scholarly journals Involvement of the thalamic reticular nucleus in prepulse inhibition of acoustic startle

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Qiang-long You ◽  
Zhou-cai Luo ◽  
Zheng-yi Luo ◽  
Ying Kong ◽  
Ze-lin Li ◽  
...  
Keyword(s):  
Prepulse Inhibition ◽  
Gabab Receptor ◽  
Acoustic Startle ◽  
Autism Spectrum ◽  
Burst Firing ◽  
Inhibitory Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Sound Stimulation ◽  
Medial Geniculate

AbstractThalamic reticular nucleus (TRN) is a group of inhibitory neurons surrounding the thalamus. Due to its important role in sensory information processing, TRN is considered as the target nucleus for the pathophysiological investigation of schizophrenia and autism spectrum disorder (ASD). Prepulse inhibition (PPI) of acoustic startle response, a phenomenon that strong stimulus-induced startle reflex is reduced by a weaker prestimulus, is always found impaired in schizophrenia and ASD. But the role of TRN in PPI modulation remains unknown. Here, we report that parvalbumin-expressing (PV+) neurons in TRN are activated by sound stimulation of PPI paradigm. Chemogenetic inhibition of PV+ neurons in TRN impairs PPI performance. Further investigations on the mechanism suggest a model of burst-rebound burst firing in TRN-auditory thalamus (medial geniculate nucleus, MG) circuitry. The burst firing is mediated by T-type calcium channel in TRN, and rebound burst firing needs the participation of GABAB receptor in MG. Overall, these findings support the involvement of TRN in PPI modulation.

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1993-2003 ◽  
Author(s):  
R. A. Warren ◽  
A. Agmon ◽  
E. G. Jones
Keyword(s):  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Initial Response ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Synaptic Interactions ◽  
Gabaa Receptor Antagonist

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

scholarly journals Two Functionally Distinct Networks of Gap Junction-Coupled Inhibitory Neurons in the Thalamic Reticular Nucleus

2014 ◽  
Vol 34 (39) ◽  
pp. 13170-13182 ◽  
Author(s):  
S.-C. Lee ◽  
S. L. Patrick ◽  
K. A. Richardson ◽  
B. W. Connors
Keyword(s):  
Gap Junction ◽  
Inhibitory Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus

Anatomic, Intrinsic, and Synaptic Properties of Dorsal and Ventral Division Neurons in Rat Medial Geniculate Body

1999 ◽  
Vol 81 (5) ◽  
pp. 1999-2016 ◽  
Author(s):  
Edward L. Bartlett ◽  
Philip H. Smith
Keyword(s):  
Membrane Potential ◽  
Nmda Receptors ◽  
Brain Slices ◽  
Medial Geniculate Body ◽  
Dendritic Tree ◽  
Dendritic Morphology ◽  
Thalamic Reticular Nucleus ◽  
Membrane Properties ◽  
Reticular Nucleus ◽  
Medial Geniculate

Anatomic, intrinsic, and synaptic properties of dorsal and ventral division neurons in rat medial geniculate body. Presently little is known about what basic synaptic and cellular mechanisms are employed by thalamocortical neurons in the two main divisions of the auditory thalamus to elicit their distinct responses to sound. Using intracellular recording and labeling methods, we characterized anatomic features, membrane properties, and synaptic inputs of thalamocortical neurons in the dorsal (MGD) and ventral (MGV) divisions in brain slices of rat medial geniculate body. Quantitative analysis of dendritic morphology demonstrated that tufted neurons in both divisions had shorter dendrites, smaller dendritic tree areas, more profuse branching, and a greater dendritic polarization compared with stellate neurons, which were only found in MGD. Tufted neuron dendritic polarization was not as strong or consistent as earlier Golgi studies suggested. MGV and MGD cells had similar intrinsic properties except for an increased prevalence of a depolarizing sag potential in MGV neurons. The sag was the only intrinsic property correlated with cell morphology, seen only in tufted neurons in either division. Many MGV and MGD neurons received excitatory and inhibitory inferior colliculus (IC) inputs (designated IN/EX or EX/IN depending on excitation/inhibition sequence). However, a significant number only received excitatory inputs (EX/O) and a few only inhibitory (IN/O). Both MGV and MGD cells displayed similar proportions of response combinations, but suprathreshold EX/O responses only were observed in tufted neurons. Excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) had multiple distinguishable amplitude levels implying convergence. Excitatory inputs activated α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) receptors the relative contributions of which were variable. For IN/EX cells with suprathreshold inputs, first-spike timing was independent of membrane potential unlike that of EX/O cells. Stimulation of corticothalamic (CT) and thalamic reticular nucleus (TRN) axons evoked a GABAA IPSP, EPSP, GABAB IPSP sequence in most neurons with both morphologies in both divisions. TRN IPSPs and CT EPSPs were graded in amplitude, again suggesting convergence. CT inputs activated AMPA and NMDA receptors. The NMDA component of both IC and CT inputs had an unusual voltage dependence with a detectable dl-2-amino-5-phosphonovaleric acid-sensitive component even below −70 mV. First-spike latencies of CT evoked action potentials were sensitive to membrane potential regardless of whether the TRN IPSP was present. Overall, our in vitro data indicate that reported regional differences in the in vivo responses of MGV and MGD cells to auditory stimuli are not well correlated with major differences in intrinsic membrane features or synaptic responses between cell types.

Corticofugal Projection Inhibits the Auditory Thalamus Through the Thalamic Reticular Nucleus

2008 ◽  
Vol 99 (6) ◽  
pp. 2938-2945 ◽  
Author(s):  
Zhuo Zhang ◽  
Chun-Hua Liu ◽  
Yan-Qin Yu ◽  
Kenji Fujimoto ◽  
Ying-Shing Chan ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Medial Geniculate Body ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Inhibitory Effects ◽  
Inhibitory Pathway ◽  
Inhibitory Postsynaptic Potentials ◽  
Medial Geniculate ◽  
Inferior Colliculi ◽  
Stimulation Of

Electrical stimulation of the auditory cortex (AC) causes both facilitatory and inhibitory effects on the medial geniculate body (MGB). The purpose of this study was to identify the corticofugal inhibitory pathway to the MGB. We assessed two potential circuits: 1) the cortico-colliculo-thalamic circuit and 2) cortico-reticulo-thalamic one. We compared intracellular responses of MGB neurons to electrical stimulation of the AC following bilateral ablation of the inferior colliculi (IC) or thalamic reticular nucleus (TRN) in anesthetized guinea pigs. Cortical stimulation with intact TRN could cause strong inhibitory effects on the MGB neurons. The corticofugal inhibition remained effective after bilateral IC ablation, but it was minimized after the TRN was lesioned with kainic acid. Synchronized TRN neuronal activity and MGB inhibitory postsynaptic potentials (IPSPs) were observed with multiple recordings. The results suggest that corticofugal inhibition traverses the corticoreticulothalamic pathway, indicating that the colliculi-geniculate inhibitory pathway is probably only for feedforward inhibition.

scholarly journals Two dynamically distinct circuits driving inhibition in sensory thalamus

2020 ◽  
Author(s):  
Rosa I. Martinez-Garcia ◽  
Bettina Voelcker ◽  
Julia B. Zaltsman ◽  
Saundra L. Patrick ◽  
Tanya R. Stevens ◽  
...  
Keyword(s):  
Sensory Information ◽  
Cell Types ◽  
Higher Order ◽  
Inhibitory Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Order Structure ◽  
Multiple Sources ◽  
Cell Groups ◽  
And Function

AbstractMost sensory information destined for the neocortex is relayed through the thalamus, where considerable transformation occurs1,2. One powerful means of transformation involves interactions between excitatory thalamocortical neurons that carry data to cortex and inhibitory neurons of the thalamic reticular nucleus (TRN) that regulate flow of those data3-6. Despite enduring recognition of its importance7-9, understanding of TRN cell types, their organization, and their functional properties has lagged that of the thalamocortical systems they control.Here we address this, investigating somatosensory and visual circuits of the TRN. In the somatosensory TRN we observed two groups of genetically defined neurons that are topographically segregated, physiologically distinct, and connect reciprocally with independent thalamocortical nuclei via dynamically divergent synapses. Calbindin-expressing cells, located in the central core, connect with the ventral posterior nucleus (VP), the primary somatosensory thalamocortical relay. In contrast, somatostatin-expressing cells, residing along the surrounding edges of TRN, synapse with the posterior medial thalamic nucleus (POM), a higher-order structure that carries both top-down and bottom-up information10-12. The two TRN cell groups process their inputs in pathway-specific ways. Synapses from VP to central TRN cells transmit rapid excitatory currents that depress deeply during repetitive activity, driving phasic spike output. Synapses from POM to edge TRN cells evoke slower, less depressing excitatory currents that drive more persistent spiking. Differences in intrinsic physiology of TRN cell types, including state-dependent bursting, contribute to these output dynamics. Thus, processing specializations of two somatosensory TRN subcircuits appear to be tuned to the signals they carry—a primary central subcircuit to discrete sensory events, and a higher-order edge subcircuit to temporally distributed signals integrated from multiple sources. The structure and function of visual TRN subcircuits closely resemble those of the somatosensory TRN. These results provide fundamental insights about how subnetworks of TRN neurons may differentially process distinct classes of thalamic information.

Functional Mapping of GABAB-Receptor Subtypes in the Thalamus

2007 ◽  
Vol 98 (6) ◽  
pp. 3791-3795 ◽  
Author(s):  
Daniel Ulrich ◽  
Valérie Besseyrias ◽  
Bernhard Bettler
Keyword(s):  
Cognitive Deficits ◽  
Gabab Receptor ◽  
Cell Activity ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Receptor Subtypes ◽  
Type B ◽  
Acid Type ◽  
Output Neurons ◽  
Electrophysiological Methods

The thalamus plays an important role in attention mechanisms and the generation of brain rhythms. γ-Aminobutyric acid type B (GABAB) receptors are known to regulate the main output neurons of the thalamus, the thalamocortical relay (TCR) cells. However, the contributions of the two predominant GABAB-receptor subtypes, GABAB(1a,2) and GABAB(1b,2), to the control of TCR cell activity are unknown. Here, we used genetic and electrophysiological methods to investigate subtype-specific GABAB effects at the inputs to TCR cells. We found that mainly GABAB(1a,2) receptors inhibit the release of glutamate from corticothalamic fibers impinging onto TCR cells. In contrast, both GABAB(1a,2) and GABAB(1b,2) receptors efficiently inhibit the release of GABA from thalamic reticular nucleus (TRN) neurons onto TCR neurons. Likewise, both GABAB(1a,2) and GABAB(1b,2) receptors efficiently activate somatodendritic K+ currents in TCR cells. In summary, our data show that GABAB(1b,2) receptors cannot compensate for the absence of GABAB(1a,2) receptors at glutamatergic inputs to TCR cells. This shows that the predominant association of GABAB(1a,2) receptors with glutamatergic terminals is a feature that is preserved at several brain synapses. Furthermore, our data indicate that the cognitive deficits observed with mice lacking GABAB(1a,2) receptors could to some extent relate to attention deficits caused by disinhibited release of glutamate onto TCR neurons.

Topography of thalamic reticular nucleus projections to the medial geniculate body

2007 ◽  
Vol 58 ◽  
pp. S156
Author(s):  
Akihisa Kimura ◽  
Tomohiro Donishi ◽  
Hiroki Imbe ◽  
Yasuhiko Tamai
Keyword(s):  
Medial Geniculate Body ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Medial Geniculate

Slow Recovery From Excitation of Thalamic Reticular Nucleus Neurons

2009 ◽  
Vol 101 (2) ◽  
pp. 980-987 ◽  
Author(s):  
Xiong-Jie Yu ◽  
Xin-Xiu Xu ◽  
Xi Chen ◽  
Shigang He ◽  
Jufang He
Keyword(s):  
Interstimulus Interval ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Auditory Stimuli ◽  
Slow Recovery ◽  
Frequent Change ◽  
Medial Geniculate ◽  
Auditory Response ◽  
Repetitive Stimulus ◽  
Fast Rhythm

Responses to repeated auditory stimuli were examined in 103 neurons in the auditory region of the thalamic reticular nucleus (TRN) and in 20 medial geniculate (MGB) neurons of anesthetized rats. A further six TRN neurons were recorded from awake rats. The TRN neurons showed strong responses to the first trial and weak responses to the subsequent trials of repeated auditory stimuli and electrical stimulation of the MGB and auditory cortex when the interstimulus interval (ISI) was short (<3 s). They responded to the second trial when the interstimulus interval was lengthened to ≥3 s. These responses contrasted to those of MGB neurons, which responded to repeated auditory stimuli of different ISIs. The TRN neurons showed a significant increase in the onset auditory response from 9.5 to 76.5 Hz when the ISI was increased from 200 ms to 10 s ( P < 0.001, ANOVA). The duration of the auditory-evoked oscillation was longer when the ISI was lengthened. The slow recovery of the TRN neurons after oscillation of burst firings to fast repetitive stimulus was a reflection of a different role than that of the thalamocortical relay neurons. Supposedly the TRN is involved in the process of attention such as attention shift; the slow recovery of TRN neurons probably limits the frequent change of the attention in a fast rhythm.

Tonotopic Control of Auditory Thalamus Frequency Tuning by Reticular Thalamic Neurons

2008 ◽  
Vol 99 (3) ◽  
pp. 1137-1151 ◽  
Author(s):  
Nathalie Cotillon-Williams ◽  
Chloé Huetz ◽  
Elizabeth Hennevin ◽  
Jean-Marc Edeline
Keyword(s):  
Frequency Tuning ◽  
Tuning Curve ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Inhibitory Input ◽  
Group Data ◽  
Level Function ◽  
Medial Geniculate ◽  
Auditory Systems ◽  
Strong Control

GABAergic cells of the thalamic reticular nucleus (TRN) can potentially exert strong control over transmission of information through thalamus to the cerebral cortex. Anatomical studies have shown that the reticulo-thalamic connections are spatially organized in the visual, somatosensory, and auditory systems. However, the issue of how inhibitory input from TRN controls the functional properties of thalamic relay cells and whether this control follows topographic rules remains largely unknown. Here we assessed the consequences of increasing or decreasing the activity of small ensembles of TRN neurons on the receptive field properties of medial geniculate (MG) neurons. For each MG cell, the frequency tuning curve and the rate-level function were tested before, during, and after microiontophoretic applications of GABA, or of glutamate, in the auditory sector of the TRN. For 66 MG cells tested during potent pharmacological control of TRN activity, group data did not reveal any significant effects. However, for a population of 20/66 cells (all but 1 recorded in the ventral, tonotopic, division), the breadth of tuning, the frequency selectivity and the acoustic threshold were significantly modified in the directions expected from removing, or reinforcing, a dominant inhibitory input onto MG cells. Such effects occurred only when the distance between the characteristic frequency of the recorded ventral MG cell and that of the TRN cells at the ejection site was <0.25 octaves; they never occurred for larger distances. This relationship indicates that the functional interactions between TRN cells and ventral MG cells rely on precise topographic connections.

scholarly journals Manipulations of MeCP2 in glutamatergic neurons highlight their contributions to Rett and other neurological disorders

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Xiangling Meng ◽  
Wei Wang ◽  
Hui Lu ◽  
Ling-jie He ◽  
Wu Chen ◽  
...  
Keyword(s):  
Mouse Models ◽  
Neurological Disorders ◽  
Acoustic Startle ◽  
Acoustic Startle Response ◽  
Autism Spectrum ◽  
Inhibitory Neurons ◽  
Loss Of Function ◽  
Glutamatergic Neurons ◽  
Excitatory Neurotransmission ◽  
Spectrum Disorders

Many postnatal onset neurological disorders such as autism spectrum disorders (ASDs) and intellectual disability are thought to arise largely from disruption of excitatory/inhibitory homeostasis. Although mouse models of Rett syndrome (RTT), a postnatal neurological disorder caused by loss-of-function mutations in MECP2, display impaired excitatory neurotransmission, the RTT phenotype can be largely reproduced in mice simply by removing MeCP2 from inhibitory GABAergic neurons. To determine what role excitatory signaling impairment might play in RTT pathogenesis, we generated conditional mouse models with Mecp2 either removed from or expressed solely in glutamatergic neurons. MeCP2 deficiency in glutamatergic neurons leads to early lethality, obesity, tremor, altered anxiety-like behaviors, and impaired acoustic startle response, which is distinct from the phenotype of mice lacking MeCP2 only in inhibitory neurons. These findings reveal a role for excitatory signaling impairment in specific neurobehavioral abnormalities shared by RTT and other postnatal neurological disorders.

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