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1

Higgs, Matthew H., and Charles J. Wilson. "Frequency-dependent entrainment of striatal fast-spiking interneurons." Journal of Neurophysiology 122, no. 3 (September 1, 2019): 1060–72. http://dx.doi.org/10.1152/jn.00369.2019.

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Striatal fast-spiking interneurons (FSIs) fire in variable-length runs of action potentials at 20–200 spikes/s separated by pauses. In vivo, or with fluctuating applied current, both runs and pauses become briefer and more variable. During runs, spikes are entrained specifically to gamma-frequency components of the input fluctuations. We stimulated parvalbumin-expressing striatal FSIs in mouse brain slices with broadband noise currents added to direct current steps and measured spike entrainment across all frequencies. As the constant current level was increased, FSIs produced longer runs and showed sharper frequency tuning, with best entrainment at the stimulus frequency matching their intrarun firing rate. We separated the contributions of previous spikes from that of the fluctuating stimulus, revealing a strong contribution of previous action potentials to gamma-frequency entrainment. In contrast, after subtraction of the effect inherited from the previous spike, the remaining stimulus contribution to spike generation was less sharply tuned, showing a larger contribution of lower frequencies. The frequency specificity of entrainment within a run was reproduced with a phase resetting model based on experimentally measured phase resetting curves of the same FSIs. In the model, broadly tuned phase entrainment for the first spike in a run evolved into sharply tuned gamma entrainment over the next few spikes. The data and modeling results indicate that for FSIs firing in brief runs and pauses firing within runs is entrained by gamma-frequency components of the input, whereas the onset timing of runs may be sensitive to a wider range of stimulus frequency components. NEW & NOTEWORTHY Specific types of neurons entrain their spikes to particular oscillation frequencies in their synaptic input. This entrainment is commonly understood in terms of the subthreshold voltage response, but how this translates to spiking is not clear. We show that in striatal fast-spiking interneurons, entrainment to gamma-frequency input depends on rhythmic spike runs and is explained by the phase resetting curve, whereas run initiation can be triggered by a broad range of input frequencies.
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2

Marche, Kévin, and Paul Apicella. "Changes in activity of fast-spiking interneurons of the monkey striatum during reaching at a visual target." Journal of Neurophysiology 117, no. 1 (January 1, 2017): 65–78. http://dx.doi.org/10.1152/jn.00566.2016.

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Recent works highlight the importance of local inhibitory interneurons in regulating the function of the striatum. In particular, fast-spiking interneurons (FSIs), which likely correspond to a subgroup of GABAergic interneurons, have been involved in the control of movement by exerting strong inhibition on striatal output pathways. However, little is known about the exact contribution of these presumed interneurons in movement preparation, initiation, and execution. We recorded the activity of FSIs in the striatum of monkeys as they performed reaching movements to a visual target under two task conditions: one in which the movement target was presented at unsignaled left or right locations, and another in which advance information about target location was available, thus allowing monkeys to react faster. Modulations of FSI activity around the initiation of movement (53% of 55 neurons) consisted mostly of increases reaching maximal firing immediately before or, less frequently, after movement onset. Another subset of FSIs showed decreases in activity during movement execution. Rarely did movement-related changes in FSI firing depend on response direction and movement speed. Modulations of FSI activity occurring relatively early in relation to movement initiation were more influenced by the preparation for movement, compared with those occurring later. Conversely, FSI activity remained unaffected, as monkeys were preparing a movement toward a specific location and instead moved to the opposite direction when the trigger occurred. These results provide evidence that changes in activity of presumed GABAergic interneurons of the primate striatum could make distinct contributions to processes involved in movement generation. NEW & NOTEWORTHY We explored the functional contributions of striatal fast-spiking interneurons (FSIs), presumed GABAergic interneurons, to distinct steps of movement generation in monkeys performing a reaching task. The activity of individual FSIs was modulated before and during the movement, consisting mostly of increased in firing rates. Changes in activity also occurred during movement preparation. We interpret this variety of modulation types at different moments of task performance as reflecting differential FSI control over distinct phases of movement.
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3

Banaie Boroujeni, Kianoush, Mariann Oemisch, Seyed Alireza Hassani, and Thilo Womelsdorf. "Fast spiking interneuron activity in primate striatum tracks learning of attention cues." Proceedings of the National Academy of Sciences 117, no. 30 (July 13, 2020): 18049–58. http://dx.doi.org/10.1073/pnas.2001348117.

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Cognitive flexibility depends on a fast neural learning mechanism for enhancing momentary relevant over irrelevant information. A possible neural mechanism realizing this enhancement uses fast spiking interneurons (FSIs) in the striatum to train striatal projection neurons to gate relevant and suppress distracting cortical inputs. We found support for such a mechanism in nonhuman primates during the flexible adjustment of visual attention in a reversal learning task. FSI activity was modulated by visual attention cues during feature-based learning. One FSI subpopulation showed stronger activation during learning, while another FSI subpopulation showed response suppression after learning, which could indicate a disinhibitory effect on the local circuit. Additionally, FSIs that showed response suppression to learned attention cues were activated by salient distractor events, suggesting they contribute to suppressing bottom-up distraction. These findings suggest that striatal fast spiking interneurons play an important role when cues are learned that redirect attention away from previously relevant to newly relevant visual information. This cue-specific activity was independent of motor-related activity and thus tracked specifically the learning of reward predictive visual features.
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Damodaran, Sriraman, Rebekah C. Evans, and Kim T. Blackwell. "Synchronized firing of fast-spiking interneurons is critical to maintain balanced firing between direct and indirect pathway neurons of the striatum." Journal of Neurophysiology 111, no. 4 (February 15, 2014): 836–48. http://dx.doi.org/10.1152/jn.00382.2013.

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The inhibitory circuits of the striatum are known to be critical for motor function, yet their contributions to Parkinsonian motor deficits are not clear. Altered firing in the globus pallidus suggests that striatal medium spiny neurons (MSN) of the direct (D1 MSN) and indirect pathway (D2 MSN) are imbalanced during dopamine depletion. Both MSN classes receive inhibitory input from each other and from inhibitory interneurons within the striatum, specifically the fast-spiking interneurons (FSI). To investigate the role of inhibition in maintaining striatal balance, we developed a biologically-realistic striatal network model consisting of multicompartmental neuron models: 500 D1 MSNs, 500 D2 MSNs and 49 FSIs. The D1 and D2 MSN models are differentiated based on published experiments of individual channel modulations by dopamine, with D2 MSNs being more excitable than D1 MSNs. Despite this difference in response to current injection, in the network D1 and D2 MSNs fire at similar frequencies in response to excitatory synaptic input. Simulations further reveal that inhibition from FSIs connected by gap junctions is critical to produce balanced firing. Although gap junctions produce only a small increase in synchronization between FSIs, removing these connections resulted in significant firing differences between D1 and D2 MSNs, and balanced firing was restored by providing synchronized cortical input to the FSIs. Together these findings suggest that desynchronization of FSI firing is sufficient to alter balanced firing between D1 and D2 MSNs.
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5

Bakhurin, Konstantin I., Victor Mac, Peyman Golshani, and Sotiris C. Masmanidis. "Temporal correlations among functionally specialized striatal neural ensembles in reward-conditioned mice." Journal of Neurophysiology 115, no. 3 (March 1, 2016): 1521–32. http://dx.doi.org/10.1152/jn.01037.2015.

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As the major input to the basal ganglia, the striatum is innervated by a wide range of other areas. Overlapping input from these regions is speculated to influence temporal correlations among striatal ensembles. However, the network dynamics among behaviorally related neural populations in the striatum has not been extensively studied. We used large-scale neural recordings to monitor activity from striatal ensembles in mice undergoing Pavlovian reward conditioning. A subpopulation of putative medium spiny projection neurons (MSNs) was found to discriminate between cues that predicted the delivery of a reward and cues that predicted no specific outcome. These cells were preferentially located in lateral subregions of the striatum. Discriminating MSNs were more spontaneously active and more correlated than their nondiscriminating counterparts. Furthermore, discriminating fast spiking interneurons (FSIs) represented a highly prevalent group in the recordings, which formed a strongly correlated network with discriminating MSNs. Spike time cross-correlation analysis showed the existence of synchronized activity among FSIs and feedforward inhibitory modulation of MSN spiking by FSIs. These findings suggest that populations of functionally specialized (cue-discriminating) striatal neurons have distinct network dynamics that sets them apart from nondiscriminating cells, potentially to facilitate accurate behavioral responding during associative reward learning.
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6

Govindaiah, Gubbi, Rong-Jian Liu, and Yanyan Wang. "Dopamine D2L Receptor Deficiency Alters Neuronal Excitability and Spine Formation in Mouse Striatum." Biomedicines 10, no. 1 (January 4, 2022): 101. http://dx.doi.org/10.3390/biomedicines10010101.

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The striatum contains several types of neurons including medium spiny projection neurons (MSNs), cholinergic interneurons (ChIs), and fast-spiking interneurons (FSIs). Modulating the activity of these neurons by the dopamine D2 receptor (D2R) can greatly impact motor control and movement disorders. D2R exists in two isoforms: D2L and D2S. Here, we assessed whether alterations in the D2L and D2S expression levels affect neuronal excitability and synaptic function in striatal neurons. We observed that quinpirole inhibited the firing rate of all three types of striatal neurons in wild-type (WT) mice. However, in D2L knockout (KO) mice, quinpirole enhanced the excitability of ChIs, lost influence on spike firing of MSNs, and remained inhibitory effect on spike firing of FSIs. Additionally, we showed mIPSC frequency (but not mIPSC amplitude) was reduced in ChIs from D2L KO mice compared with WT mice, suggesting spontaneous GABA release is reduced at GABAergic terminals onto ChIs in D2L KO mice. Furthermore, we found D2L deficiency resulted in reduced dendritic spine density in ChIs, suggesting D2L activation plays a role in the formation/maintenance of dendritic spines of ChIs. These findings suggest new molecular and cellular mechanisms for causing ChIs abnormality seen in Parkinson’s disease or drug-induced dyskinesias.
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Xiao, Guihua, Yilin Song, Yu Zhang, Yu Xing, Shengwei Xu, Mixia Wang, Junbo Wang, Deyong Chen, Jian Chen, and Xinxia Cai. "Dopamine and Striatal Neuron Firing Respond to Frequency-Dependent DBS Detected by Microelectrode Arrays in the Rat Model of Parkinson’s Disease." Biosensors 10, no. 10 (September 28, 2020): 136. http://dx.doi.org/10.3390/bios10100136.

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(1) Background: Deep brain stimulation (DBS) is considered as an efficient treatment method for alleviating motor symptoms in Parkinson’s disease (PD), while different stimulation frequency effects on the specific neuron patterns at the cellular level remain unknown. (2) Methods: In this work, nanocomposites-modified implantable microelectrode arrays (MEAs) were fabricated to synchronously record changes of dopamine (DA) concentration and striatal neuron firing in the striatum during subthalamic nucleus DBS, and different responses of medium spiny projecting neurons (MSNs) and fast spiking interneurons (FSIs) to DBS were analyzed. (3) Results: DA concentration and striatal neuron spike firing rate showed a similar change as DBS frequency changed from 10 to 350 Hz. Note that the increases in DA concentration (3.11 ± 0.67 μM) and neural spike firing rate (15.24 ± 2.71 Hz) were maximal after the stimulation at 100 Hz. The MSNs firing response to DBS was significant, especially at 100 Hz, while the FSIs remained stable after various stimulations. (4) Conclusions: DBS shows the greatest regulatory effect on DA concentration and MSNs firing rate at 100 Hz stimulation. This implantable MEA in the recording of the neurotransmitter and neural spike pattern response to DBS provides a new insight to understand the mechanism of PD at the cellular level.
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8

Shaheen, Hina, and Roderick Melnik. "Deep Brain Stimulation with a Computational Model for the Cortex-Thalamus-Basal-Ganglia System and Network Dynamics of Neurological Disorders." Computational and Mathematical Methods 2022 (February 13, 2022): 1–17. http://dx.doi.org/10.1155/2022/8998150.

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Deep brain stimulation (DBS) can alleviate the movement disorders like Parkinson’s disease (PD). Indeed, it is known that aberrant beta (13-30 Hz) oscillations and the loss of dopaminergic neurons in the basal ganglia-thalamus (BGTH) and cortex characterize the akinesia symptoms of PD. However, the relevant biophysical mechanism behind this process still remains unclear. Based on the prior striatal inhibitory model, we propose an extended BGTH model incorporating medium spine neurons (MSNs) and fast-spiking interneurons (FSIs) along with the effect of DBS. We are focusing in this paper on an open-loop DBS mode, where the stimulation parameters stay constant independent of variations in the disease state, and modifications of parameters rely mainly on trial and error of medical experts. Additionally, we propose a novel combined model of the cerebellar-basal-ganglia thalamocortical network, MSNs, and FSIs and show new results that indicate that Parkinsonian oscillations in the beta-band frequency range emerge from the dynamics of such a network. Our model predicts that DBS can be used to suppress beta oscillations in globus pallidus pars interna (GPi) neurons. This research will help our better understanding of the changes in the brain activity caused by DBS, providing new insight for studying PD in the future.
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9

Kunimatsu, Jun, Shinya Yamamoto, Kazutaka Maeda, and Okihide Hikosaka. "Environment-based object values learned by local network in the striatum tail." Proceedings of the National Academy of Sciences 118, no. 4 (January 19, 2021): e2013623118. http://dx.doi.org/10.1073/pnas.2013623118.

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Basal ganglia contribute to object-value learning, which is critical for survival. The underlying neuronal mechanism is the association of each object with its rewarding outcome. However, object values may change in different environments and we then need to choose different objects accordingly. The mechanism of this environment-based value learning is unknown. To address this question, we created an environment-based value task in which the value of each object was reversed depending on the two scene-environments (X and Y). After experiencing this task repeatedly, the monkeys became able to switch the choice of object when the scene-environment changed unexpectedly. When we blocked the inhibitory input from fast-spiking interneurons (FSIs) to medium spiny projection neurons (MSNs) in the striatum tail by locally injecting IEM-1460, the monkeys became unable to learn scene-selective object values. We then studied the mechanism of the FSI-MSN connection. Before and during this learning, FSIs responded to the scenes selectively, but were insensitive to object values. In contrast, MSNs became able to discriminate the objects (i.e., stronger response to good objects), but this occurred clearly in one of the two scenes (X or Y). This was caused by the scene-selective inhibition by FSI. As a whole, MSNs were divided into two groups that were sensitive to object values in scene X or in scene Y. These data indicate that the local network of striatum tail controls the learning of object values that are selective to the scene-environment. This mechanism may support our flexible switching behavior in various environments.
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10

Bryson, Alexander, Samuel F. Berkovic, Steven Petrou, and David B. Grayden. "State transitions through inhibitory interneurons in a cortical network model." PLOS Computational Biology 17, no. 10 (October 15, 2021): e1009521. http://dx.doi.org/10.1371/journal.pcbi.1009521.

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Inhibitory interneurons shape the spiking characteristics and computational properties of cortical networks. Interneuron subtypes can precisely regulate cortical function but the roles of interneuron subtypes for promoting different regimes of cortical activity remains unclear. Therefore, we investigated the impact of fast spiking and non-fast spiking interneuron subtypes on cortical activity using a network model with connectivity and synaptic properties constrained by experimental data. We found that network properties were more sensitive to modulation of the fast spiking population, with reductions of fast spiking excitability generating strong spike correlations and network oscillations. Paradoxically, reduced fast spiking excitability produced a reduction of global excitation-inhibition balance and features of an inhibition stabilised network, in which firing rates were driven by the activity of excitatory neurons within the network. Further analysis revealed that the synaptic interactions and biophysical features associated with fast spiking interneurons, in particular their rapid intrinsic response properties and short synaptic latency, enabled this state transition by enhancing gain within the excitatory population. Therefore, fast spiking interneurons may be uniquely positioned to control the strength of recurrent excitatory connectivity and the transition to an inhibition stabilised regime. Overall, our results suggest that interneuron subtypes can exert selective control over excitatory gain allowing for differential modulation of global network state.
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11

Krimer, Leonid S., Aleksey V. Zaitsev, Gabriela Czanner, Sven Kröner, Guillermo González-Burgos, Nadezhda V. Povysheva, Satish Iyengar, German Barrionuevo, and David A. Lewis. "Cluster Analysis–Based Physiological Classification and Morphological Properties of Inhibitory Neurons in Layers 2–3 of Monkey Dorsolateral Prefrontal Cortex." Journal of Neurophysiology 94, no. 5 (November 2005): 3009–22. http://dx.doi.org/10.1152/jn.00156.2005.

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In primates, little is known about intrinsic electrophysiological properties of neocortical neurons and their morphological correlates. To classify inhibitory cells (interneurons) in layers 2–3 of monkey dorsolateral prefrontal cortex we used whole cell voltage recordings and intracellular labeling in slice preparation with subsequent morphological reconstructions. Regular spiking pyramidal cells have been also included in the sample. Neurons were successfully segregated into three physiological clusters: regular-, intermediate-, and fast-spiking cells using cluster analysis as a multivariate exploratory technique. When morphological types of neurons were mapped on the physiological clusters, the cluster of regular spiking cells contained all pyramidal cells, whereas the intermediate- and fast-spiking clusters consisted exclusively of interneurons. The cluster of fast-spiking cells contained all of the chandelier cells and the majority of local, medium, and wide arbor (basket) interneurons. The cluster of intermediate spiking cells predominantly consisted of cells with the morphology of neurogliaform or vertically oriented (double-bouquet) interneurons. Thus a quantitative approach enabled us to demonstrate that intrinsic electrophysiological properties of neurons in the monkey prefrontal cortex define distinct cell types, which also display distinct morphologies.
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12

Larimer, Phillip, Julien Spatazza, Michael P. Stryker, Arturo Alvarez-Buylla, and Andrea R. Hasenstaub. "Development and long-term integration of MGE-lineage cortical interneurons in the heterochronic environment." Journal of Neurophysiology 118, no. 1 (July 1, 2017): 131–39. http://dx.doi.org/10.1152/jn.00096.2017.

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Interneuron precursors transplanted into visual cortex induce network plasticity during their heterochronic maturation. Such plasticity can have a significant impact on the function of the animal and is normally present only during a brief critical period in early postnatal development. Elucidating the synaptic and physiological properties of interneuron precursors as they mature is key to understanding how long-term circuit changes are induced by transplants. We studied the development of transplant-derived interneurons and compared it to endogenously developing interneurons (those that are born and develop in the same animal) at parallel developmental time points, using patch-clamp recordings in acute cortical slices. We found that transplant-derived interneurons develop into fast-spiking and non-fast-spiking neurons characteristic of the medial ganglionic eminence (MGE) lineage. Transplant-derived interneurons matured more rapidly than endogenously developing interneurons, as shown by more hyperpolarized membrane potentials, smaller input resistances, and narrower action potentials at a juvenile age. In addition, transplant-derived fast-spiking interneurons have more quickly saturating input-output relationships and lower maximal firing rates in adulthood, indicating a possible divergence in function. Transplant-derived interneurons both form inhibitory synapses onto host excitatory neurons and receive excitatory synapses from host pyramidal cells. Unitary connection properties are similar to those of host interneurons. These transplant-derived interneurons, however, were less densely functionally connected onto host pyramidal cells than were host interneurons and received fewer spontaneous excitatory inputs from host cells. These findings suggest that many physiological characteristics of interneurons are autonomously determined, while some factors impacting their circuit function may be influenced by the environment in which they develop. NEW & NOTEWORTHY Transplanting embryonic interneurons into older brains induces a period of plasticity in the recipient animal. We find that these interneurons develop typical fast-spiking and non-fast-spiking phenotypes by the end of adolescence. However, the input-output characteristics of transplant-derived neurons diverged from endogenously developing interneurons during adulthood, and they showed lower connection rates to local pyramidal cells at all time points. This suggests a unique and ongoing role of transplant-derived interneurons in host circuits, enabling interneuron transplant therapies.
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13

Bracci, Enrico, Diego Centonze, Giorgio Bernardi, and Paolo Calabresi. "Dopamine Excites Fast-Spiking Interneurons in the Striatum." Journal of Neurophysiology 87, no. 4 (April 1, 2002): 2190–94. http://dx.doi.org/10.1152/jn.00754.2001.

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The striatum is the main recipient of dopaminergic innervation. Striatal projection neurons are controlled by cholinergic and GABAergic interneurons. The effects of dopamine on projection neurons and cholinergic interneurons have been described. Its action on GABAergic interneurons, however, is still unknown. We studied the effects of dopamine on fast-spiking (FS) GABAergic interneurons in vitro, with intracellular recordings. Bath application of dopamine elicited a depolarization accompanied by an increase in membrane input resistance (an effect that persisted in the presence of tetrodotoxin) and action-potential discharge. These effects were mimicked by the D1-like dopamine receptor agonist SKF38393 but not by the D2-like agonist quinpirole. Evoked corticostriatal glutamatergic synaptic currents were not affected by dopamine. Conversely, GABAergic currents evoked by intrastriatal stimulation were reversibly depressed by dopamine and D2-like, but not D1-like, agonists. Cocaine elicited effects similar to those of dopamine on membrane potential and synaptic currents. These results show that endogenous dopamine exerts a dual excitatory action on FS interneurons, by directly depolarizing them (through D1-like receptors) and by reducing their synaptic inhibition (through presynaptic D2-like receptors).
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14

Kann, Oliver, Ismini E. Papageorgiou, and Andreas Draguhn. "Highly Energized Inhibitory Interneurons are a Central Element for Information Processing in Cortical Networks." Journal of Cerebral Blood Flow & Metabolism 34, no. 8 (June 4, 2014): 1270–82. http://dx.doi.org/10.1038/jcbfm.2014.104.

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Gamma oscillations (~30 to 100 Hz) provide a fundamental mechanism of information processing during sensory perception, motor behavior, and memory formation by coordination of neuronal activity in networks of the hippocampus and neocortex. We review the cellular mechanisms of gamma oscillations about the underlying neuroenergetics, i.e., high oxygen consumption rate and exquisite sensitivity to metabolic stress during hypoxia or poisoning of mitochondrial oxidative phosphorylation. Gamma oscillations emerge from the precise synaptic interactions of excitatory pyramidal cells and inhibitory GABAergic interneurons. In particular, specialized interneurons such as parvalbumin-positive basket cells generate action potentials at high frequency (‘fast-spiking’) and synchronize the activity of numerous pyramidal cells by rhythmic inhibition (‘clockwork’). As prerequisites, fast-spiking interneurons have unique electrophysiological properties and particularly high energy utilization, which is reflected in the ultrastructure by enrichment with mitochondria and cytochrome c oxidase, most likely needed for extensive membrane ion transport and γ-aminobutyric acid metabolism. This supports the hypothesis that highly energized fast-spiking interneurons are a central element for cortical information processing and may be critical for cognitive decline when energy supply becomes limited (‘interneuron energy hypothesis’). As a clinical perspective, we discuss the functional consequences of metabolic and oxidative stress in fast-spiking interneurons in aging, ischemia, Alzheimer's disease, and schizophrenia.
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Di Garbo, Angelo, Michele Barbi, and Santi Chillemi. "Signal processing properties of fast spiking interneurons." Biosystems 86, no. 1-3 (October 2006): 27–37. http://dx.doi.org/10.1016/j.biosystems.2006.03.009.

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Urban-Ciecko, Joanna, Małgorzata Kossut, and Jerzy W. Mozrzymas. "Sensory Learning Differentially Affects GABAergic Tonic Currents in Excitatory Neurons and Fast Spiking Interneurons in Layer 4 of Mouse Barrel Cortex." Journal of Neurophysiology 104, no. 2 (August 2010): 746–54. http://dx.doi.org/10.1152/jn.00988.2009.

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Pairing tactile stimulation of whiskers with a tail shock is known to result in expansion of cortical representation of stimulated vibrissae and in the increase in synaptic GABAergic transmission. However, the impact of such sensory learning in classical conditioning paradigm on GABAergic tonic currents has not been addressed. To this end, we performed whole cell patch-clamp slice recordings of tonic currents from neurons (excitatory regular spiking, regular spiking nonpyramidal, and fast spiking interneurons) of layer 4 of the barrel cortex from naive and trained mice. Interestingly, endogenous tonic GABAergic currents measured from the excitatory neurons in the cortical representation of “trained” vibrissae were larger than in the “naïve” or pseudoconditioned ones. On the contrary, sensory learning markedly reduced tonic currents in the fast spiking interneurons but not in regular spiking nonpyramidal neurons. Changes of tonic currents were accompanied by changes in the input resistances—decrease in regular spiking and increase in fast spiking neurons, respectively. Applications of nipecotic acid, a GABA uptake blocker, enhanced the tonic currents, but the impact of the sensory learning remained qualitatively the same as in the case of the tonic currents. Similar to endogenous tonic currents, sensory learning enhanced currents induced by THIP (superagonist for δ subunit–containing GABAA receptors) in regular spiking neurons, whereas the opposite was observed for the fast spiking interneurons. In conclusion, our data show that the sensory learning strongly affects the GABAergic tonic currents in a cell-specific manner and suggest that the underlying mechanism involves regulation of expression of δ subunit–containing GABAA receptors.
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Blomeley, Craig P., and Enrico Bracci. "Serotonin excites fast-spiking interneurons in the striatum." European Journal of Neuroscience 29, no. 8 (April 2009): 1604–14. http://dx.doi.org/10.1111/j.1460-9568.2009.06725.x.

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Di Garbo, Angelo, Michele Barbi, and Santi Chillemi. "Synchronization in a network of fast-spiking interneurons." Biosystems 67, no. 1-3 (October 2002): 45–53. http://dx.doi.org/10.1016/s0303-2647(02)00062-x.

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Maguire, Jamie. "Fast-Spiking Interneurons Exposed in Tumor-Associated Epilepsy." Epilepsy Currents 19, no. 2 (March 2019): 119–21. http://dx.doi.org/10.1177/1535759719835351.

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Pisansky, Marc T., Emilia M. Lefevre, Cassandra L. Retzlaff, Brian H. Trieu, David W. Leipold, and Patrick E. Rothwell. "Nucleus Accumbens Fast-Spiking Interneurons Constrain Impulsive Action." Biological Psychiatry 86, no. 11 (December 2019): 836–47. http://dx.doi.org/10.1016/j.biopsych.2019.07.002.

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Povysheva, Nadezhda V., and Jon W. Johnson. "Tonic NMDA receptor-mediated current in prefrontal cortical pyramidal cells and fast-spiking interneurons." Journal of Neurophysiology 107, no. 8 (April 15, 2012): 2232–43. http://dx.doi.org/10.1152/jn.01017.2011.

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Tonically activated neuronal currents mediated by N-methyl-d-aspartate receptors (NMDARs) have been hypothesized to contribute to normal neuronal function as well as to neuronal pathology resulting from excessive activation of glutamate receptors (e.g., excitotoxicity). Whereas cortical excitatory cells are very vulnerable to excitotoxic insult, the data regarding resistance of inhibitory cells (or interneurons) are inconsistent. Types of neurons with more pronounced tonic NMDAR current potentially associated with the activation of extrasynaptic NMDARs could be expected to be more vulnerable to excessive activation by glutamate. In this study, we compared tonic activation of NMDARs in excitatory pyramidal cells and inhibitory fast-spiking interneurons in prefrontal cortical slices. We assessed tonic NMDAR current by measuring holding current shift as well as noise reduction following NMDAR blockade after removal of spontaneous glutamate release. In addition, we compared NMDAR miniature excitatory postsynaptic currents (EPSCs) in both cell types. We have demonstrated for the first time that tonic NMDAR currents are present in inhibitory fast-spiking interneurons. We found that the magnitude of tonic NMDAR current is similar in pyramidal cells and fast-spiking interneurons, and that quantal release of glutamate does not significantly impact tonic NMDAR current.
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Bjorefeldt, Andreas, Pontus Wasling, Henrik Zetterberg, and Eric Hanse. "Neuromodulation of fast-spiking and non-fast-spiking hippocampal CA1 interneurons by human cerebrospinal fluid." Journal of Physiology 594, no. 4 (January 18, 2016): 937–52. http://dx.doi.org/10.1113/jp271553.

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Zhou, Fu-Wen, and Steven N. Roper. "Reduced chemical and electrical connections of fast-spiking interneurons in experimental cortical dysplasia." Journal of Neurophysiology 112, no. 6 (September 15, 2014): 1277–90. http://dx.doi.org/10.1152/jn.00126.2014.

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Aberrant neural connections are regarded as a principal factor contributing to epileptogenesis. This study examined chemical and electrical connections between fast-spiking (FS), parvalbumin (PV)-immunoreactive (FS-PV) interneurons and regular-spiking (RS) neurons (pyramidal neurons or spiny stellate neurons) in a rat model of prenatal irradiation-induced cortical dysplasia. Presynaptic action potentials were evoked by current injection and the elicited unitary inhibitory or excitatory postsynaptic potentials (uIPSPs or uEPSPs) were recorded in the postsynaptic cell. In dysplastic cortex, connection rates between presynaptic FS-PV interneurons and postsynaptic RS neurons and FS-PV interneurons, and uIPSP amplitudes were significantly smaller than controls, but both failure rates and coefficient of variation of uIPSP amplitudes were larger than controls. In contrast, connection rates from RS neurons to FS-PV interneurons and uEPSPs amplitude were similar in the two groups. Assessment of the paired pulse ratio showed a significant decrease in synaptic release probability at FS-PV interneuronal terminals, and the density of terminal boutons on axons of biocytin-filled FS-PV interneurons was also decreased, suggesting presynaptic dysfunction in chemical synapses formed by FS-PV interneurons. Electrical connections were observed between FS-PV interneurons, and the connection rates and coupling coefficients were smaller in dysplastic cortex than controls. In dysplastic cortex, we found a reduced synaptic efficiency for uIPSPs originating from FS-PV interneurons regardless of the type of target cell, and impaired electrical connections between FS-PV interneurons. This expands our understanding of the fundamental impairment of inhibition in this model and may have relevance for certain types of human cortical dysplasia.
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Nomura, Masaki, Tomoki Fukai, and Toshio Aoyagi. "Synchrony of Fast-Spiking Interneurons Interconnected by GABAergic and Electrical Synapses." Neural Computation 15, no. 9 (September 1, 2003): 2179–98. http://dx.doi.org/10.1162/089976603322297340.

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Fast-spiking (FS) interneurons have specific types (Kv3.1/3.2 type) of the delayed potassium channel, which differ from the conventional Hodgkin-Huxley (HH) type potassium channel (Kv1.3 type) in several aspects. In this study, we show dramatic effects of the Kv3.1/3.2 potassium channel on the synchronization of the FS interneurons. We show analytically that two identical electrically coupled FS interneurons modeled with Kv3.1/3.2 channel fire synchronously at arbitrary firing frequencies, unlike similarly coupled FS neurons modeled with Kv1.3 channel that show frequency-dependent synchronous and antisynchronous firing states. Introducing GABA A receptor-mediated synaptic connections into an FS neuron pair tends to induce an antisynchronous firing state, even if the chemical synapses are bidirectional. Accordingly, an FS neuron pair connected simultaneously by electrical and chemical synapses achieves both synchronous firing state and antisynchronous firing state in a physiologically plausible range of the conductance ratio between electrical and chemical synapses. Moreover, we find that a large-scale network of FS interneurons connected by gap junctions and bidirectional GABAergic synapses shows similar bistability in the range of gamma frequencies (30–70 Hz).
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Cabungcal, J. H., P. Steullet, H. Morishita, R. Kraftsik, M. Cuenod, T. K. Hensch, and K. Q. Do. "Perineuronal nets protect fast-spiking interneurons against oxidative stress." Proceedings of the National Academy of Sciences 110, no. 22 (May 13, 2013): 9130–35. http://dx.doi.org/10.1073/pnas.1300454110.

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Golomb, David, Karnit Donner, Liron Shacham, Dan Shlosberg, Yael Amitai, and David Hansel. "Mechanisms of Firing Patterns in Fast-Spiking Cortical Interneurons." PLoS Computational Biology 3, no. 8 (August 10, 2007): e156. http://dx.doi.org/10.1371/journal.pcbi.0030156.

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Golomb, David, Karnit Donner, Liron Shacham, Dan Shlosberg, Yael Amitai, and David Hansel. "Mechanisms of Firing Patterns in Fast-Spiking Cortical Interneurons." PLoS Computational Biology preprint, no. 2007 (2005): e156. http://dx.doi.org/10.1371/journal.pcbi.0030156.eor.

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28

Gittis, A. H., D. K. Leventhal, B. A. Fensterheim, J. R. Pettibone, J. D. Berke, and A. C. Kreitzer. "Selective Inhibition of Striatal Fast-Spiking Interneurons Causes Dyskinesias." Journal of Neuroscience 31, no. 44 (November 2, 2011): 15727–31. http://dx.doi.org/10.1523/jneurosci.3875-11.2011.

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Guo, Daqing, Mingming Chen, Matjaž Perc, Shengdun Wu, Chuan Xia, Yangsong Zhang, Peng Xu, Yang Xia, and Dezhong Yao. "Firing regulation of fast-spiking interneurons by autaptic inhibition." EPL (Europhysics Letters) 114, no. 3 (May 1, 2016): 30001. http://dx.doi.org/10.1209/0295-5075/114/30001.

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Peng, Yangfan, Federico J. Barreda Tomas, Paul Pfeiffer, Moritz Drangmeister, Susanne Schreiber, Imre Vida, and Jörg R. P. Geiger. "Spatially structured inhibition defined by polarized parvalbumin interneuron axons promotes head direction tuning." Science Advances 7, no. 25 (June 2021): eabg4693. http://dx.doi.org/10.1126/sciadv.abg4693.

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In cortical microcircuits, it is generally assumed that fast-spiking parvalbumin interneurons mediate dense and nonselective inhibition. Some reports indicate sparse and structured inhibitory connectivity, but the computational relevance and the underlying spatial organization remain unresolved. In the rat superficial presubiculum, we find that inhibition by fast-spiking interneurons is organized in the form of a dominant super-reciprocal microcircuit motif where multiple pyramidal cells recurrently inhibit each other via a single interneuron. Multineuron recordings and subsequent 3D reconstructions and analysis further show that this nonrandom connectivity arises from an asymmetric, polarized morphology of fast-spiking interneuron axons, which individually cover different directions in the same volume. Network simulations assuming topographically organized input demonstrate that such polarized inhibition can improve head direction tuning of pyramidal cells in comparison to a “blanket of inhibition.” We propose that structured inhibition based on asymmetrical axons is an overarching spatial connectivity principle for tailored computation across brain regions.
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Burket, Jessica A., Jason D. Webb, and Stephen I. Deutsch. "Perineuronal Nets and Metal Cation Concentrations in the Microenvironments of Fast-Spiking, Parvalbumin-Expressing GABAergic Interneurons: Relevance to Neurodevelopment and Neurodevelopmental Disorders." Biomolecules 11, no. 8 (August 18, 2021): 1235. http://dx.doi.org/10.3390/biom11081235.

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Because of their abilities to catalyze generation of toxic free radical species, free concentrations of the redox reactive metals iron and copper are highly regulated. Importantly, desired neurobiological effects of these redox reactive metal cations occur within very narrow ranges of their local concentrations. For example, synaptic release of free copper acts locally to modulate NMDA receptor-mediated neurotransmission. Moreover, within the developing brain, iron is critical to hippocampal maturation and the differentiation of parvalbumin-expressing neurons, whose soma and dendrites are surrounded by perineuronal nets (PNNs). The PNNs are a specialized component of brain extracellular matrix, whose polyanionic character supports the fast-spiking electrophysiological properties of these parvalbumin-expressing GABAergic interneurons. In addition to binding cations and creation of the Donnan equilibrium that support the fast-spiking properties of this subset of interneurons, the complex architecture of PNNs also binds metal cations, which may serve a protective function against oxidative damage, especially of these fast-spiking neurons. Data suggest that pathological disturbance of the population of fast-spiking, parvalbumin-expressing GABAergic inhibitory interneurons occur in at least some clinical presentations, which leads to disruption of the synchronous oscillatory output of assemblies of pyramidal neurons. Increased expression of the GluN2A NMDA receptor subunit on parvalbumin-expressing interneurons is linked to functional maturation of both these neurons and the perineuronal nets that surround them. Disruption of GluN2A expression shows increased susceptibility to oxidative stress, reflected in redox dysregulation and delayed maturation of PNNs. This may be especially relevant to neurodevelopmental disorders, including autism spectrum disorder. Conceivably, binding of metal redox reactive cations by the perineuronal net helps to maintain safe local concentrations, and also serves as a reservoir buffering against second-to-second fluctuations in their concentrations outside of a narrow physiological range.
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Beatty, Joseph A., Soomin C. Song, and Charles J. Wilson. "Cell-type-specific resonances shape the responses of striatal neurons to synaptic input." Journal of Neurophysiology 113, no. 3 (February 1, 2015): 688–700. http://dx.doi.org/10.1152/jn.00827.2014.

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Neurons respond to synaptic inputs in cell-type-specific ways. Each neuron type may thus respond uniquely to shared patterns of synaptic input. We applied statistically identical barrages of artificial synaptic inputs to four striatal cell types to assess differences in their responses to a realistic input pattern. Each interneuron type fired in phase with a specific input-frequency component. The fast-spiking interneuron fired in relation to the gamma-band (and higher) frequencies, the low-threshold spike interneuron to the beta-band frequencies, and the cholinergic neurons to the delta-band frequencies. Low-threshold spiking and cholinergic interneurons showed input impedance resonances at frequencies matching their spiking resonances. Fast-spiking interneurons showed resonance of input impedance but at lower than gamma frequencies. The spiny projection neuron's frequency preference did not have a fixed frequency but instead tracked its own firing rate. Spiny cells showed no input impedance resonance. Striatal interneurons are each tuned to a specific frequency band corresponding to the major frequency components of local field potentials. Their influence in the circuit may fluctuate along with the contribution of that frequency band to the input. In contrast, spiny neurons may tune to any of the frequency bands by a change in firing rate.
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33

Börgers, Christoph, Steven Epstein, and Nancy J. Kopell. "Gamma oscillations mediate stimulus competition and attentional selection in a cortical network model." Proceedings of the National Academy of Sciences 105, no. 46 (November 12, 2008): 18023–28. http://dx.doi.org/10.1073/pnas.0809511105.

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Simultaneous presentation of multiple stimuli can reduce the firing rates of neurons in extrastriate visual cortex below the rate elicited by a single preferred stimulus. We describe computational results suggesting how this remarkable effect may arise from strong excitatory drive to a substantial local population of fast-spiking inhibitory interneurons, which can lead to a loss of coherence in that population and thereby raise the effectiveness of inhibition. We propose that in attentional states fast-spiking interneurons may be subject to a bath of inhibition resulting from cholinergic activation of a second class of inhibitory interneurons, restoring conditions needed for gamma rhythmicity. Oscillations and coherence are emergent features, not assumptions, in our model. The gamma oscillations in turn support stimulus competition. The mechanism is a form of “oscillatory selection,” in which neural interactions change phase relationships that regulate firing rates, and attention shapes those neural interactions.
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34

Erisir, A., D. Lau, B. Rudy, and C. S. Leonard. "Function of Specific K+ Channels in Sustained High-Frequency Firing of Fast-Spiking Neocortical Interneurons." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2476–89. http://dx.doi.org/10.1152/jn.1999.82.5.2476.

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Fast-spiking GABAergic interneurons of the neocortex and hippocampus fire high-frequency trains of brief action potentials with little spike-frequency adaptation. How these striking properties arise is unclear, although recent evidence suggests K+ channels containing Kv3.1-Kv3.2 proteins play an important role. We investigated the role of these channels in the firing properties of fast-spiking neocortical interneurons from mouse somatosensory cortex using a pharmacological and modeling approach. Low tetraethylammonium (TEA) concentrations (≤1 mM), which block only a few known K+channels including Kv3.1-Kv3.2, profoundly impaired action potential repolarization and high-frequency firing. Analysis of the spike trains evoked by steady depolarization revealed that, although TEA had little effect on the initial firing rate, it strongly reduced firing frequency later in the trains. These effects appeared to be specific to Kv3.1 and Kv3.2 channels, because blockade of dendrotoxin-sensitive Kv1 channels and BK Ca2+-activated K+ channels, which also have high TEA sensitivity, produced opposite or no effects. Voltage-clamp experiments confirmed the presence of a Kv3.1-Kv3.2–like current in fast-spiking neurons, but not in other interneurons. Analysis of spike shape changes during the spike trains suggested that Na+ channel inactivation plays a significant role in the firing-rate slowdown produced by TEA, a conclusion that was supported by computer simulations. These findings indicate that the unique properties of Kv3.1-Kv3.2 channels enable sustained high-frequency firing by facilitating the recovery of Na+ channel inactivation and by minimizing the duration of the afterhyperpolarization in neocortical interneurons.
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35

Cho, Kwang-Hyun, Jin Hwa Jang, Hyun-Jong Jang, Myung-Jun Kim, Shin Hee Yoon, Takaichi Fukuda, Frank Tennigkeit, Wolf Singer, and Duck-Joo Rhie. "Subtype-Specific Dendritic Ca2+ Dynamics of Inhibitory Interneurons in the Rat Visual Cortex." Journal of Neurophysiology 104, no. 2 (August 2010): 840–53. http://dx.doi.org/10.1152/jn.00146.2010.

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The Ca2+ increase in dendrites that is evoked by the backpropagation of somatic action potentials (APs) is involved in the activity-dependent modulation of dendritic and synaptic functions that are location dependent. In the present study, we investigated dendritic Ca2+ dynamics evoked by backpropagating APs (bAPs) in four subtypes of inhibitory interneurons classified by their spiking patterns: fast spiking (FS), late spiking (LS), burst spiking (BS), and regular-spiking nonpyramidal (RSNP) cells. Cluster analysis, single-cell RT-PCR, and immunohistochemistry confirmed the least-overlapping nature of the grouped cell populations. Somatic APs evoked dendritic Ca2+ transients in all subtypes of inhibitory interneurons with different spatial profiles along the tree: constantly linear in FS and LS cells, increasing to a plateau in BS cells and bell-shaped in RSNP cells. The increases in bAP-evoked dendritic Ca2+ transients brought about by the blocking of A-type K+ channels were similar in whole dendritic trees of each subtype of inhibitory interneurons. However, in RSNP cells, the increases in the distal dendrites were larger than those in the proximal dendrites. On cholinergic activation, nicotinic inhibition of bAP-evoked dendritic Ca2+ transients was observed only in BS cells expressing cholecystokinin and vasoactive intestinal peptide mRNAs, with no muscarinic modulation in all subtypes of inhibitory interneurons. Cell subtype-specific differential spatial profiles and their modulation in bAP-evoked dendritic Ca2+ transients might be important for the domain-specific modulation of segregated inputs in inhibitory interneurons and differential control between the excitatory and inhibitory networks in the visual cortex.
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36

Povysheva, Nadezhda V., Aleksey V. Zaitsev, Guillermo Gonzalez-Burgos, and David A. Lewis. "Electrophysiological Heterogeneity of Fast-Spiking Interneurons: Chandelier versus Basket Cells." PLoS ONE 8, no. 8 (August 12, 2013): e70553. http://dx.doi.org/10.1371/journal.pone.0070553.

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37

Okaty, B. W., M. N. Miller, K. Sugino, C. M. Hempel, and S. B. Nelson. "Transcriptional and Electrophysiological Maturation of Neocortical Fast-Spiking GABAergic Interneurons." Journal of Neuroscience 29, no. 21 (May 27, 2009): 7040–52. http://dx.doi.org/10.1523/jneurosci.0105-09.2009.

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38

Owen, Scott F., Sebnem N. Tuncdemir, Patrick L. Bader, Natasha N. Tirko, Gord Fishell, and Richard W. Tsien. "Oxytocin enhances hippocampal spike transmission by modulating fast-spiking interneurons." Nature 500, no. 7463 (August 2013): 458–62. http://dx.doi.org/10.1038/nature12330.

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39

del Pino, Isabel, Cristina García-Frigola, Nathalie Dehorter, Jorge R. Brotons-Mas, Efrén Alvarez-Salvado, María Martínez de Lagrán, Gabriele Ciceri, et al. "Erbb4 Deletion from Fast-Spiking Interneurons Causes Schizophrenia-like Phenotypes." Neuron 79, no. 6 (September 2013): 1152–68. http://dx.doi.org/10.1016/j.neuron.2013.07.010.

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40

Gage, Gregory J., Colin R. Stoetzner, Alexander B. Wiltschko, and Joshua D. Berke. "Selective Activation of Striatal Fast-Spiking Interneurons during Choice Execution." Neuron 67, no. 3 (August 2010): 466–79. http://dx.doi.org/10.1016/j.neuron.2010.06.034.

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41

Roberts, Bradley M., Michael G. White, Mary H. Patton, Rong Chen, and Brian N. Mathur. "Ensemble encoding of action speed by striatal fast-spiking interneurons." Brain Structure and Function 224, no. 7 (June 26, 2019): 2567–76. http://dx.doi.org/10.1007/s00429-019-01908-7.

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42

Szydlowski, S. N., I. Pollak Dorocic, H. Planert, M. Carlen, K. Meletis, and G. Silberberg. "Target Selectivity of Feedforward Inhibition by Striatal Fast-Spiking Interneurons." Journal of Neuroscience 33, no. 4 (January 23, 2013): 1678–83. http://dx.doi.org/10.1523/jneurosci.3572-12.2013.

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43

Lewis, Timothy J., and John Rinzel. "Dendritic effects in networks of electrically coupled fast-spiking interneurons." Neurocomputing 58-60 (June 2004): 145–50. http://dx.doi.org/10.1016/j.neucom.2004.01.035.

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44

Fujiwara-Tsukamoto, Y., Y. Isomura, M. Imanishi, T. Ninomiya, M. Tsukada, Y. Yanagawa, T. Fukai, and M. Takada. "Prototypic Seizure Activity Driven by Mature Hippocampal Fast-Spiking Interneurons." Journal of Neuroscience 30, no. 41 (October 13, 2010): 13679–89. http://dx.doi.org/10.1523/jneurosci.1523-10.2010.

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45

Koós, Tibor, and James M. Tepper. "Dual Cholinergic Control of Fast-Spiking Interneurons in the Neostriatum." Journal of Neuroscience 22, no. 2 (January 15, 2002): 529–35. http://dx.doi.org/10.1523/jneurosci.22-02-00529.2002.

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46

Rotaru, Diana C., Cameron Olezene, Takeaki Miyamae, Nadezhda V. Povysheva, Aleksey V. Zaitsev, David A. Lewis, and Guillermo Gonzalez-Burgos. "Functional properties of GABA synaptic inputs onto GABA neurons in monkey prefrontal cortex." Journal of Neurophysiology 113, no. 6 (March 15, 2015): 1850–61. http://dx.doi.org/10.1152/jn.00799.2014.

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In rodent cortex GABAA receptor (GABAAR)-mediated synapses are a significant source of input onto GABA neurons, and the properties of these inputs vary among GABA neuron subtypes that differ in molecular markers and firing patterns. Some features of cortical interneurons are different between rodents and primates, but it is not known whether inhibition of GABA neurons is prominent in the primate cortex and, if so, whether these inputs show heterogeneity across GABA neuron subtypes. We thus studied GABAAR-mediated miniature synaptic events in GABAergic interneurons in layer 3 of monkey dorsolateral prefrontal cortex (DLPFC). Interneurons were identified on the basis of their firing pattern as fast spiking (FS), regular spiking (RS), burst spiking (BS), or irregular spiking (IS). Miniature synaptic events were common in all of the recorded interneurons, and the frequency of these events was highest in FS neurons. The amplitude and kinetics of miniature inhibitory postsynaptic potentials (mIPSPs) also differed between DLPFC interneuron subtypes in a manner correlated with their input resistance and membrane time constant. FS neurons had the fastest mIPSP decay times and the strongest effects of the GABAAR modulator zolpidem, suggesting that the distinctive properties of inhibitory synaptic inputs onto FS cells are in part conferred by GABAARs containing α1 subunits. Moreover, mIPSCs differed between FS and RS interneurons in a manner consistent with the mIPSP findings. These results show that in the monkey DLPFC GABAAR-mediated synaptic inputs are prominent in layer 3 interneurons and may differentially regulate the activity of different interneuron subtypes.
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47

Goldberg, Jesse H., and Michale S. Fee. "Singing-Related Neural Activity Distinguishes Four Classes of Putative Striatal Neurons in the Songbird Basal Ganglia." Journal of Neurophysiology 103, no. 4 (April 2010): 2002–14. http://dx.doi.org/10.1152/jn.01038.2009.

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The striatum—the primary input nucleus of the basal ganglia—plays a major role in motor control and learning. Four main classes of striatal neuron are thought to be essential for normal striatal function: medium spiny neurons, fast-spiking interneurons, cholinergic tonically active neurons, and low-threshold spiking interneurons. However, the nature of the interaction of these neurons during behavior is poorly understood. The songbird area X is a specialized striato-pallidal basal ganglia nucleus that contains two pallidal cell types as well as the same four cell types found in the mammalian striatum. We recorded 185 single units in Area X of singing juvenile birds and, based on singing-related firing patterns and spike waveforms, find six distinct cell classes—two classes of putative pallidal neuron that exhibited a high spontaneous firing rate (>60 Hz), and four cell classes that exhibited low spontaneous firing rates characteristic of striatal neurons. In this study, we examine in detail the four putative striatal cell classes. Type-1 neurons were the most frequently encountered and exhibited sparse temporally precise singing-related activity. Type-2 neurons were distinguished by their narrow spike waveforms and exhibited brief, high-frequency bursts during singing. Type-3 neurons were tonically active and did not burst, whereas type-4 neurons were inactive outside of singing and during singing generated long high-frequency bursts that could reach firing rates over 1 kHz. Based on comparison to the mammalian literature, we suggest that these four putative striatal cell classes correspond, respectively, to the medium spiny neurons, fast-spiking interneurons, tonically active neurons, and low-threshold spiking interneurons that are known to reside in area X.
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48

Imbrosci, Barbara, Angela Neitz, and Thomas Mittmann. "Focal Cortical Lesions Induce Bidirectional Changes in the Excitability of Fast Spiking and Non Fast Spiking Cortical Interneurons." PLoS ONE 9, no. 10 (October 27, 2014): e111105. http://dx.doi.org/10.1371/journal.pone.0111105.

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49

Gonzalez-Burgos, G., S. Kroener, J. K. Seamans, D. A. Lewis, and G. Barrionuevo. "Dopaminergic Modulation of Short-Term Synaptic Plasticity in Fast-Spiking Interneurons of Primate Dorsolateral Prefrontal Cortex." Journal of Neurophysiology 94, no. 6 (December 2005): 4168–77. http://dx.doi.org/10.1152/jn.00698.2005.

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Dopaminergic regulation of primate dorsolateral prefrontal cortex (PFC) activity is essential for cognitive functions such as working memory. However, the cellular mechanisms of dopamine neuromodulation in PFC are not well understood. We have studied the effects of dopamine receptor activation during persistent stimulation of excitatory inputs onto fast-spiking GABAergic interneurons in monkey PFC. Stimulation at 20 Hz induced short-term excitatory postsynaptic potential (EPSP) depression. The D1 receptor agonist SKF81297 (5 μM) significantly reduced the amplitude of the first EPSP but not of subsequent responses in EPSP trains, which still displayed significant depression. Dopamine (DA; 10 μM) effects were similar to those of SKF81297 and were abolished by the D1 antagonist SCH23390 (5 μM), indicating a D1 receptor-mediated effect. DA did not alter miniature excitatory postsynaptic currents, suggesting that its effects were activity dependent and presynaptic action potential dependent. In contrast to previous findings in pyramidal neurons, in fast-spiking cells, contribution of N-methyl-d-aspartate receptors to EPSPs at subthreshold potentials was not significant and fast-spiking cell depolarization decreased EPSP duration. In addition, DA had no significant effects on temporal summation. The selective decrease in the amplitude of the first EPSP in trains delivered every 10 s suggests that in fast-spiking neurons, DA reduces the amplitude of EPSPs evoked at low frequency but not of EPSPs evoked by repetitive stimulation. DA may therefore improve detection of EPSP bursts above background synaptic activity. EPSP bursts displaying short-term depression may transmit spike-timing-dependent temporal codes contained in presynaptic spike trains. Thus DA neuromodulation may increase the signal-to-noise ratio at fast-spiking cell inputs.
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50

Szegedi, Viktor, Emőke Bakos, Szabina Furdan, Bálint H. Kovács, Dániel Varga, Miklós Erdélyi, Pál Barzó, Attila Szücs, Gábor Tamás, and Karri Lamsa. "HCN channels at the cell soma ensure the rapid electrical reactivity of fast-spiking interneurons in human neocortex." PLOS Biology 21, no. 2 (February 6, 2023): e3002001. http://dx.doi.org/10.1371/journal.pbio.3002001.

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Accumulating evidence indicates that there are substantial species differences in the properties of mammalian neurons, yet theories on circuit activity and information processing in the human brain are based heavily on results obtained from rodents and other experimental animals. This knowledge gap may be particularly important for understanding the neocortex, the brain area responsible for the most complex neuronal operations and showing the greatest evolutionary divergence. Here, we examined differences in the electrophysiological properties of human and mouse fast-spiking GABAergic basket cells, among the most abundant inhibitory interneurons in cortex. Analyses of membrane potential responses to current input, pharmacologically isolated somatic leak currents, isolated soma outside-out patch recordings, and immunohistochemical staining revealed that human neocortical basket cells abundantly express hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel isoforms HCN1 and HCN2 at the cell soma membrane, whereas these channels are sparse at the rodent basket cell soma membrane. Antagonist experiments showed that HCN channels in human neurons contribute to the resting membrane potential and cell excitability at the cell soma, accelerate somatic membrane potential kinetics, and shorten the lag between excitatory postsynaptic potentials and action potential generation. These effects are important because the soma of human fast-spiking neurons without HCN channels exhibit low persistent ion leak and slow membrane potential kinetics, compared with mouse fast-spiking neurons. HCN channels speed up human cell membrane potential kinetics and help attain an input–output rate close to that of rodent cells. Computational modeling demonstrated that HCN channel activity at the human fast-spiking cell soma membrane is sufficient to accelerate the input–output function as observed in cell recordings. Thus, human and mouse fast-spiking neurons exhibit functionally significant differences in ion channel composition at the cell soma membrane to set the speed and fidelity of their input–output function. These HCN channels ensure fast electrical reactivity of fast-spiking cells in human neocortex.
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