Academic literature on the topic 'Rat synapse mechanisms'
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Journal articles on the topic "Rat synapse mechanisms"
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Herrera-López, Gabriel, Ernesto Griego, and Emilio J. Galván. "Lactate induces synapse-specific potentiation on CA3 pyramidal cells of rat hippocampus." PLOS ONE 15, no. 11 (November 12, 2020): e0242309. http://dx.doi.org/10.1371/journal.pone.0242309.
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Neuronal activity within the physiologic range stimulates lactate production that, via metabolic pathways or operating through an array of G-protein-coupled receptors, regulates intrinsic excitability and synaptic transmission. The recent discovery that lactate exerts a tight control of ion channels, neurotransmitter release, and synaptic plasticity-related intracellular signaling cascades opens up the possibility that lactate regulates synaptic potentiation at central synapses. Here, we demonstrate that extracellular lactate (1–2 mM) induces glutamatergic potentiation on the recurrent collateral synapses of hippocampal CA3 pyramidal cells. This potentiation is independent of lactate transport and further metabolism, but requires activation of NMDA receptors, postsynaptic calcium accumulation, and activation of a G-protein-coupled receptor sensitive to cholera toxin. Furthermore, perfusion of 3,5- dihydroxybenzoic acid, a lactate receptor agonist, mimics this form of synaptic potentiation. The transduction mechanism underlying this novel form of synaptic plasticity requires G-protein βγ subunits, inositol-1,4,5-trisphosphate 3-kinase, PKC, and CaMKII. Activation of these signaling cascades is compartmentalized in a synapse-specific manner since lactate does not induce potentiation at the mossy fiber synapses of CA3 pyramidal cells. Consistent with this synapse-specific potentiation, lactate increases the output discharge of CA3 neurons when recurrent collaterals are repeatedly activated during lactate perfusion. This study provides new insights into the cellular mechanisms by which lactate, acting via a membrane receptor, contributes to the memory formation process.
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Hardingham, Neil R., Giles E. Hardingham, Kevin D. Fox, and Julian J. B. Jack. "Presynaptic Efficacy Directs Normalization of Synaptic Strength in Layer 2/3 Rat Neocortex After Paired Activity." Journal of Neurophysiology 97, no. 4 (April 2007): 2965–75. http://dx.doi.org/10.1152/jn.01352.2006.
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Paired neuronal activity is known to induce changes in synaptic strength that result in the synapse in question having different properties to unmodified synapses. Here we show that in layer 2/3 excitatory connections in young adult rat cortex paired activity acts to normalize the strength and quantal parameters of connections. Paired action potential firing produces long-term potentiation in only a third of connections, whereas a third remain with their amplitude unchanged and a third exhibit long-term depression. Furthermore, the direction of plasticity can be predicted by the initial strength of the connection: weak connections potentiate and strong connections depress. A quantal analysis reveals that changes in synaptic efficacy were predominantly presynaptic in locus and that the key determinant of the direction and magnitude of synaptic modification was the initial release probability ( Pr) of the synapse, which correlated inversely with change in Pr after pairing. Furthermore, distal synapses also exhibited larger potentiations including postsynaptic increases in efficacy, whereas more proximal inputs did not. This may represent a means by which distal synapses preferentially increase their efficacy to achieve equal weighting at the soma. Paired activity thus acts to normalize synaptic strength, by both pre- and postsynaptic mechanisms.
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Mandela, Prashant, and Xin-Ming Ma. "Kalirin, a Key Player in Synapse Formation, Is Implicated in Human Diseases." Neural Plasticity 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/728161.
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Synapse formation is considered to be crucial for learning and memory. Understanding the underlying molecular mechanisms of synapse formation is a key to understanding learning and memory. Kalirin-7, a major isoform of Kalirin in adult rodent brain, is an essential component of mature excitatory synapses. Kalirin-7 interacts with multiple PDZ-domain-containing proteins including PSD95, spinophilin, and GluR1 through its PDZ-binding motif. In cultured hippocampal/cortical neurons, overexpression of Kalirin-7 increases spine density and spine size whereas reduction of endogenous Kalirin-7 expression decreases synapse number, and spine density. In Kalirin-7 knockout mice, spine length, synapse number, and postsynaptic density (PSD) size are decreased in hippocampal CA1 pyramidal neurons; these morphological alterations are accompanied by a deficiency in long-term potentiation (LTP) and a decreased spontaneous excitatory postsynaptic current (sEPSC) frequency. Human Kalirin-7, also known as Duo or Huntingtin-associated protein-interacting protein (HAPIP), is equivalent to rat Kalirin-7. Recent studies show that Kalirin is relevant to many human diseases such as Huntington’s Disease, Alzheimer’s Disease, ischemic stroke, schizophrenia, depression, and cocaine addiction. This paper summarizes our recent understanding of Kalirin function.
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Betz, W. J., R. R. Ribchester, and R. M. A. P. Ridge. "Competitive mechanisms underlying synapse elimination in the lumbrical muscle of the rat." Journal of Neurobiology 21, no. 1 (January 1990): 1–17. http://dx.doi.org/10.1002/neu.480210102.
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Oshima-Takago, Tomoko, and Hideki Takago. "NMDA receptor-dependent presynaptic inhibition at the calyx of Held synapse of rat pups." Open Biology 7, no. 7 (July 2017): 170032. http://dx.doi.org/10.1098/rsob.170032.
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N -Methyl- d -aspartate receptors (NMDARs) play diverse roles in synaptic transmission, synaptic plasticity, neuronal development and neurological diseases. In addition to their postsynaptic expression, NMDARs are also expressed in presynaptic terminals at some central synapses, and their activation modulates transmitter release. However, the regulatory mechanisms of NMDAR-dependent synaptic transmission remain largely unknown. In the present study, we demonstrated that activation of NMDARs in a nerve terminal at a central glutamatergic synapse inhibits presynaptic Ca 2+ currents (I Ca ) in a GluN2C/2D subunit-dependent manner, thereby decreasing nerve-evoked excitatory postsynaptic currents. Neither presynaptically loaded fast Ca 2+ chelator BAPTA nor non-hydrolysable GTP analogue GTPγS affected NMDAR-mediated I Ca inhibition. In the presence of a glutamate uptake blocker, the decline in I Ca amplitude evoked by repetitive depolarizing pulses at 20 Hz was attenuated by an NMDAR competitive antagonist, suggesting that endogenous glutamate has a potential to activate presynaptic NMDARs. Moreover, NMDA-induced inward currents at a negative holding potential (−80 mV) were abolished by intra-terminal loading of the NMDAR open channel blocker MK-801, indicating functional expression of presynaptic NMDARs. We conclude that presynaptic NMDARs can attenuate glutamate release by inhibiting voltage-gated Ca 2+ channels at a relay synapse in the immature rat auditory brainstem.
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Gao, Bao-Xi, Gong Cheng, and Lea Ziskind-Conhaim. "Development of Spontaneous Synaptic Transmission in the Rat Spinal Cord." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2277–87. http://dx.doi.org/10.1152/jn.1998.79.5.2277.
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Gao, Bao-Xi, Gong Cheng, and Lea Ziskind-Conhaim. Development of spontaneous synaptic transmission in the rat spinal cord. J. Neurophysiol. 79: 2277–2287, 1998. Dorsal root afferents form synaptic connections on motoneurons a few days after motoneuron clustering in the rat lumbar spinal cord, but frequent spontaneous synaptic potentials are detected only after birth. To increase our understanding of the mechanisms underlying the differentiation of synaptic transmission, we examined the developmental changes in properties of spontaneous synaptic transmission at early stages of synapse formation. Spontaneous postsynaptic currents (PSCs) and tetrodotoxin (TTX)-resistant miniature PSCs (mPSCs) were measured in spinal motoneurons of embryonic and postnatal rats using whole cell patch-clamp recordings. Spontaneous PSC frequencies were higher than mPSC frequencies in both embryonic and postnatal motoneurons, suggesting that even at embryonic stages, when action-potential firing rate was low, presynaptic action potentials played an important role in triggering spontaneous PSCs. After birth, the twofold increase in spontaneous PSC frequency was attributed to an increase in action-potential–independent quantal release rather than to a higher rate of action-potential firing. In embryonic motoneurons, the fluctuations in peak amplitude of spontaneous PSCs were normally distributed around single peaks with modal values similar to those of mPSCs. These data indicated that early in synapse differentiation spontaneous PSCs were primarily composed of currents generated by quantal release. After birth, mean mPSC amplitude increased by 50% but mean quantal current amplitude did not change. Synchronous, multiquantal release was apparent in postnatal motoneurons only in high-K+ extracellular solution. Comparison of the properties of miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) demonstrated that mean mEPSC frequency was higher than mIPSC frequency, suggesting that either excitatory synapses outnumbered inhibitory synapses or that the probability of excitatory transmitter release was higher than the release of inhibitory neurotransmitters. The finding that mIPSC duration was several-fold longer than mEPSC duration implied that despite their lower frequency, inhibitory currents could modulate motoneuron synaptic integration by shunting incoming excitatory inputs for prolonged time intervals.
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McCoy, Portia A., and Lori L. McMahon. "Muscarinic Receptor–Dependent Long-Term Depression in Rat Visual Cortex Is PKC Independent but Requires ERK1/2 Activation and Protein Synthesis." Journal of Neurophysiology 98, no. 4 (October 2007): 1862–70. http://dx.doi.org/10.1152/jn.00510.2007.
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Intact cholinergic innervation of visual cortex is critical for normal processing of visual information and for spatial memory acquisition and retention. However, a complete description of the mechanisms by which the cholinergic system modifies synaptic function in visual cortex is lacking. Previously it was shown that activation of the m1 subtype of muscarinic receptor induces an activity-dependent and partially N-methyl-d-aspartate receptor (NMDAR)-dependent long-term depression (LTD) at layer 4–layer 2/3 synapses in rat visual cortex slices in vitro. The cellular mechanisms downstream of the Gαq coupled m1 receptor required for induction of this LTD (which we term mLTD) are currently unknown. Here, we confirm a role for m1 receptors in mLTD induction and use a series of pharmacological tools to study the signaling molecules downstream of m1 receptor activation in mLTD induction. We found that mLTD is prevented by inhibitors of L-type Ca2+ channels, the Src kinase family, and the mitogen-activated kinase/extracellular kinase. mLTD is also partially dependent on phospholipase C but is unaffected by blocking protein kinase C. mLTD expression can be long-lasting (>2 h) and its long-term maintenance requires translation. Thus we report the signaling mechanisms underlying induction of an m1 receptor-dependent LTD in visual cortex and the requirement of protein synthesis for long-term expression. This plasticity could be a mechanism by which the cholinergic system modifies glutamatergic synapse function to permit normal visual system processing required for cognition.
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Bolanos, Sandra, Hiroshi Saito, John Papaconstantinou, and Thomas A. Kent. "Transcriptional Responses in Recovery from Stroke." Stroke 32, suppl_1 (January 2001): 316. http://dx.doi.org/10.1161/str.32.suppl_1.316.
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1 Multiple lines of evidence support synaptic reorganization of the brain after stroke and a role in functional recovery. Molecular, pharmacological, especially norardrenergic, and behavioral methods have shown promise in enhancing recovery in animal or clinical studies. However, the mechanisms underlying stimulation of new synapses remain largely unknown, information that is critical to optimize interventions, including stem cell transplant, drug therapy or other approaches. We investigated two potential such mechanisms in a rat model of middle cerebral artery occlusion (MCAO) in which we have previously shown robust new expression of the pre-synaptic vesicle protein synaptophysin in the peri-infarct and contralateral homotopic regions. One candidate signal for stimulation of new synaptic formation is the polysialated form of neuronal cell adhesion molecules (PSCAM) that is expressed during synaptic development. Immunostaining for PSCAM after MCAO and recovery failed to demonstrate expression. The possibility that signal molecules potentially released following ischemia, may be involved in synaptic generation analogous to long term potentiation (LTP), was next investigated. The C/EBP (CCAAT enhancer binding protein) family of transcription factors is an important intermediary for glutamate stimulation of synapses in LTP. After distal MCAO in rats, we found dramatic expression of the C/EBP α subtype in the peri-infarct region at 3 days, and expression by Western blot of a 30 kD C/EBP α isoform in cultured PC12 cells induced to differentiate into neurite and synapses. We suggest the possibility that C/EBP, stimulated by biochemical events in the peri-infarct region, is a potential signal for new synapses following stroke. We are in the process of assessing the effect of overexpression of this isoform on synapse formation in cultured PC12 cells. C/EBP α and other signals may provide targets for intervention to enhance expression. The importance of these results as related to the effects of glutamate also support our previous finding that glutamate-blockade, although limiting infarct size, may also interfere with synapse formation in the long term (Bolanos & Kent, JCBF & Met Suppl, 1999).
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Yao, Lijun, and Takeshi Sakaba. "cAMP Modulates Intracellular Ca2+ Sensitivity of Fast-Releasing Synaptic Vesicles at the Calyx of Held Synapse." Journal of Neurophysiology 104, no. 6 (December 2010): 3250–60. http://dx.doi.org/10.1152/jn.00685.2010.
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cAMP potentiates neurotransmitter release from the presynaptic terminal in many CNS synapses, but the underlying mechanisms remain unclear. Here we addressed this issue quantitatively by performing double patch-clamp recordings from the pre- and postsynaptic compartments of the calyx of Held synapse in rat brain stem slices in combination with Ca2+ uncaging. We found that elevation of cAMP increased intracellular Ca2+ sensitivity for transmitter release especially at lower Ca2+ concentrations. The change in Ca2+ sensitivity was limited to the fast-releasing synaptic vesicles, which could be released rapidly on action potentials. cAMP did not affect the slowly releasing vesicles. Fit of the data using a simplified allosteric model indicated that cAMP increased the fusion “willingness,” thereby facilitating transmitter release. We suggest that synaptic vesicles have to be positionally primed to the release sites close to the Ca2+ channel cluster for cAMP to modulate intracellular Ca2+ sensitivity of transmitter release.
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Hong, Fashui, Xiao Ze, Xu Mu, and Yuguan Ze. "Titanium Dioxide Inhibits Hippocampal Neuronal Synapse Growth Through the Brain-Derived Neurotrophic Factor-Tyrosine Kinase Receptor B Signaling Pathway." Journal of Biomedical Nanotechnology 17, no. 1 (January 1, 2021): 37–52. http://dx.doi.org/10.1166/jbn.2021.2999.
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Nanoparticulate titanium dioxide (nano-TiO2) is a commonly used nanoparticle material and has been widely used in the fields of medicine, cosmetics, construction, and environmental protection. Numerous studies have demonstrated that nano-TiO2 has toxic effects on neuronal development, which lead to defects in learning and memory functions. However, it is still unclear whether nano-TiO2 inhibits the development of synapse and the underlying molecular mechanism is still unknown. In this study, nano-TiO2 was administered to rat primary hippocampal neurons for 24 h to investigate the underlying molecular mechanisms behind the inhibition of neuronal synaptic development by nano-TiO2. We used hippocampal neurons as a model to study the effect of nano-TiO2 on synaptic development. Our results demonstrated that dendritic development that represented synaptic plasticity in hippocampal neurons was significantly inhibited in a concentration-dependent manner after exposure to nano-TiO2 for 24 h. Experiments with varying concentrations of nano-TiO2 (5, 15, and 30 g/mL) indicated that the apoptotic rate of hippocampal neurons increased, development of neuronal synapses were inhibited, and synaptic densities decreased by 24.29%, 54.29%, and 72.86%, respectively, in post-treatment with nano-TiO2. Furthermore, the results indicated that the expressions of Synapsin I (SYN I) and postsynaptic density 95 (PSD95) in neuron synapse were also significantly inhibited, particularly SYN I decreased by 18.43%, 37.2%, and 51.6%, and PSD95 decreased by 16.02%, 24.06%, and 38.74% after treatment with varying concentrations of nano-TiO2, respectively. In addition, experiments to assess the BDNF-TrkB signaling pathway indicated that nano-TiO2 inhibited the expressions of key proteins in the downstream MEK/ERK and PI3K/Akt signaling pathways by inhibiting the expression of BDNF. With concentrations of nano-TiO2 at 5, 15, and 30 μg/mL, the expression of BDNF decreased by 22.64%, 33.3%, and 53.58% compared with the control group. Further, the expression ratios of downstream key proteins p-CREB/CREB decreased by 3.03%, 18.11%, and 30.57%; p-ERK1/2/ERK1/2 ratios decreased by 19.11%, 28.82%, and 58.09%, and p-Akt1/Akt1 ratios decreased by 1.92%, 27.79%, and 41.33%, respectively. These results demonstrated that nano-TiO2 inhibited the normal function of the BDNF-TrkB signaling pathway, which is closely related to neuronal synapse. Thus, it can be hypothesized that the inhibition of neuronal synaptic growth by nano-TiO2 may be related to the inhibition of BDNF-TrkB signaling pathway.
Dissertations / Theses on the topic "Rat synapse mechanisms"
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Clowry, G. J. "Studies of neuronal connectivity in the superior cervical sympathetic ganglion of the rat." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382701.
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Dobie, Frederick Andrew. "Molecular and cellular mechanisms of inhibitory synapse formation in developing rat hippocampal neurons." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/41933.
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The proper functioning of the brain and central nervous system (CNS) requires the precise formation of synapses between neurons. The two main neurotransmitter systems for fast synaptic communication in the CNS are excitatory glutamate and inhibitory gamma-aminobutyric acid. A growing body of evidence has begun to uncover several shared and divergent rules for the establishment of each of these two types of synapses.
At the molecular level, a number of key proteins have been shown to be involved in the initial formation and subsequent development of synaptic connection, including cell adhesion molecules (CAMs). Among the CAMs, neurexins and neuroligins are important synaptogenic proteins that act trans-synaptically to organize synapses: binding of axonal beta-neurexins by neuroligins is sufficient to cause development of a presynaptic specialization at that site, while binding of dendritic neuroligin-1 or neuroligin-2 by beta-neurexins is sufficient to cause development of postsynaptic excitatory or inhibitory specializations, respectively. In Chapter 2, we explore the role of alpha-neurexins in synapse organization. We find alpha-neurexins are able to specifically induce the formation of inhibitory synapses, presumably through clustering of postsynaptic neuroligin-2. Moreover, we find that the expression of various splice variants of alpha- and beta-neurexins is regulated both during development and by activity, suggesting a physiological role for alternative splicing in the modulation of synapse assembly.
At the cellular level, it is now clear from live imaging studies that synapses and their formation are highly dynamic processes. A number of studies have established the temporal recruitment of pre- and postsynaptic components to nascent synapses and how synapse formation can influence neuron growth. However, these studies have focused on excitatory synapses. In Chapter 3, we explore the cellular mechanisms of inhibitory synapse formation and modulation. We find that entire synapses are highly mobile and can undergo dynamic structural modulation. New synapses are formed by gradual accumulation of components from diffuse cytoplasmic pools, with a significant contribution of presynaptic vesicles from previously recycling sites. These results provide new insights into the mechanisms of inhibitory synapse formation and how it is both similar and different from excitatory synapse formation.
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Bender, Kevin James. "Mechanisms of deprivation-induced map plasticity at layer 4 to layer 2/3 synapses in rat barrel cortex /." Diss., Connected to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3187822.
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Thesis (Ph. D.)--University of California, San Diego, 2005.Title from first page of PDF file (viewed January 11, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Barri, Alessandro. "Network mechanisms of memory storage in the balanced cortex." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T060/document.
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Pas de résumé en françaisIt is generally maintained that one of cortex’ functions is the storage of a large number of memories. In this picture, the physical substrate of memories is thought to be realised in pattern and strengths of synaptic connections among cortical neurons. Memory recall is associated with neuronal activity that is shaped by this connectivity. In this framework, active memories are represented by attractors in the space of neural activity. Electrical activity in cortical neurones in vivo exhibits prominent temporal irregularity. A standard way to account for this phenomenon is to postulate that recurrent synaptic excitation and inhibition as well as external inputs are balanced. In the common view, however, these balanced networks do not easily support the coexistence of multiple attractors. This is problematic in view of memory function. Recently, theoretical studies showed that balanced networks with synapses that exhibit short-term plasticity (STP) are able to maintain multiple stable states. In order to investigate whether experimentally obtained synaptic parameters are consistent with model predictions, we developed a new methodology that is capable to quantify both response variability and STP at the same synapse in an integrated and statistically-principled way. This approach yields higher parameter precision than standard procedures and allows for the use of more efficient stimulation protocols. However, the findings with respect to STP parameters do not allow to make conclusive statements about the validity of synaptic theories of balanced working memory. In the second part of this thesis an alternative theory of cortical memory storage is developed. The theory is based on the assumptions that memories are stored in attractor networks, and that memories are not represented by network states differing in their average activity levels, but by micro-states sharing the same global statistics. Different memories differ with respect to their spatial distributions of firing rates. From this the main result is derived: the balanced state is a necessary condition for extensive memory storage. Furthermore, we analytically calculate memory storage capacities of rate neurone networks. Remarkably, it can be shown that crucial properties of neuronal activity and physiology that are consistent with experimental observations are directly predicted by the theory if optimal memory storage capacity is required
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Wadel, Kristian. "The mechanism mediating fast neurotransmitter release at the calyx of Held synapse." Doctoral thesis, 2008. http://hdl.handle.net/11858/00-1735-0000-0006-B4F6-F.
Full textBook chapters on the topic "Rat synapse mechanisms"
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Soderling, Scott H., and Linda Van Aelst. "Principles Driving the Spatial Organization of Rho GTPase Signaling at Synapses." In Ras Superfamily Small G Proteins: Biology and Mechanisms 1, 395–419. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1806-1_17.
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Laughlin, Simon B. "Fly Optic Lamina as a Guide to Neural Circuit Design." In Handbook of Brain Microcircuits, edited by Gordon M. Shepherd and Sten Grillner, 285–92. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190636111.003.0023.
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Lamina circuits are designed to transfer information effectively and efficiently from photoreceptors to interneurons in the face of two neural constraints: limited dynamic range and synaptic noise. The design uses analogue signals to achieve high information rates, high gain synapses releasing vesicles at high rate to reduce the effects of synaptic noise, and predictive coding to remove redundancy. To increase synaptic efficiency predictive coding is implemented pre-synaptically, using unorthodox non-vesicular mechanisms. To optimize information uptake, the lamina circuit continuously adapts to input statistics over a wide range of input levels. The lamina circuit demonstrates a widely employed circuit motif because its equivalent, in the vertebrate retina’s outer plexiform layer (OPL) has similar properties. The motif’s functional advantages were established in lamina because it is more amenable to reverse engineering. Indeed, the fly lamina exemplifies several principles of neural design that apply widely throughout brains.
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Cheshire, William P. "Autonomic Physiology." In Clinical Neurophysiology, 617–28. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780195385113.003.0035.
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The autonomic nervous system consists of three divisions: the sympathetic (thoracolumbar), parasympathetic (craniosacral), and enteric nervous systems. The sympathetic and parasympathetic autonomic outflows involve a two-neuron pathway with a synapse in an autonomic ganglion. Preganglionic sympathetic neurons are organized into various functional units that control specific targets and include skin vasomotor, muscle vasomotor, visceromotor, pilomotor, and sudomotor units. Microneurographic techniques allow recording of postganglionic sympathetic nerve activity in humans. Skin sympathetic activity is a mixture of sudomotor and vasoconstrictor impulses and is regulated mainly by environmental temperature and emotional influences. Muscle sympathetic activity is composed of vasoconstrictor impulses that are strongly modulated by arterial baroreceptors. Heart rate is controlled by vagal parasympathetic and thoracic sympathetic inputs. Vagal influence on the heart rate is strongly modulated by respiration; it is more marked during expiration and is absent during inspiration. This is the basis for the so-called respiratory sinus arrhythmia, which is an important index of vagal innervation of the heart. Power spectral analysis of heart rate fluctuations allows noninvasive assessment of beat-to-beat modulation of neuronal activity affecting the heart. Arterial baroreflex, cardiopulmonary reflexes, venoarteriolar reflex, and ergoreflexes control sympathetic and parasympathetic influences on cardiovascular effectors. The main regulatory mechanism that prevents orthostatic hypotension is reflex arterial vasoconstriction in the splanchnic, renal, and muscular beds triggered by a decrease in transmural pressure at the level of carotid sinus baroreceptors.
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Koch, Christof. "Unconventional Computing." In Biophysics of Computation. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195104912.003.0026.
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As discussed in the introduction to this book, any (bio)physical mechanism that transforms some physical variable, such as the electrical potential across the membrane, in such a way that it can be mapped onto a meaningful formal mathematical operation, such as delayand- correlate or convolution, can be treated as a computation. Traditionally only Vm, spike trains, and the firing rate f(t) have been thought to play this role in the computations performed by the nervous system. Due to the recent and widespread usage of high-resolution calcium-dependent fluorescent dyes, the concentration of free intracellular calcium [Ca2+]i in presynaptic terminals, dendrites, and cell bodies has been promoted into the exalted rank of a variable that can act as a short-term memory and that can be manipulated using buffers, calcium-dependent enzymes, and diffusion in ways that can be said to instantiate specific computations. But why stop here? Why not consider the vast number of signaling molecules that are localized to specific intra- or extracellular compartments to instantiate specific computations that can act over particular spatial and temporal time scales? And what about the peptides and hormones that are released into large areas of the brain or that circulate in the bloodstream? In this penultimate chapter, we will acquaint the reader with several examples of computations that use such unconventional means. The computation in question constitutes a molecular switch that stores a few bits of information at each of the thousands of synapses on a typical cortical cell. In order to describe its principle of operation, it will be necessary to introduce the reader to some basic concepts in biochemistry. The ability of individual synapses to potentially store analog variables is important enough that this modest intellectual investment will pay off. (For an introduction to biochemistry, consult Stryer, 1995).