Journal articles on the topic 'Feedback neuron'

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1

Vidybida, Alexander. "Relation Between Firing Statistics of Spiking Neuron with Instantaneous Feedback and Without Feedback." Fluctuation and Noise Letters 14, no. 04 (November 9, 2015): 1550034. http://dx.doi.org/10.1142/s0219477515500340.

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We consider a class of spiking neuron models, defined by a set of conditions which are typical for basic threshold-type models like leaky integrate-and-fire, or binding neuron model and also for some artificial neurons. A neuron is fed with a point renewal process. A relation between the three probability density functions (PDF): (i) PDF of input interspike intervals ISIs, (ii) PDF of output interspike intervals of a neuron with a feedback and (iii) PDF for that same neuron without feedback is derived. This allows to calculate any one of the three PDFs provided the remaining two are given. Similar relation between corresponding means and variances is derived. The relations are checked exactly for the binding neuron model stimulated with Poisson stream.
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2

Spencer, Robert M., and Dawn M. Blitz. "Network feedback regulates motor output across a range of modulatory neuron activity." Journal of Neurophysiology 115, no. 6 (June 1, 2016): 3249–63. http://dx.doi.org/10.1152/jn.01112.2015.

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Modulatory projection neurons alter network neuron synaptic and intrinsic properties to elicit multiple different outputs. Sensory and other inputs elicit a range of modulatory neuron activity that is further shaped by network feedback, yet little is known regarding how the impact of network feedback on modulatory neurons regulates network output across a physiological range of modulatory neuron activity. Identified network neurons, a fully described connectome, and a well-characterized, identified modulatory projection neuron enabled us to address this issue in the crab ( Cancer borealis) stomatogastric nervous system. The modulatory neuron modulatory commissural neuron 1 (MCN1) activates and modulates two networks that generate rhythms via different cellular mechanisms and at distinct frequencies. MCN1 is activated at rates of 5–35 Hz in vivo and in vitro. Additionally, network feedback elicits MCN1 activity time-locked to motor activity. We asked how network activation, rhythm speed, and neuron activity levels are regulated by the presence or absence of network feedback across a physiological range of MCN1 activity rates. There were both similarities and differences in responses of the two networks to MCN1 activity. Many parameters in both networks were sensitive to network feedback effects on MCN1 activity. However, for most parameters, MCN1 activity rate did not determine the extent to which network output was altered by the addition of network feedback. These data demonstrate that the influence of network feedback on modulatory neuron activity is an important determinant of network output and feedback can be effective in shaping network output regardless of the extent of network modulation.
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3

Vidybida, Alexander, and Olha Shchur. "Relation Between Firing Statistics of Spiking Neuron with Delayed Fast Inhibitory Feedback and Without Feedback." Fluctuation and Noise Letters 17, no. 01 (January 23, 2018): 1850005. http://dx.doi.org/10.1142/s0219477518500050.

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We consider a class of spiking neuronal models, defined by a set of conditions typical for basic threshold-type models, such as the leaky integrate-and-fire or the binding neuron model and also for some artificial neurons. A neuron is fed with a Poisson process. Each output impulse is applied to the neuron itself after a finite delay [Formula: see text]. This impulse acts as being delivered through a fast Cl-type inhibitory synapse. We derive a general relation which allows calculating exactly the probability density function (pdf) [Formula: see text] of output interspike intervals of a neuron with feedback based on known pdf [Formula: see text] for the same neuron without feedback and on the properties of the feedback line (the [Formula: see text] value). Similar relations between corresponding moments are derived.Furthermore, we prove that the initial segment of pdf [Formula: see text] for a neuron with a fixed threshold level is the same for any neuron satisfying the imposed conditions and is completely determined by the input stream. For the Poisson input stream, we calculate that initial segment exactly and, based on it, obtain exactly the initial segment of pdf [Formula: see text] for a neuron with feedback. That is the initial segment of [Formula: see text] is model-independent as well. The obtained expressions are checked by means of Monte Carlo simulation. The course of [Formula: see text] has a pronounced peculiarity, which makes it impossible to approximate [Formula: see text] by Poisson or another simple stochastic process.
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4

HAYOT, FERNAND, and DANIEL TRANCHINA. "Modeling corticofugal feedback and the sensitivity of lateral geniculate neurons to orientation discontinuity." Visual Neuroscience 18, no. 6 (November 2001): 865–77. http://dx.doi.org/10.1017/s0952523801186037.

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We model feedback from primary visual cortex to the dorsal lateral geniculate nucleus (dLGN). This feedback makes dLGN neurons sensitive to orientation discontinuity (Sillito et al., 1993; Cudeiro & Sillito, 1996). In the model, each dLGN neuron receives retinotopic input driven by layer 6 cortical neurons in a full set of orientation columns. Excitation is monosynaptic, while inhibition is through perigeniculate neurons and dLGN interneurons. The stimulus consists of drifting gratings, one within and the other outside a circular region centered over the receptive field of the model dLGN relay neuron we study. They appear as a single grating when they are aligned with equal contrast. The model reproduces experimental results showing an increasing inhibitory effect of feedback on the firing rate of dLGN neurons as the two gratings move towards the aligned position. Moreover, enhancement of dLGN cell center-surround antagonism by feedback is revealed by measuring the responses to drifting gratings inside a circular window, as a function of window radius. This effect is related to the observed length tuning of dLGN cells. Sensitivity to orientation discontinuity could be mediated in the model by feedback from either simple or complex cells. The model puts constraints on the feedback synaptic footprint and shows that its elongated shape does not play a crucial role in sensitivity to orientation discontinuity. The inhibitory component of feedback must predominate overall, but the feedback signal from a cortical neuron to a dLGN neuron with the same or nearby receptive-field center can be dominated by excitation. Predictions of the model include (1) robust stimuli for layer 6 cortical neurons give pronounced nonlinearities in the responses of dLGN neurons; (2) the sensitivity to orientation discontinuity at low contrast is twice that at high contrast.
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5

Blitz, Dawn M. "Circuit feedback increases activity level of a circuit input through interactions with intrinsic properties." Journal of Neurophysiology 118, no. 2 (August 1, 2017): 949–63. http://dx.doi.org/10.1152/jn.00772.2016.

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Feedback from central pattern generator (CPG) circuits patterns activity of their projection neuron inputs. However, whether the intraburst firing rate between rhythmic feedback inhibition is also impacted by CPG feedback was not known. I establish that CPG feedback can alter the projection neuron intraburst firing rate through interactions with projection neuron intrinsic properties. The contribution of feedback to projection neuron activity level is specific to the modulatory condition, demonstrating a state dependence for this novel role of circuit feedback.
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6

Torres-Treviño, Luis M., Angel Rodríguez-Liñán, Luis González-Estrada, and Gustavo González-Sanmiguel. "Single Gaussian Chaotic Neuron: Numerical Study and Implementation in an Embedded System." Discrete Dynamics in Nature and Society 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/318758.

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Artificial Gaussian neurons are very common structures of artificial neural networks like radial basis function. These artificial neurons use a Gaussian activation function that includes two parameters called the center of mass (cm) and sensibility factor (λ). Changes on these parameters determine the behavior of the neuron. When the neuron has a feedback output, complex chaotic behavior is displayed. This paper presents a study and implementation of this particular neuron. Stability of fixed points, bifurcation diagrams, and Lyapunov exponents help to determine the dynamical nature of the neuron, and its implementation on embedded system illustrates preliminary results toward embedded chaos computation.
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7

Xu, Yao-Qun, Xin-Xin Zhen, and Meng Tang. "Dynamical System in Chaotic Neurons with Time Delay Self-Feedback and Its Application in Color Image Encryption." Complexity 2022 (July 1, 2022): 1–28. http://dx.doi.org/10.1155/2022/2832104.

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The time delay caused by transmission in neurons is often ignored, but it is demonstrated by theories and practices that time delay is unavoidable. A new chaotic neuron model with time delay self-feedback is proposed based on Chen’s chaotic neuron. The bifurcation diagram and Lyapunov exponential diagram are used to analyze the chaotic characteristics of neurons in the model when they receive the output signals at different times. The experimental results exhibit that it has a rich dynamic behavior. In addition, the randomness of chaotic series generated by chaotic neurons with time delay self-feedback under different conditions is verified. In order to investigate the application of this model in image encryption, an image encryption scheme is proposed. The security analysis of the simulation results shows that the encryption algorithm has an excellent anti-attack ability. Therefore, it is necessary and practical to study chaotic neurons with time delay self-feedback.
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8

Cardi, P., and F. Nagy. "A rhythmic modulatory gating system in the stomatogastric nervous system of Homarus gammarus. III. Rhythmic control of the pyloric CPG." Journal of Neurophysiology 71, no. 6 (June 1, 1994): 2503–16. http://dx.doi.org/10.1152/jn.1994.71.6.2503.

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1. Two modulatory neurons, P and commissural pyloric (CP), known to be involved in the long-term maintenance of pyloric central pattern generator operation in the rock lobster Homarus gammarus, are members of the commissural pyloric oscillator (CPO), a higher-order oscillator influencing the pyloric network. 2. The CP neuron was endogenously oscillating in approximately 30% of the preparations in which its cell body was impaled. Rhythmic inhibitory feedback from the pyloric pacemaker anterior burster (AB) neuron stabilized the CP neuron's endogenous rhythm. 3. The organization of the CPO is described. Follower commissural neurons, the F cells, and the CP neuron receive a common excitatory postsynaptic potential from another commissural neuron, the large exciter (LE). When in oscillatory state, CP in turn excites the LE neuron. This positive feedback may maintain long episodes of CP oscillations. 4. The pyloric pacemaker neurons follow the CPO rhythm with variable coordination modes (i.e., 1:1, 1:2) and switch among these modes when their membrane potential is modified. The CPO inputs strongly constrain the pyloric period, which as a result may adopt only a few discrete values. This effect is based on mechanisms of entrainment between the CPO and the pyloric oscillator. 5. Pyloric constrictor neurons show differential sensitivity from the pyloric pacemaker neurons with respect to the CPO inputs. Consequently, their bursting period can be a shorter harmonic of the bursting period of the pyloric pacemakers neurons. 6. The CPO neurons seem to be the first example of modulatory gating neurons that also give timing cues to a rhythmic pattern generating network.
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9

Rybak, Ilya A., Julian F. R. Paton, and James S. Schwaber. "Modeling Neural Mechanisms for Genesis of Respiratory Rhythm and Pattern. II. Network Models of the Central Respiratory Pattern Generator." Journal of Neurophysiology 77, no. 4 (April 1, 1997): 2007–26. http://dx.doi.org/10.1152/jn.1997.77.4.2007.

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Rybak, Ilya A., Julian F. R. Paton, and James S. Schwaber. Modeling neural mechanisms for genesis of respiratory rhythm and pattern. II. Network models of the central respiratory pattern generator. J. Neurophysiol. 77: 2007–2026, 1997. The present paper describes several models of the central respiratory pattern generator (CRPG) developed employing experimental data and current hypotheses for respiratory rhythmogenesis. Each CRPG model includes a network of respiratory neuron types (e.g., early inspiratory; ramp inspiratory; late inspiratory; decrementing expiratory; postinspiratory; stage II expiratory; stage II constant firing expiratory; preinspiratory) and simplified models of lung and pulmonary stretch receptors (PSR), which provide feedback to the respiratory network. The used models of single respiratory neurons were developed in the Hodgkin-Huxley style as described in the previous paper. The mechanism for termination of inspiration (the inspiratory off-switch) in all models operates via late-I neuron, which is considered to be the inspiratory off-switching neuron. Several two- and three-phase CRPG models have been developed using different accepted hypotheses of the mechanism for termination of expiration. The key elements in the two-phase models are the early-I and dec-E neurons. The expiratory off-switch mechanism in these models is based on the mutual inhibitory connections between early-I and dec-E and adaptive properties of the dec-E neuron. The difference between the two-phase models concerns the mechanism for ramp firing patterns of E2 neurons resulting either from the intrinsic neuronal properties of the E2 neuron or from disinhibition from the adapting dec-E neuron. The key element of the three-phase models is the pre-I neuron, which acts as the expiratory off-switching neuron. The three-phase models differ by the mechanisms used for termination of expiration and for the ramp firing patterns of E2 neurons. Additional CRPG models were developed employing a dual switching neuron that generates two bursts per respiratory cycle to terminate both inspiration and expiration. Although distinctly different each model generates a stable respiratory rhythm and shows physiologically plausible firing patterns of respiratory neurons with and without PSR feedback. Using our models, we analyze the roles of different respiratory neuron types and their interconnections for the respiratory rhythm and pattern generation. We also investigate the possible roles of intrinsic biophysical properties of different respiratory neurons in controlling the duration of respiratory phases and timing of switching between them. We show that intrinsic membrane properties of respiratory neurons are integrated with network properties of the CRPG at three hierarchical levels: at the cellular level to provide the specific firing patterns of respiratory neurons (e.g., ramp firing patterns); at the network level to provide switching between the respiratory phases; and at the systems level to control the duration of inspiration and expiration under different conditions (e.g., lack of PSR feedback).
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10

Chambers, Jordan D., Joel C. Bornstein, Henrik Sjövall, and Evan A. Thomas. "Recurrent networks of submucous neurons controlling intestinal secretion: a modeling study." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 5 (May 2005): G887—G896. http://dx.doi.org/10.1152/ajpgi.00491.2004.

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Secretomotor neurons, immunoreactive for vasoactive intestinal peptide (VIP), are important in controlling chloride secretion in the small intestine. These neurons form functional synapses with other submucosal VIP neurons and transmit via slow excitatory postsynaptic potentials (EPSPs). Thus they form a recurrent network with positive feedback. Intrinsic sensory neurons within the submucosa are also likely to form recurrent networks with positive feedback, provide substantial output to VIP neurons, and receive input from VIP neurons. If positive feedback within recurrent networks is sufficiently large, then neurons in the network respond to even small stimuli by firing at their maximum possible rate, even after the stimulus is removed. However, it is not clear whether such a mechanism operates within the recurrent networks of submucous neurons. We investigated this question by performing computer simulations of realistic models of VIP and intrinsic sensory neuron networks. In the expected range of electrophysiological properties, we found that activity in the VIP neuron network decayed slowly after cessation of a stimulus, indicating that positive feedback is not strong enough to support the uncontrolled firing state. The addition of intrinsic sensory neurons produced a low stable firing rate consistent with the common finding that basal secretory activity is, in part, neurogenic. Changing electrophysiological properties enables these recurrent networks to support the uncontrolled firing state, which may have implications with hypersecretion in the presence of enterotoxins such as cholera-toxin.
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11

Wang, Chunni, Shengli Guo, Ying Xu, Jun Ma, Jun Tang, Faris Alzahrani, and Aatef Hobiny. "Formation of Autapse Connected to Neuron and Its Biological Function." Complexity 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/5436737.

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Autapse is a specific synapse connected to the neuron via close loop, and its functional adjusting is described by applying time-delayed feedback on the membrane potential of the neuron. This paper discussed the possible formation mechanism and biological function of autapse connection on neurons. We believe that the formation and growth of autapse connected to neuron can be associated with injury on axon and blocking in signal transmission; thus auxiliary loop is developed to form an autapse. When autapse is set up, it can propagate the signals and change the modes of electrical activities under self-adaption. Based on the cable neuron model, the injury on axon is generated by poisoning and blocking in ion channels (of sodium); thus the conductance of ion channels are changed to form injury-associated defects. Furthermore, auxiliary loop with time delay is designed to restore and enhance signal propagation by setting different time delays and feedback gains. The numerical studies confirmed that appropriate time delay and feedback gain in electric or chemical autapse can help signal (or wave generated by external forcing) propagation across the blocked area. As a result, formation of autapse could be dependent on the injury of neuron and further enhances the self-adaption to external stimuli.
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12

HERRMANN, CHRISTOPH S., and ANDREAS KLAUS. "AUTAPSE TURNS NEURON INTO OSCILLATOR." International Journal of Bifurcation and Chaos 14, no. 02 (February 2004): 623–33. http://dx.doi.org/10.1142/s0218127404009338.

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Recently, neurobiologists have discovered axons on neurons which synapse on the same neuron's dendrites — so-called autapses. It is not yet clear what functional significance autapses offer for neural behavior. This is an ideal case for using a physical simulation to investigate how an autapse alters the firing of a neuron. We simulated a neural basket cell via the Hodgkin–Huxley equations and implemented an autapse which feeds back onto the soma of the neuron. The behavior of the cell was compared with and without autaptic feedback. Our artificial autapse neuron (AAN) displays oscillatory behavior which is not observed for the same model neuron without autapse. The neuron oscillates between two functional states: one where it fires at high frequency and another where firing is suppressed. This behavior is called "spike bursting" and represents a common pattern recorded from cerebral neurons.
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13

Shchur, Olha, and Alexander Vidybida. "First Passage Time Distribution for Spiking Neuron with Delayed Excitatory Feedback." Fluctuation and Noise Letters 19, no. 01 (July 11, 2019): 2050005. http://dx.doi.org/10.1142/s0219477520500054.

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A class of spiking neuronal models with threshold 2 is considered. It is defined by a set of conditions typical for basic threshold-type models, such as the leaky integrate-and-fire (LIF) or the binding neuron model, and also for some artificial neurons. A neuron is stimulated with a Poisson stream of excitatory impulses. Each output impulse is conveyed through the feedback line to the neuron input after finite delay [Formula: see text]. This impulse is identical to those delivered from the input stream. We have obtained a general relation allowing calculating exactly the probability density function (PDF) [Formula: see text] for distribution of the first passage time of crossing the threshold, which is the distribution of output interspike intervals (ISI) values for this neuron. The calculation is based on known PDF [Formula: see text] for that same neuron without feedback, intensity of the input stream [Formula: see text] and properties of the feedback line. Also, we derive exact relation for calculating the moments of [Formula: see text] based on known moments of [Formula: see text]. The obtained general expression for [Formula: see text] is checked numerically using Monte Carlo simulation for the case of LIF model. The course of [Formula: see text] has a [Formula: see text]-function-type peculiarity. This fact contributes to the discussion about the possibility to model neuronal activity with Poisson process, supporting the “no” answer.
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14

Xu, Ying, Ya Jia, John Billy Kirunda, Jian Shen, Mengyan Ge, Lulu Lu, and Qiming Pei. "Dynamic Behaviors in Coupled Neuron System with the Excitatory and Inhibitory Autapse under Electromagnetic Induction." Complexity 2018 (July 26, 2018): 1–13. http://dx.doi.org/10.1155/2018/3012743.

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The induced current produced by electromagnetic induction can adjust the membrane potential of neuron through the feedback of a magnetic flux-controlled memristor. We adopt the numerical simulation method with the aim of investigating the synchronous behavior in the neuronal system that is coupled by chemical and electrical synapses under electromagnetic induction. Within the improved model, the effects of electromagnetic induction on neurons are described with additive memristive current on the membrane variable, and the memristive current is dependent on the variation of magnetic flow. The simulation results show that the two coupling modes play an important role in the synchronization of the system. By increasing the chemical synaptic feedback gain, we observe a transition from mixed oscillatory to periodic state at a critical value. In addition, two Hopf bifurcation points are found with the change of the external stimuli, and the state of neuron discharge is influenced by initial values. Furthermore, there is a domain of coupling strength and feedback gain values, in which the two coupled neuron system is synchronized and longer time lag is not conducive to the system synchronization.
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15

Vidybida, Alexander, and Kseniia Kravchuk. "Spiking Statistics of Excitatory Neuron with Feedback." International Journal of Organizational and Collective Intelligence 3, no. 2 (April 2012): 1–42. http://dx.doi.org/10.4018/joci.2012040101.

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Firing statistics of excitatory binding neuron (BN) is considered. The neuron is driven externally by a Poisson stream. Influence of feedback, which conveys every output impulse to the input with time delay , on the statistics of output spikes is studied. The resulting output stream is not Poissonian, and the authors obtain its inter-spike intervals (ISI) distribution for the case of BN, BN with instantaneous, , and delayed, , feedback. Output statistics of neuron with delayed feedback differs essentially from that found for the case of no feedback as well as from the case of instantaneous feedback. ISI distributions, found for delayed feedback, are characterized with jumps, derivative discontinuities and include -function type singularity. Also, for non-zero refractory time, the authors obtain multiple-ISI conditional probability density and prove, that delayed feedback presence results in non-Markovian statistics of neuronal firing. It is concluded, that delayed feedback presence can radically change neuronal firing statistics.
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16

Taylan, Osman, Mona Abusurrah, Ehsan Eftekhari-Zadeh, Ehsan Nazemi, Farheen Bano, and Ali Roshani. "Controlling Effects of Astrocyte on Neuron Behavior in Tripartite Synapse Using VHDL–AMS." Mathematics 9, no. 21 (October 25, 2021): 2700. http://dx.doi.org/10.3390/math9212700.

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Astrocyte cells form the largest cell population in the brain and can influence neuron behavior. These cells provide appropriate feedback control in regulating neuronal activities in the Central Nervous System (CNS). This paper presents a set of equations as a model to describe the interactions between neurons and astrocyte. A VHDL–AMS-based tripartite synapse model that includes a pre-synaptic neuron, the synaptic terminal, a post-synaptic neuron, and an astrocyte cell is presented. In this model, the astrocyte acts as a controller module for neurons and can regulates the spiking activity of them. Simulation results show that by regulating the coupling coefficients of astrocytes, spiking frequency of neurons can be reduced and the activity of neuronal cells is modulated.
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17

Ruka, Kristen A., Laura L. Burger, and Suzanne M. Moenter. "Both Estrogen and Androgen Modify the Response to Activation of Neurokinin-3 and κ-Opioid Receptors in Arcuate Kisspeptin Neurons From Male Mice." Endocrinology 157, no. 2 (November 12, 2015): 752–63. http://dx.doi.org/10.1210/en.2015-1688.

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Abstract Gonadal steroids regulate the pattern of GnRH secretion. Arcuate kisspeptin (kisspeptin, neurokinin B, and dynorphin [KNDy]) neurons may convey steroid feedback to GnRH neurons. KNDy neurons increase action potential firing upon the activation of neurokinin B receptors (neurokinin-3 receptor [NK3R]) and decrease firing upon the activation of dynorphin receptors (κ-opioid receptor [KOR]). In KNDy neurons from intact vs castrated male mice, NK3R-mediated stimulation is attenuated and KOR-mediated inhibition enhanced, suggesting gonadal secretions are involved. Estradiol suppresses spontaneous GnRH neuron firing in male mice, but the mediators of the effects on firing in KNDy neurons are unknown. We hypothesized the same gonadal steroids affecting GnRH firing pattern would regulate KNDy neuron response to NK3R and KOR agonists. To test this possibility, extracellular recordings were made from KNDy neurons in brain slices from intact, untreated castrated or castrated adult male mice treated in vivo with steroid receptor agonists. As observed previously, the stimulation of KNDy neurons by the NK3R agonist senktide was attenuated in intact vs castrated mice and suppression by dynorphin was enhanced. In contrast to observations of steroid effects on the GnRH neuron firing pattern, both estradiol and DHT suppressed senktide-induced KNDy neuron firing and enhanced the inhibition caused by dynorphin. An estrogen receptor-α agonist but not an estrogen receptor-β agonist mimicked the effects of estradiol on NK3R activation. These observations suggest the steroid modulation of responses to activation of NK3R and KOR as mechanisms for negative feedback in KNDy neurons and support the contribution of these neurons to steroid-sensitive elements of a GnRH pulse generator.
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18

White, Rachel S., Robert M. Spencer, Michael P. Nusbaum, and Dawn M. Blitz. "State-dependent sensorimotor gating in a rhythmic motor system." Journal of Neurophysiology 118, no. 5 (November 1, 2017): 2806–18. http://dx.doi.org/10.1152/jn.00420.2017.

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Sensory feedback influences motor circuits and/or their projection neuron inputs to adjust ongoing motor activity, but its efficacy varies. Currently, less is known about regulation of sensory feedback onto projection neurons that control downstream motor circuits than about sensory regulation of the motor circuit neurons themselves. In this study, we tested whether sensory feedback onto projection neurons is sensitive only to activation of a motor system, or also to the modulatory state underlying that activation, using the crab Cancer borealis stomatogastric nervous system. We examined how proprioceptor neurons (gastropyloric receptors, GPRs) influence the gastric mill (chewing) circuit neurons and the projection neurons (MCN1, CPN2) that drive the gastric mill rhythm. During gastric mill rhythms triggered by the mechanosensory ventral cardiac neurons (VCNs), GPR was shown previously to influence gastric mill circuit neurons, but its excitation of MCN1/CPN2 was absent. In this study, we tested whether GPR effects on MCN1/CPN2 are also absent during gastric mill rhythms triggered by the peptidergic postoesophageal commissure (POC) neurons. The VCN and POC pathways both trigger lasting MCN1/CPN2 activation, but their distinct influence on circuit feedback to these neurons produces different gastric mill motor patterns. We show that GPR excites MCN1 and CPN2 during the POC-gastric mill rhythm, altering their firing rates and activity patterns. This action changes both phases of the POC-gastric mill rhythm, whereas GPR only alters one phase of the VCN-gastric mill rhythm. Thus sensory feedback to projection neurons can be gated as a function of the modulatory state of an active motor system, not simply switched on/off with the onset of motor activity. NEW & NOTEWORTHY Sensory feedback influences motor systems (i.e., motor circuits and their projection neuron inputs). However, whether regulation of sensory feedback to these projection neurons is consistent across different versions of the same motor pattern driven by the same motor system was not known. We found that gating of sensory feedback to projection neurons is determined by the modulatory state of the motor system, and not simply by whether the system is active or inactive.
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19

Christian, Catherine A., and Suzanne M. Moenter. "Vasoactive Intestinal Polypeptide Can Excite Gonadotropin-Releasing Hormone Neurons in a Manner Dependent on Estradiol and Gated by Time of Day." Endocrinology 149, no. 6 (March 6, 2008): 3130–36. http://dx.doi.org/10.1210/en.2007-1098.

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A surge of GnRH release signals the LH surge that triggers ovulation. The GnRH surge is dependent on a switch in estradiol feedback from negative to positive and, in rodents, a daily neural signal, likely from the suprachiasmatic nuclei. Vasoactive intestinal polypeptide (VIP) may be involved in suprachiasmatic nuclei-GnRH neuron communication. Here we assessed the effects of acute VIP (5 min treatment) on GnRH neuron function using targeted extracellular recordings of firing activity of GnRH neurons in brain slices. We examined the effect of VIP on firing rate at different times of day using an established ovariectomized, estradiol-treated (OVX+E) mouse model that exhibits daily LH surges timed to the late afternoon. Cells from OVX animals (no estradiol) did not respond to VIP, regardless of time of day. With estradiol, the effect of VIP on GnRH neurons was dependent on the time of recording. During negative feedback, OVX+E cells did not respond. VIP increased firing in cells recorded during surge onset, but this excitatory response was reduced at surge peak. Acute treatment of OVX+E cells during surge peak with a VIP receptor antagonist decreased GnRH neuron firing. This suggests endogenous VIP may both increase GnRH neuron firing during the surge and occlude response to exogenous VIP. These data provide functional evidence for VIP effects on GnRH neurons and indicate that both estradiol and time of day gate the GnRH neuron response to this peptide. VIP may provide an excitatory signal from the circadian clock that helps time the GnRH surge.
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20

Takahashi, T., O. Koizumi, Y. Ariura, A. Romanovitch, T. C. Bosch, Y. Kobayakawa, S. Mohri, et al. "A novel neuropeptide, Hym-355, positively regulates neuron differentiation in Hydra." Development 127, no. 5 (March 1, 2000): 997–1005. http://dx.doi.org/10.1242/dev.127.5.997.

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During the course of a systematic screening of peptide signaling molecules in Hydra a novel peptide, Hym-355 (FPQSFLPRG-NH(2)), was identified. A cDNA encoding the peptide was isolated and characterized. Using both in situ hybridization and immunohistochemistry, Hym-355 was shown to be expressed in neurons and hence is a neuropeptide. The peptide was shown to specifically enhance neuron differentiation throughout the animal by inducing interstitial cells to enter the neuron pathway. Further, co-treatment with a PW peptide, which inhibits neuron differentiation, nullified the effects of both peptides, suggesting that they act in an antagonistic manner. This effect is discussed in terms of a feedback mechanism for maintaining the steady state neuron population in Hydra.
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21

LIN, WEI, and TIANPING CHEN. "CONTROLLING CHAOS IN A CHAOTIC NEURON MODEL." International Journal of Bifurcation and Chaos 15, no. 08 (August 2005): 2611–21. http://dx.doi.org/10.1142/s0218127405013551.

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In this paper we investigate several methods for controlling chaos in Aihara's chaotic neuron model. We first discuss the stability of exponential feedback control method for this model. To obviate predetermining the unstable periodic orbits of the system, two other methods are developed. We analyze why the conventional delayed feedback control method cannot be employed here, and then give a modified form for recursive delayed feedback control and apply it to control chaos in this model. To obtain high-periodic orbits more easily, a delayed exponential feedback control method is proposed, by which we can obtain different periodic orbits by changing parameters. Computer simulations show good control effects and robustness against noise.
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Kumar, Devesh, Michael Candlish, Vinod Periasamy, Nergiz Avcu, Christian Mayer, and Ulrich Boehm. "Specialized Subpopulations of Kisspeptin Neurons Communicate With GnRH Neurons in Female Mice." Endocrinology 156, no. 1 (January 1, 2015): 32–38. http://dx.doi.org/10.1210/en.2014-1671.

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Abstract The neuropeptide kisspeptin is a potent stimulator of GnRH neurons and has been implicated as a major regulator of the hypothalamus-pituitary-gonadal axis. There are mainly two anatomically segregated populations of neurons that express kisspeptin in the female hypothalamus: one in the anteroventral periventricular nucleus (AVPV) and the other in the arcuate nucleus (ARC). Distinct roles have been proposed for AVPV and ARC kisspeptin neurons during reproductive maturation and in mediating estrogen feedback on the hypothalamus-pituitary-gonadal axis in adults. Despite their pivotal role in the regulation of reproductive physiology, little is known about kisspeptin neuron connectivity. Although previous data suggest heterogeneity within the AVPV and ARC kisspeptin neuron populations, how many and which of these potential kisspeptin neuron subpopulations are actually communicating with GnRH neurons is not known. Here we used a combinatorial genetic transsynaptic tracing strategy to start to analyze the connectivity of individual kisspeptin neurons with the GnRH neuron population in female mice with a single-cell resolution. We find that only subsets of AVPV and ARC kisspeptin neurons are synaptically connected with GnRH neurons. We demonstrate that the majority of kisspeptin neurons within the AVPV and ARC does not communicate with GnRH neurons. Furthermore, we show that all kisspeptin neurons within the AVPV connected to GnRH neurons are estrogen sensitive and that most of these express tyrosine hydroxylase. Our data demonstrate functional specialization within the two kisspeptin neuron populations.
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HSU, CHENG-HSIUNG, SUH-YUH YANG, TING-HUI YANG, and TZI-SHENG YANG. "ON PERIODIC SOLUTIONS OF A TWO-NEURON NETWORK SYSTEM WITH SIGMOIDAL ACTIVATION FUNCTIONS." International Journal of Bifurcation and Chaos 16, no. 05 (May 2006): 1405–17. http://dx.doi.org/10.1142/s0218127406015386.

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In this paper we study the existence, uniqueness and stability of periodic solutions for a two-neuron network system with or without external inputs. The system consists of two identical neurons, each possessing nonlinear feedback and connected to the other neuron via a nonlinear sigmoidal activation function. In the absence of external inputs but with appropriate conditions on the feedback and connection strengths, we prove the existence, uniqueness and stability of periodic solutions by using the Poincaré–Bendixson theorem together with Dulac's criterion. On the other hand, for the system with periodic external inputs, combining the techniques of the Liapunov function with the contraction mapping theorem, we propose some sufficient conditions for establishing the existence, uniqueness and exponential stability of the periodic solutions. Some numerical results are also provided to demonstrate the theoretical analysis.
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CHAKRAVARTHY, NIRANJAN, SHIVKUMAR SABESAN, LEON IASEMIDIS, and KOSTAS TSAKALIS. "CONTROLLING SYNCHRONIZATION IN A NEURON-LEVEL POPULATION MODEL." International Journal of Neural Systems 17, no. 02 (April 2007): 123–38. http://dx.doi.org/10.1142/s0129065707000993.

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We have studied coupled neural populations in an effort to understand basic mechanisms that maintain their normal synchronization level despite changes in the inter-population coupling levels. Towards this goal, we have incorporated coupling and internal feedback structures in a neuron-level population model from the literature. We study two forms of internal feedback — regulation of excitation, and compensation of excessive excitation with inhibition. We show that normal feedback actions quickly regulate/compensate an abnormally high coupling between the neural populations, whereas a pathology in these feedback actions can lead to abnormal synchronization and "seizure"-like high amplitude oscillations. We then develop an external control paradigm, termed feedback decoupling, as a robust synchronization control strategy. The external feedback decoupling controller acts to achieve the operational objective of maintaining normal-level synchronous behavior irrespective of the pathology in the internal feedback mechanisms. Results from such an analysis have an interesting physical interpretation and specific implications for the treatment of diseases such as epilepsy. The proposed remedy is consistent with a variety of recent observations in the human and animal epileptic brain, and with theories from nonlinear systems, adaptive systems, optimization, and neurophysiology.
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Moore, Aleisha M., Melanie Prescott, and Rebecca E. Campbell. "Estradiol Negative and Positive Feedback in a Prenatal Androgen-Induced Mouse Model of Polycystic Ovarian Syndrome." Endocrinology 154, no. 2 (December 19, 2012): 796–806. http://dx.doi.org/10.1210/en.2012-1954.

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Gonadal steroid hormone feedback is impaired in polycystic ovarian syndrome (PCOS), a common endocrine disorder characterized by hyperandrogenism and an associated increase in LH pulse frequency. Using a prenatal androgen (PNA)-treated mouse model of PCOS, we aimed to investigate negative and positive feedback effects of estrogens on the hypothalamic-pituitary axis regulation of LH. PNA-treated mice exhibited severely disrupted estrous cycles, hyperandrogenism, significantly reduced fertility, and altered ovarian morphology. To assess the negative feedback effects of estrogens, LH was measured before and after ovariectomy and after estradiol (E2) administration. Compared with controls, PNA-treated mice exhibited a blunted postcastration rise in LH (P < .001) and an absence of LH suppression after E2 administration. To assess E2-positive feedback, control and PNA-treated GnRH-green fluorescent protein transgenic mice were subjected to a standard ovariectomy with E2-replacement regimen, and both plasma and perfusion-fixed brains were collected at the time of the expected GnRH/LH surge. Immunocytochemistry and confocal imaging of cFos and green fluorescent protein were used to assess GnRH neuron activation and spine density. In the surged group, both control and PNA-treated mice had significantly increased LH and cFos activation in GnRH neurons (P < .05) compared with nonsurged animals. Spine density was quantified in cFos-positive and -negative GnRH neurons to examine whether there was an increase in spine density in cFos-expressing GnRH neurons of surged mice as expected. A significant increase in spine density in cFos-expressing GnRH neurons was evident in control animals; however, no significant increase was observed in the PNA-treated mice because spine density was elevated across all GnRH neurons. These data support that PNA treatment results in a PCOS-like phenotype that includes impaired E2-negative feedback. Additionally, although E2-positive feedback capability is retained in PNA mice, elevated GnRH neuron spine density may reflect altered synaptic regulation.
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Cheong, Rachel Y., Robert Porteous, Pierre Chambon, István Ábrahám, and Allan E. Herbison. "Effects of Neuron-Specific Estrogen Receptor (ER) α and ERβ Deletion on the Acute Estrogen Negative Feedback Mechanism in Adult Female Mice." Endocrinology 155, no. 4 (April 1, 2014): 1418–27. http://dx.doi.org/10.1210/en.2013-1943.

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The negative feedback mechanism through which 17β-estradiol (E2) acts to suppress the activity of the GnRH neurons remains unclear. Using inducible and cell-specific genetic mouse models, we examined the estrogen receptor (ER) isoforms expressed by neurons that mediate acute estrogen negative feedback. Adult female mutant mice in which ERα was deleted from all neurons in the neonatal period failed to exhibit estrous cycles or negative feedback. Adult mutant female mice with neonatal neuronal ERβ deletion exhibited normal estrous cycles, but a failure of E2 to suppress LH secretion was seen in ovariectomized mice. Mutant mice with a GnRH neuron–selective deletion of ERβ exhibited normal cycles and negative feedback, suggesting no critical role for ERβ in GnRH neurons in acute negative feedback. To examine the adult roles of neurons expressing ERα, an inducible tamoxifen-based Cre-LoxP approach was used to ablate ERα from neurons that express calmodulin kinase IIα in adults. This resulted in mice with no estrous cycles, a normal increase in LH after ovariectomy, but an inability of E2 to suppress LH secretion. Finally, acute administration of ERα- and ERβ-selective agonists to adult ovariectomized wild-type mice revealed that activation of ERα suppressed LH secretion, whereas ERβ agonists had no effect. This study highlights the differences in adult reproductive phenotypes that result from neonatal vs adult ablation of ERα in the brain. Together, these experiments expand previous global knockout studies by demonstrating that neurons expressing ERα are essential and probably sufficient for the acute estrogen negative feedback mechanism in female mice.
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Pielecka, Justyna, Samuel D. Quaynor, and Suzanne M. Moenter. "Androgens Increase Gonadotropin-Releasing Hormone Neuron Firing Activity in Females and Interfere with Progesterone Negative Feedback." Endocrinology 147, no. 3 (March 1, 2006): 1474–79. http://dx.doi.org/10.1210/en.2005-1029.

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GnRH neurons are the central regulators of fertility, and their activity is modulated by steroid feedback. In women with hyperandrogenemic infertility and in animal models of these disorders, elevated androgen levels interfere with progesterone (P) negative feedback. Our previous work showed that steroids altered the frequency and amplitude of γ-aminobutyric acid (GABA) transmission to GnRH neurons. Specifically, P inhibited GABA transmission, which can excite GnRH neurons, whereas dihydrotestosterone (DHT) increased GABA transmission. In this study the GnRH neuron firing rate was examined in the same animal models. Adult (>2 months) female mice were ovariectomized and treated for 8–12 d with implants containing estradiol (E), E and P, E and DHT, or E, P, and DHT. Targeted extracellular recordings were used to examine the long-term firing activity of green fluorescent protein-identified GnRH neurons in brain slices from these mice. In comparing E alone to E plus P animals, P increased the percentage of time that GnRH neurons were quiescent and reduced the area under the curve of the firing rate and the instantaneous firing frequency, suggesting that P provides additional negative feedback over E alone. The addition of DHT markedly increased GnRH neuron activity in both the presence and absence of P. DHT also altered the firing pattern of GnRH neurons, such that peaks in the firing rate detected by the Cluster8 algorithm were approximately doubled in frequency and amplitude. These data support and extend our previous findings and are consistent with the hypothesis that the changes in GABAergic transmission observed in these animal models impact upon the activity of GnRH neurons, and central androgen action probably stimulates GnRH release.
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Zhang, Yongkui, and Nobuo Suga. "Corticofugal Feedback for Collicular Plasticity Evoked by Electric Stimulation of the Inferior Colliculus." Journal of Neurophysiology 94, no. 4 (October 2005): 2676–82. http://dx.doi.org/10.1152/jn.00549.2005.

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Focal electric stimulation of the auditory cortex, 30-min repetitive acoustic stimulation, and auditory fear conditioning each evoke shifts of the frequency-tuning curves [hereafter, best frequency (BF) shifts] of cortical and collicular neurons. The short-term collicular BF shift is produced by the corticofugal system and primarily depends on the relationship in BF between a recorded collicular and a stimulated cortical neuron or between the BF of a recorded collicular neuron and the frequency of an acoustic stimulus. However, it has been unknown whether focal electric stimulation of the inferior colliculus evokes the collicular BF shift and whether the collicular BF shift, if evoked, depends on corticofugal feedback. In our present research with the awake big brown bat, we found that focal electric stimulation of collicular neurons evoked the BF shifts of collicular neurons located near the stimulated ones; that there were two types of BF shifts: centripetal and centrifugal BF shifts, i.e., shifts toward and shifts away from the BF of stimulated neurons, respectively; and that the development of these collicular BF shifts was blocked by inactivation of the auditory cortex. Our data indicate that the collicular BF shifts (plasticity) evoked by collicular electric stimulation depended on corticofugal feedback. It should be noted that collicular BF shifts also depend on acetylcholine because it has been demonstrated that atropine (an antagonist of muscarinic acetylcholine receptors) applied to the IC blocks the development of collicular BF shifts.
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29

Vidybida, A. K. "Output stream of binding neuron with instantaneous feedback." European Physical Journal B 65, no. 4 (October 2008): 577–84. http://dx.doi.org/10.1140/epjb/e2008-00360-1.

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Vidybida, A. K., and K. G. Kravchuk. "Output stream of binding neuron with delayed feedback." European Physical Journal B 72, no. 2 (September 17, 2009): 279–87. http://dx.doi.org/10.1140/epjb/e2009-00309-x.

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31

Nunemaker, Craig S., R. Anthony DeFazio, and Suzanne M. Moenter. "Estradiol-Sensitive Afferents Modulate Long-Term Episodic Firing Patterns of GnRH Neurons." Endocrinology 143, no. 6 (June 1, 2002): 2284–92. http://dx.doi.org/10.1210/endo.143.6.8869.

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Abstract GnRH neurons comprise the final common pathway of an estrogen-sensitive pattern generator controlling fertility. To determine estradiol effects on GnRH neuron firing patterns, adult transgenic mice were ovariectomized (OVX), and half were treated with estradiol (OVX+E). One week later targeted single-unit extracellular recordings were made from GnRH neurons identified by green fluorescent protein expression. Estradiol markedly affected GnRH neuron firing patterns, increasing the percentage and duration of time these cells were quiescent (≤1 action current/min). Estradiol increased the interval between episodes of increased firing rate determined by Cluster analysis of recordings more than 45 min (OVX+E 38.8 ± 7.2 min, OVX 16.7 ± 2.1 min, n = 6 each). Possible mechanisms of estradiol modulation were examined by simultaneously blocking ionotropic secretion of γ-aminobutyric acid and glutamatergic receptors. This treatment had no effect on cells from OVX mice (n = 10), indicating episodic firing of GnRH neurons is not driven by activation of these receptors. Receptor blockade eliminated estradiol effects on GnRH neurons in the midventral preoptic area (n = 7) but not elsewhere (n = 7). Individual GnRH neurons thus display episodic firing patterns at intervals previously reported for secretory pulses. Estradiol modulates episode frequency to exert feedback control; in a substantial subset of GnRH neurons, estradiol feedback is enforced via GABAergic and/or glutamatergic afferents.
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32

Gaskins, Garrett T., and Suzanne M. Moenter. "Orexin A Suppresses Gonadotropin-Releasing Hormone (GnRH) Neuron Activity in the Mouse." Endocrinology 153, no. 8 (June 6, 2012): 3850–60. http://dx.doi.org/10.1210/en.2012-1300.

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GnRH neurons are critical for the central regulation of fertility, integrating steroidal, metabolic and other cues. GnRH neurons appear to lack receptors for many of these cues, suggesting involvement of afferent systems to convey information. Orexin A (orexin) is of interest in this regard as a neuromodulator that up-regulates metabolic activity, increases wakefulness, and affects GnRH/LH release. We examined the electrophysiological response of GnRH neurons to orexin application and how this response changes with estradiol and time of day in a defined animal model. Mice were either ovariectomized (OVX) or OVX and implanted with estradiol capsules (OVX+E). GnRH neurons from OVX+E mice exhibit low firing rates in the morning, due to estradiol-negative feedback, and high firing rates in the evening, due to positive feedback. Orexin inhibited activity of GnRH neurons from OVX mice independent of time of day. In GnRH neurons from OVX+E mice, orexin was inhibitory during the evening, suggesting orexin inhibition is not altered by estradiol. No effect of orexin was observed in OVX+E morning recordings, due to low basal GnRH activity. Inhibitory effects of orexin were mediated by the type 1 orexin receptor, but antagonism of this receptor did not increase GnRH neuron activity during estradiol-negative feedback. Spike pattern analysis revealed orexin increases interevent interval by reducing the number of single spikes and bursts. Orexin reduced spikes/burst and burst duration but did not affect intraburst interval. This suggests orexin may reduce overall firing rate by suppressing spike initiation and burst maintenance in GnRH neurons.
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33

Blitz, Dawn M., Andrew E. Christie, Aaron P. Cook, Patsy S. Dickinson, and Michael P. Nusbaum. "Similarities and differences in circuit responses to applied Gly1-SIFamide and peptidergic (Gly1-SIFamide) neuron stimulation." Journal of Neurophysiology 121, no. 3 (March 1, 2019): 950–72. http://dx.doi.org/10.1152/jn.00567.2018.

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Microcircuit modulation by peptides is well established, but the cellular/synaptic mechanisms whereby identified neurons with identified peptide transmitters modulate microcircuits remain unknown for most systems. Here, we describe the distribution of GYRKPPFNGSIFamide (Gly1-SIFamide) immunoreactivity (Gly1-SIFamide-IR) in the stomatogastric nervous system (STNS) of the crab Cancer borealis and the Gly1-SIFamide actions on the two feeding-related circuits in the stomatogastric ganglion (STG). Gly1-SIFamide-IR localized to somata in the paired commissural ganglia (CoGs), two axons in the nerves connecting each CoG with the STG, and the CoG and STG neuropil. We identified one Gly1-SIFamide-IR projection neuron innervating the STG as the previously identified modulatory commissural neuron 5 (MCN5). Brief (~10 s) MCN5 stimulation excites some pyloric circuit neurons. We now find that bath applying Gly1-SIFamide to the isolated STG also enhanced pyloric rhythm activity and activated an imperfectly coordinated gastric mill rhythm that included unusually prolonged bursts in two circuit neurons [inferior cardiac (IC), lateral posterior gastric (LPG)]. Furthermore, longer duration (>30 s) MCN5 stimulation activated a Gly1-SIFamide-like gastric mill rhythm, including prolonged IC and LPG bursting. The prolonged LPG bursting decreased the coincidence of its activity with neurons to which it is electrically coupled. We also identified local circuit feedback onto the MCN5 axon terminals, which may contribute to some distinctions between the responses to MCN5 stimulation and Gly1-SIFamide application. Thus, MCN5 adds to the few identified projection neurons that modulate a well-defined circuit at least partly via an identified neuropeptide transmitter and provides an opportunity to study peptide regulation of electrical coupled neurons in a functional context. NEW & NOTEWORTHY Limited insight exists regarding how identified peptidergic neurons modulate microcircuits. We show that the modulatory projection neuron modulatory commissural neuron 5 (MCN5) is peptidergic, containing Gly1-SIFamide. MCN5 and Gly1-SIFamide elicit similar output from two well-defined motor circuits. Their distinct actions may result partly from circuit feedback onto the MCN5 axon terminals. Their similar actions include eliciting divergent activity patterns in normally coactive, electrically coupled neurons, providing an opportunity to examine peptide modulation of electrically coupled neurons in a functional context.
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34

Aronowitz, Jake V., Alice Perez, Christopher O’Brien, Siaresh Aziz, Erica Rodriguez, Kobi Wasner, Sissi Ribeiro, Dovounnae Green, Farhana Faruk, and Carolyn L. Pytte. "Unilateral vocal nerve resection alters neurogenesis in the avian song system in a region-specific manner." PLOS ONE 16, no. 8 (August 31, 2021): e0256709. http://dx.doi.org/10.1371/journal.pone.0256709.

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New neurons born in the adult brain undergo a critical period soon after migration to their site of incorporation. During this time, the behavior of the animal may influence the survival or culling of these cells. In the songbird song system, earlier work suggested that adult-born neurons may be retained in the song motor pathway nucleus HVC with respect to motor progression toward a target song during juvenile song learning, seasonal song restructuring, and experimentally manipulated song variability. However, it is not known whether the quality of song per se, without progressive improvement, may also influence new neuron survival. To test this idea, we experimentally altered song acoustic structure by unilateral denervation of the syrinx, causing a poor quality song. We found no effect of aberrant song on numbers of new neurons in HVC, suggesting that song quality does not influence new neuron culling in this region. However, aberrant song resulted in the loss of left-side dominance in new neurons in the auditory region caudomedial nidopallium (NCM), and a bilateral decrease in new neurons in the basal ganglia nucleus Area X. Thus new neuron culling may be influenced by behavioral feedback in accordance with the function of new neurons within that region. We propose that studying the effects of singing behaviors on new neurons across multiple brain regions that differentially subserve singing may give rise to general rules underlying the regulation of new neuron survival across taxa and brain regions more broadly.
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35

Nagy, F., P. Cardi, and I. Cournil. "A rhythmic modulatory gating system in the stomatogastric nervous system of Homarus gammarus. I. Pyloric-related neurons in the commissural ganglia." Journal of Neurophysiology 71, no. 6 (June 1, 1994): 2477–89. http://dx.doi.org/10.1152/jn.1994.71.6.2477.

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1. Operation of the pyloric neural network in the crustacean stomatogastric ganglion (STG) depends on constant firing of modulatory inputs from anterior ganglia. We have identified two bilaterally symmetrical pairs of these inputs in the commissural ganglia (COGs) of the European rock lobster Homarus gammarus. During operation of the pyloric CPG, they fired in pyloric time, out of phase with the pyloric pacemakers. 2. One of the pair was the commissural pyloric (CP) neuron and the other was homologous to the P neuron described in the spiny lobster Panulirus interruptus. We describe their morphology and location in the COG. The CP neuron projected to the STG via the superior esophageal nerve (son) and the stomatogastric nerve (stn), whereas the P neuron projected via the inferior esophageal nerve (ion) and stn. 3. To determine the total number of commissural neurons projecting to the STG, we used cobalt and Lucifer yellow backfilling from their cut axons in the stn. With the ion cut, there were between 8 to 12 labeled somata in each COG including CP cell body, whereas only 2 somata (including P) were labeled with the son cut. Among these neurons, CP and P appeared to be the only commissural neurons that fired in pyloric time and projected in the STG on the pyloric network. 4. The CP neuron produced monosynaptic excitatory postsynaptic potentials (EPSPs) on the pyloric dilator (PD), lateral pyloric (LP), and inferior cardiac (IC) neurons, whereas the P neuron produced monosynaptic EPSPs on all pyloric motoneurons but IC. The P neuron was gamma-aminobutyric acid immunoreactive, and the P-derived EPSPs in pyloric neurons were reversibly blocked by bicuculline, picrotoxin, and D-tubocurarine. 5. The CP and P neurons were electrically coupled, and modification of membrane potential in either one of them appreciably changed the firing frequency of the coupled neuron. 6. A negative-feedback loop from the pyloric anterior burster (AB) interneuron provoked simultaneous rhythmic inhibitions in the P and CP neurons. Together with the electrical coupling, the rhythmic inhibition contributed to synchronize firing of the two commissural neurons. 7. The following papers in the series of describe the modulatory and rhythmic control exerted by the P and CP neurons over the pyloric pattern generator.
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36

Mahesh, Virendra B. "Hirsutism, virilism, polycystic ovarian disease, and the steroid-gonadotropin-feedback system: a career retrospective." American Journal of Physiology-Endocrinology and Metabolism 302, no. 1 (January 1, 2012): E4—E18. http://dx.doi.org/10.1152/ajpendo.00488.2011.

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This career retrospective describes how the initial work on the mechanism of hormone action provided the tools for the study of hirsutism, virilism, and polycystic ovarian disease. After excessive ovarian and or adrenal androgen secretion in polycystic ovarian disease had been established, the question whether the disease was genetic or acquired, methods to manage hirsutism and methods for the induction of ovulation were addressed. Recognizing that steroid gonadotropin feedback was an important regulatory factor, initial studies were done on the secretion of LH and FSH in the ovulatory cycle. This was followed by the study of basic mechanisms of steroid-gonadotropin feedback system, using castration and steroid replacement and the events surrounding the natural onset of puberty. Studies in ovariectomized rats showed that progesterone was a pivotal enhancer of estrogen-induced gonadotropin release, thus accounting for the preovulatory gonadotropin surge. The effects of progesterone were manifested by depletion of the occupied estrogen receptors of the anterior pituitary, release of hypothalamic LHRH, and inhibition of enzymes that degrade LHRH. Progesterone also promoted the synthesis of FSH in the pituitary. The 3α,5α-reduced metabolite of progesterone brought about selective LH release and acted using the GABAA receptor system. The 5α-reduced metabolite of progesterone brought about selective FSH release; the ability of progesterone to bring about FSH release was dependent on its 5α-reduction. The GnRH neuron does not have steroid receptors; the steroid effect was shown to be mediated through the excitatory amino acid glutamate, which in turn stimulated nitric oxide. These observations led to the replacement of the long-accepted belief that ovarian steroids acted directly on the GnRH neuron by the novel concept that the steroid feedback effect was exerted at the glutamatergic neuron, which in turn regulated the GnRH neuron. The neuroprotective effects of estrogens on brain neurons are of considerable interest.
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Thirumalai, Vatsala, Astrid A. Prinz, Christian D. Johnson, and Eve Marder. "Red Pigment Concentrating Hormone Strongly Enhances the Strength of the Feedback to the Pyloric Rhythm Oscillator But Has Little Effect on Pyloric Rhythm Period." Journal of Neurophysiology 95, no. 3 (March 2006): 1762–70. http://dx.doi.org/10.1152/jn.00764.2005.

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The neuropeptide, red pigment concentrating hormone (RPCH), strengthened the inhibitory synapse from the lateral pyloric (LP) neuron to the pyloric dilator (PD) neurons in the pyloric network of the stomatogastric ganglion (STG) of the lobster, Homarus americanus. RPCH produced several-fold increases in the amplitude of both action potential–mediated and non–impulse-mediated transmission that persisted for as long as the peptide remained present. Because the LP to PD synapse is the only feedback to the pacemaker kernel of the pyloric network, which consists of the electrically coupled two PD neurons and the anterior burster (AB) neuron, it might have been expected that strengthening the LP to PD synapse would increase the period of the pyloric rhythm. However, the period of the pyloric rhythm increased only transiently in RPCH, and a transient increase in cycle period was observed even when the LP neuron was hyperpolarized. Phase response curves were measured using the dynamic clamp to create artificial inhibitory inputs of variable strength and duration to the PD neurons. Synaptic conductance values seen in normal saline were ineffective at changing the pyloric period throughout the pyloric cycle. Conductances similar to those seen in 10−6 M RPCH also did not evoke phase resets at phases when the LP neuron is typically active. Thus the dramatic effects of RPCH on synaptic strength have little role in modulation of the period of the pyloric rhythm under normal operating conditions but may help to stabilize the rhythm when the cycle period is too slow or too fast.
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Sun, Jianli, and Suzanne M. Moenter. "Progesterone Treatment Inhibits and Dihydrotestosterone (DHT) Treatment Potentiates Voltage-Gated Calcium Currents in Gonadotropin-Releasing Hormone (GnRH) Neurons." Endocrinology 151, no. 11 (August 25, 2010): 5349–58. http://dx.doi.org/10.1210/en.2010-0385.

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GnRH neurons are central regulators of fertility, and their activity is modulated by steroid feedback. In normal females, GnRH secretion is regulated by estradiol and progesterone (P). Excess androgens present in hyperandrogenemic fertility disorders may disrupt communication of negative feedback signals from P and/or independently stimulate GnRH release. Voltage-gated calcium channels (VGCCs) are important in regulating excitability and hormone release. Estradiol alters VGCCs in a time-of-day-dependent manner. To further elucidate ovarian steroid modulation of GnRH neuron VGCCs, we studied the effects of dihydrotestosterone (DHT) and P. Adult mice were ovariectomized (OVX) or OVX and treated with implants containing DHT (OVXD), estradiol (OVXE), estradiol and DHT (OVXED), estradiol and P (OVXEP), or estradiol, DHT, and P (OVXEDP). Macroscopic calcium current (ICa) was recorded in the morning or afternoon 8–12 d after surgery using whole-cell voltage-clamp. ICa was increased in afternoon vs. morning in GnRH neurons from OVXE mice but this increase was abolished in cells from OVXEP mice. ICa in cells from OVXD mice was increased regardless of time of day; there was no additional effect in OVXED mice. P reduced N-type and DHT potentiated N- and R-type VGCCs; P blocked the DHT potentiation of N-type-mediated current. These data suggest P and DHT have opposing actions on VGCCs in GnRH neurons, but in the presence of both steroids, P dominates. VGCCs are targets of ovarian steroid feedback modulation of GnRH neuron activity and, more specifically, a potential mechanism whereby androgens could activate GnRH neuronal function.
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39

Skorupski, P., B. M. Rawat, and B. M. Bush. "Heterogeneity and central modulation of feedback reflexes in crayfish motor pool." Journal of Neurophysiology 67, no. 3 (March 1, 1992): 648–63. http://dx.doi.org/10.1152/jn.1992.67.3.648.

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1. Movement of the crayfish thoracocoxal leg joint is monitored by a muscle receptor organ (TCMRO) and a chordotonal organ (TCCO). Both receptors span the joint in parallel but signal opposite directions of leg movement. The TCMRO is innervated by afferents responsive to lengthening, which corresponds to leg remotion, whereas TCCO afferents are responsive to shortening of the chordotonal strand, which corresponds to leg promotion. 2. When both receptors are stimulated in parallel, in an otherwise isolated preparation, reflex responses of coxal promoter and remotor motor neurons occur on both stretch and release. By comparison with experiments where one or the other of these receptors is stimulated selectively, we conclude that reflexes evoked by stretch of the two receptors are due to the TCMRO and reflexes evoked by release are due to the TCCO. 3. Reflexes mediated by these receptors are both state dependent and phase dependent. In preparations that produce patterns of reciprocal motor activity in promotor and remotor motor neurons (the active state), the reflex effect depends on the phase of this centrally generated activity. In preparations that are quiescent, or that produce only tonic motor output (the inactive state), the reflex effect is stable, corresponding to a typical resistance (negative feedback) reflex for both directions of receptor movement. 4. In the active state, coxal promotor motor neurons are both excited and inhibited in a phase-dependent manner by stretching the TCMRO. A subgroup of promotor motor neurons is excited by shortening the TCCO. One subgroup of the antagonistic coxal remotor motor neurons receives phase-dependent excitation from stretch of the TCMRO, whereas a second subgroup receives phase-dependent excitation from shortening the TCCO. 5. There are, therefore, at least two ways in which reflex effects can be modulated. At the level of a single motor neuron, the reflex response can vary in gain, and in some cases in sign, in a manner depending on centrally generated motor activity. In addition, at the level of a pool of synergistic motor neurons, the reflex effect is not uniform; instead, different subgroups of motor neurons display different reflex effects, so that the relative levels of excitability of different motor neuron reflex subgroups can also determine the net reflex effect. 6. Excitation of promotor motor neurons by TCCO shortening and of remotor motor neurons by TCMRO lengthening are positive feedback reflexes. The subgroups of motor neurons in which positive feedback reflexes can be evoked in both promotor and remotor pools are termed group 1.(ABSTRACT TRUNCATED AT 400 WORDS)
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40

BHATTACHARJEE, ANINDITA, M. K. DAS, and SUBHENDU GHOSH. "SYNCHRONIZATION IN A RING OF UNIDIRECTIONALLY COUPLED FITZHUGH–NAGUMO NEURONS." International Journal of Biomathematics 07, no. 01 (January 2014): 1450009. http://dx.doi.org/10.1142/s1793524514500090.

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Synchronization behavior of an ensemble of unidirectionally coupled neurons with a constant input is investigated. Chemical synapses are considered for coupling. Each neuron is also considered to be exposed to a self-delayed feedback. The synchronization phenomenon is analyzed by the error dynamics of the response trajectories of the system. The effect of various model parameters e.g. coupling strength, feedback gain and time delay, on synchronization is also investigated and a measure of synchrony is computed in each cases. It is shown that the synchronization is not only achieved by increasing the coupling strength, the system also required to have a suitable feedback gain and time delay for synchrony. Robustness of the parameters for synchrony is verified for larger systems.
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41

Gao, Zhongquan, Zhixuan Yuan, Zuo Wang, and Peihua Feng. "Modulation of Astrocytes on Mode Selection of Neuron Firing Driven by Electromagnetic Induction." Neural Plasticity 2020 (December 1, 2020): 1–18. http://dx.doi.org/10.1155/2020/8899577.

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Both of astrocytes and electromagnetic induction are magnificent to modulate neuron firing by introducing feedback currents to membrane potential. An improved astro-neuron model considering both of the two factors is employed to investigate their different roles in modulation. The mixing mode, defined by combination of period bursting and depolarization blockage, characterizes the effect of astrocytes. Mixing mode and period bursting alternatively appear in parameter space with respect to the amplitude of feedback current on neuron from astrocyte modulation. However, magnetic flux obviously plays a role of neuron firing inhibition. It not only repels the mixing mode but also suppresses period bursting. The mixing mode becomes period bursting mode and even resting state when astrocytes are hyperexcitable. Abnormal activities of astrocytes are capable to induce depolarization blockage to compose the mixing mode together with bursting mode. But electromagnetic induction shows its strong ability of inhibition of neuron firing, which is also illustrated in the bifurcation diagram. Indeed, the combination of the two factors and appropriate choice of parameters show the great potential to control disorder of neuron firing like epilepsy.
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42

Mao, Jia-Wei, and Dong-Liang Hu. "Vibrational Resonance and Electrical Activity Behavior of a Fractional-Order FitzHugh–Nagumo Neuron System." Mathematics 10, no. 1 (December 27, 2021): 87. http://dx.doi.org/10.3390/math10010087.

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Making use of the numerical simulation method, the phenomenon of vibrational resonance and electrical activity behavior of a fractional-order FitzHugh–Nagumo neuron system excited by two-frequency periodic signals are investigated. Based on the definition and properties of the Caputo fractional derivative, the fractional L1 algorithm is applied to numerically simulate the phenomenon of vibrational resonance in the neuron system. Compared with the integer-order neuron model, the fractional-order neuron model can relax the requirement for the amplitude of the high-frequency signal and induce the phenomenon of vibrational resonance by selecting the appropriate fractional exponent. By introducing the time-delay feedback, it can be found that the vibrational resonance will occur with periods in the fractional-order neuron system, i.e., the amplitude of the low-frequency response periodically changes with the time-delay feedback. The weak low-frequency signal in the system can be significantly enhanced by selecting the appropriate time-delay parameter and the fractional exponent. In addition, the original integer-order model is extended to the fractional-order model, and the neuron system will exhibit rich dynamical behaviors, which provide a broader understanding of the neuron system.
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43

Roberts, A., M. J. Tunstall, and E. Wolf. "Properties of networks controlling locomotion and significance of voltage dependency of NMDA channels: stimulation study of rhythm generation sustained by positive feedback." Journal of Neurophysiology 73, no. 2 (February 1, 1995): 485–95. http://dx.doi.org/10.1152/jn.1995.73.2.485.

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1. We have built a realistic 24-neuron model based on data from the spinal pattern generator for swimming in Xenopus embryos with the use of the SWIM programs. The neurons have dendrite, soma, and axon compartments with voltage-gated Na+ and K+ channels. Dendritic synapses were modeled as modulated ionic conductances with currents that have different reversal levels. One of these conductances was voltage dependent to model N-methyl-D-aspartate ("NMDA") synapses in the presence of Mg2+. 2. In this model, rhythm generation is initiated by a brief excitation, depends on rebound from reciprocal inhibition, and is sustained by long-duration "NMDA-dependent" feedback excitation. 3. Without NMDA voltage dependency, rhythmic activity is stable over a wide range of synaptic conductances. Its frequency decreases with more inhibition and increases with more excitation. The introduction of normally distributed variation in soma size or excitatory synaptic conductance extends the lower stable frequency range. Without such variation the frequency of the 24-neuron model is the same as a 4-neuron model provided that the synaptic conductances for each neuron are the same. 4. The effect of introducing NMDA voltage dependency on rebound after negative current injections or synaptic inhibition was investigated in single depolarized model neurons. With NMDA voltage dependency, hyperpolarizations and rebound spike responses were increased. 5. Network activity with NMDA voltage dependency was similar to that without it, but inhibitory postsynaptic potentials (IPSPs) and spikes were larger, and frequencies were lower and more sensitive to changes in excitatory and inhibitory conductance. 6. We conclude that in the model, mutual reexcitation among excitatory spinal interneurons can sustain rhythm generation by positive feedback and that NMDA voltage dependency can enhance postinhibitory rebound, stabilize swimming activity and extend its lower frequency range, and steepen the dependency of frequency on synaptic drive.
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44

Wang, Guan Ping, Wu Yin Jin, and Chi Bing Hu. "The Influence of Parameters on an Individual Neuron Firing Patterns." Applied Mechanics and Materials 239-240 (December 2012): 1095–99. http://dx.doi.org/10.4028/www.scientific.net/amm.239-240.1095.

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The influence of parameters to the firing patterns of time-delayed linear and compound Hindmarsh-Rose(HR) model neuron are studied in this work. For an individual neuron, it can be found from different Intervalspike Interval (ISI) maps that the firing patterns transform among resting state, busting firing, tonic firing, and chaotic spiking, especially, the transfer of the firing patters are speeded up under feedback mechanism, it is easier to get into the chaotic firing state compared with linear feedback.
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45

García-Crescioni, Keyla, Timothy J. Fort, Estee Stern, Vladimir Brezina, and Mark W. Miller. "Feedback From Peripheral Musculature to Central Pattern Generator in the Neurogenic Heart of the Crab Callinectes sapidus: Role of Mechanosensitive Dendrites." Journal of Neurophysiology 103, no. 1 (January 2010): 83–96. http://dx.doi.org/10.1152/jn.00561.2009.

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The neurogenic heart of decapod crustaceans is a very simple, self-contained, model central pattern generator (CPG)-effector system. The CPG, the nine-neuron cardiac ganglion (CG), is embedded in the myocardium itself; it generates bursts of spikes that are transmitted by the CG's five motor neurons to the periphery of the system, the myocardium, to produce its contractions. Considerable evidence suggests that a CPG-peripheral loop is completed by a return feedback pathway through which the contractions modify, in turn, the CG motor pattern. One likely pathway is provided by dendrites, presumably mechanosensitive, that the CG neurons project into the adjacent myocardial muscle. Here we have tested the role of this pathway in the heart of the blue crab, Callinectes sapidus . We performed “de-efferentation” experiments in which we cut the motor neuron axons to the myocardium and “de-afferentation” experiments in which we cut or ligated the dendrites. In the isolated CG, these manipulations had no effect on the CG motor pattern. When the CG remained embedded in the myocardium, however, these manipulations, interrupting either the efferent or afferent limb of the CPG-peripheral loop, decreased contraction amplitude, increased the frequency of the CG motor neuron spike bursts, and decreased the number of spikes per burst and burst duration. Finally, passive stretches of the myocardium likewise modulated the spike bursts, an effect that disappeared when the dendrites were cut. We conclude that feedback through the dendrites indeed operates in this system and suggest that it completes a loop through which the system self-regulates its activity.
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Guo, Fang, Junwei Yu, Hyung Jae Jung, Katharine C. Abruzzi, Weifei Luo, Leslie C. Griffith, and Michael Rosbash. "Circadian neuron feedback controls the Drosophila sleep–activity profile." Nature 536, no. 7616 (August 2016): 292–97. http://dx.doi.org/10.1038/nature19097.

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47

Mellen, Nicholas M., and Jack L. Feldman. "Phasic Vagal Sensory Feedback Transforms Respiratory Neuron ActivityIn Vitro." Journal of Neuroscience 21, no. 18 (September 15, 2001): 7363–71. http://dx.doi.org/10.1523/jneurosci.21-18-07363.2001.

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48

Moldovan, Adrian, Angel Caţaron, and Răzvan Andonie. "Learning in Convolutional Neural Networks Accelerated by Transfer Entropy." Entropy 23, no. 9 (September 16, 2021): 1218. http://dx.doi.org/10.3390/e23091218.

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Recently, there is a growing interest in applying Transfer Entropy (TE) in quantifying the effective connectivity between artificial neurons. In a feedforward network, the TE can be used to quantify the relationships between neuron output pairs located in different layers. Our focus is on how to include the TE in the learning mechanisms of a Convolutional Neural Network (CNN) architecture. We introduce a novel training mechanism for CNN architectures which integrates the TE feedback connections. Adding the TE feedback parameter accelerates the training process, as fewer epochs are needed. On the flip side, it adds computational overhead to each epoch. According to our experiments on CNN classifiers, to achieve a reasonable computational overhead–accuracy trade-off, it is efficient to consider only the inter-neural information transfer of the neuron pairs between the last two fully connected layers. The TE acts as a smoothing factor, generating stability and becoming active only periodically, not after processing each input sample. Therefore, we can consider the TE is in our model a slowly changing meta-parameter.
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Yu, Yangyang, Zhixuan Yuan, Yongchen Fan, Jiajia Li, and Ying Wu. "Dynamic Transitions in Neuronal Network Firing Sustained by Abnormal Astrocyte Feedback." Neural Plasticity 2020 (November 22, 2020): 1–13. http://dx.doi.org/10.1155/2020/8864246.

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Astrocytes play a crucial role in neuronal firing activity. Their abnormal state may lead to the pathological transition of neuronal firing patterns and even induce seizures. However, there is still little evidence explaining how the astrocyte network modulates seizures caused by structural abnormalities, such as gliosis. To explore the role of gliosis of the astrocyte network in epileptic seizures, we first established a direct astrocyte feedback neuronal network model on the basis of the hippocampal CA3 neuron-astrocyte model to simulate the condition of gliosis when astrocyte processes swell and the feedback to neurons increases in an abnormal state. We analyzed the firing pattern transitions of the neuronal network when astrocyte feedback starts to change via increases in both astrocyte feedback intensity and the connection probability of astrocytes to neurons in the network. The results show that as the connection probability and astrocyte feedback intensity increase, neuronal firing transforms from a nonepileptic synchronous firing state to an asynchronous firing state, and when astrocyte feedback starts to become abnormal, seizure-like firing becomes more severe and synchronized; meanwhile, the synchronization area continues to expand and eventually transforms into long-term seizure-like synchronous firing. Therefore, our results prove that astrocyte feedback can regulate the firing of the neuronal network, and when the astrocyte network develops gliosis, there will be an increase in the induction rate of epileptic seizures.
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50

Peng, Jiankui, and Suoping Li. "Dynamics Analysis and Intermittent Energy Feedback Control of m-HR Neuron Model under Electromagnetic Induction." Complexity 2022 (September 23, 2022): 1–11. http://dx.doi.org/10.1155/2022/5446369.

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It is of great practical significance to fully reveal the global discharge characteristics of neurons in electromagnetic environment and design effective energy feedback strategy for accurate prediction of neural information. Considering the effect of electromagnetic induction, a four-dimensional modified Hindmarsh–Rose (m-HR) neuron model is established, and its discharge mechanism is revealed by analyzing the existence and stability of equilibrium point of the model. Extensive numerical results confirm that the model has classical period-doubling bifurcation, period-adding bifurcation, and comb-shaped chaotic structure. Importantly, a new intermittent energy feedback controller is designed by improving the traditional energy feedback control strategy, which can effectively modulate the desired discharge modes under the cost-optimal energy consumption. Meanwhile, it should be emphasized that the intermittent control scheme has a wider range of regulation and robustness, which can be applied to other dynamical systems to obtain the desired oscillation modes. This will improve the beneficial discussion for the construction of brain-like intelligent network and efficient regulation.
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