Self–sustained rhythmic activity in the thalamic reticular nucleus mediated by depolarizing GABAA receptor potentials

10.1038/5729 ◽  
1999 ◽  
Vol 2 (2) ◽  
pp. 168-174 ◽  
Author(s):  
M. Bazhenov ◽  
I. Timofeev ◽  
M. Steriade ◽  
T.J. Sejnowski
Keyword(s):  
Gabaa Receptor ◽  
Rhythmic Activity ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus

scholarly journals Vasoactive Intestinal Peptide Selectively Depolarizes Thalamic Relay Neurons and Attenuates Intrathalamic Rhythmic Activity

2003 ◽  
Vol 90 (2) ◽  
pp. 1224-1234 ◽  
Author(s):  
Sang-Hun Lee ◽  
Charles L. Cox
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Information Transfer ◽  
Slow Wave Sleep ◽  
Rhythmic Activity ◽  
Absence Epilepsy ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Unit Recording ◽  
Recording Techniques ◽  
Relay Neurons

The reciprocal synaptic relationship between the relay thalamus and surrounding thalamic reticular nucleus can lead to the generation of various rhythmic activities that are associated with different levels of behavioral states as well as certain pathophysiological conditions. Intrathalamic rhythmic activities may be attenuated by numerous neuromodulators that arise from a variety of brain stem nuclei. This study focuses on the potential role of a particular neuropeptide, vasoactive intestinal peptide (VIP). VIP and its receptors are localized within the thalamic circuit and thus may serve as an endogenous modulator of the rhythmic activity. Using extracellular multiple-unit recording techniques, we found that VIP strongly attenuated the slow, 2- to 4-Hz intrathalamic rhythm. This rhythm is similar to that observed during slow wave sleep and certain pathophysiological conditions such as generalized absence epilepsy. Using intracellular recording techniques, we found that VIP selectively depolarized relay neurons in the ventrobasal nucleus but had negligible actions on neurons in thalamic reticular nucleus. The VIP-mediated depolarization is produced via an enhancement of the nonselective cation conductance, Ih. The antioscillatory actions of VIP likely occur by shifting the membrane potential to decrease the probability of burst discharge by relay neurons, a requirement to maintain the rhythmic activity. Not only does VIP alter the intrathalamic rhythmic activity, this peptide that is endogenous to the thalamic circuit may also play a significant role in the regulation of information transfer through the thalamocortical circuit.

scholarly journals TRPM4 conductances in thalamic reticular nucleus neurons generate persistent firing during slow oscillations

2020 ◽  
Author(s):  
John J. O’Malley ◽  
Frederik Seibt ◽  
Jeannie Chin ◽  
Michael Beierlein
Keyword(s):  
Rhythmic Activity ◽  
Thalamic Reticular Nucleus ◽  
Oscillatory Activity ◽  
Reticular Nucleus ◽  
Plateau Potentials ◽  
Slow Oscillations ◽  
Synaptic Circuits ◽  
Ventrobasal Thalamus ◽  
Persistent Firing

AbstractDuring sleep, neurons in the thalamic reticular nucleus (TRN) participate in distinct types of oscillatory activity. While the reciprocal synaptic circuits between TRN and sensory relay nuclei are known to underlie the generation of sleep spindles, the mechanisms regulating slow (<1 Hz) forms of thalamic oscillations are not well understood. Under in vitro conditions, TRN neurons can generate slow oscillations in a cell-intrinsic manner, with postsynaptic Group 1 metabotropic glutamate receptor (mGluR) activation leading to the generation of plateau potentials mediated by both T-type Ca2+ currents and Ca2+ -activated nonselective cation currents (ICAN). However, the identity of ICAN and the possible contribution of thalamic circuits to slow rhythmic activity remain unclear. Using thalamic slices derived from adult mice of either sex, we recorded slow forms of rhythmic activity in TRN neurons, which were mediated by fast glutamatergic thalamoreticular inputs but did not require postsynaptic mGluR activation. For a significant fraction of TRN neurons, synaptic inputs or brief depolarizing current steps led to long-lasting plateau potentials and persistent firing (PF), and in turn, resulted in sustained synaptic inhibition in postsynaptic relay neurons of the ventrobasal thalamus (VB). Pharmacological approaches indicated that plateau potentials were triggered by Ca2+ influx through T-type Ca2+ channels and mediated by Ca2+ and voltage-dependent transient receptor potential melastatin 4 (TRPM4) channels. Taken together, our results suggest that thalamic circuits can generate slow oscillatory activity, mediated by an interplay of TRN-VB synaptic circuits that generate rhythmicity and TRN cell-intrinsic mechanisms that control PF and oscillation frequency.Significance StatementSlow forms of thalamocortical rhythmic activity are thought to be essential for memory consolidation during sleep and the efficient removal of potentially toxic metabolites. In vivo, thalamic slow oscillations are regulated by strong bidirectional synaptic pathways linking neocortex and thalamus. Therefore, in vitro studies in the isolated thalamus can offer important insights about the ability of individual neurons and local circuits to generate different forms of rhythmic activity. We found that circuits formed by GABAergic neurons in the thalamic reticular nucleus (TRN) and glutamatergic relay neurons in the ventrobasal thalamus generated slow oscillatory activity, which was accompanied by persistent firing in TRN neurons. Our results identify both cell-intrinsic and synaptic mechanisms that mediate slow forms of rhythmic activity in thalamic circuits.

GABAA receptor mediated transmission in the thalamic reticular nucleus of rats with genetic absence epilepsy shows regional differences: Functional implications

2006 ◽  
Vol 1111 (1) ◽  
pp. 213-221 ◽  
Author(s):  
Rezzan Gülhan Aker ◽  
Hazan B. Özyurt ◽  
Hasan R. Yananli ◽  
Yusuf Özgür Çakmak ◽  
Aydan E. Özkaynakçi ◽  
...  
Keyword(s):  
Gabaa Receptor ◽  
Regional Differences ◽  
Absence Epilepsy ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Functional Implications

Thalamic Reticular Nucleus in Caiman crocodilus: Immunohistochemical Staining

2018 ◽  
Vol 92 (3-4) ◽  
pp. 142-166 ◽  
Author(s):  
Michael B. Pritz
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Immunohistochemical Staining ◽  
Medial Forebrain Bundle ◽  
Transverse Plane ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Acid Decarboxylase ◽  
Caiman Crocodilus ◽  
Monoclonal Mouse

The thalamic reticular nucleus in reptiles, Caiman crocodilus, shares a number of morphological similarities with its counterpart in mammals. In view of the immunohistochemical properties of this nucleus in mammals and the more recently identified complexity of this neuronal aggregate in Caiman, this nucleus was investigated using a number of antibodies. These results were compared with findings described for other amniotes. The following antibodies gave consistent and reproducible results: polyclonal sheep anti-parvalbumin (PV), monoclonal mouse anti-PV, and polyclonal sheep anti-glutamic acid decarboxylase (GAD). In the transverse plane, this nucleus is divided into two. In each part, a compact group of cells sits on top of the fibers of the forebrain bundle with scattered cells among these fibers. In the lateral forebrain bundle, this neuronal aggregate is represented by the dorsal peduncular nucleus and the perireticular nucleus while, in the medial forebrain bundle, these parts are the interstitial nucleus and the scattered cells in this fiber tract. The results of this study are the following. First, the thalamic reticular nucleus of Caiman contains GAD(+) and PV(+) neurons, which is similar to what has been described in other amniotes. Second, the morphology and distribution of many GAD(+) and PV(+) neurons in the dorsal peduncular and perireticular nuclei are similar and suggest that these neurons colocalize these markers. Third, neurons in the interstitial nucleus and in the medial forebrain bundle are GAD(+) and PV(+). At the caudal pole of the thalamic reticular nucleus, PV immunoreactive cells predominated and avoided the central portion of this nucleus where GAD(+) cells were preferentially located. However, GAD(+) cells were sparse when compared with PV(+) cells. This immunohistochemically different area in the caudal pole is considered to be an area separate from the thalamic reticular nucleus.

scholarly journals The therapeutic mechanism of epilepsy seizures in different target areas: Research on a theoretical model

2021 ◽  
Vol 29 ◽  
pp. 455-461
Author(s):  
Bing Hu ◽  
Zhizhi Wang ◽  
Minbo Xu ◽  
Luyao Zhu ◽  
Dingjiang Wang
Keyword(s):  
Pyramidal Neurons ◽  
Control Mechanism ◽  
Difficult Problem ◽  
Calculation Model ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Theoretical Support ◽  
Therapeutic Mechanism ◽  
Optimal Target ◽  
Selection Of

BACKGROUND: The selection of optimal target areas in the surgical treatment of epilepsy is always a difficult problem in medicine. OBJECTIVE: We employed a theoretical calculation model to explore the control mechanism of seizures by an external voltage stimulus acting in different nerve nuclei. METHODS: Theoretical analysis and numerical simulation were combined. RESULTS: The globus pallidus, excitatory pyramidal neurons, striatal D1 neurons, thalamic reticular nucleus and specific relay nuclei were selected, we analyzed that the electrical stimulation has different effects in these target areas. CONCLUSIONS: The data selected were reasonable in study, the results may give a theoretical support for similar studies in clinical.

scholarly journals Synaptic properties of the feedback connections from the thalamic reticular nucleus to the dorsal lateral geniculate nucleus

2020 ◽  
Vol 124 (2) ◽  
pp. 404-417 ◽  
Author(s):  
Peter W. Campbell ◽  
Gubbi Govindaiah ◽  
Sean P. Masterson ◽  
Martha E. Bickford ◽  
William Guido
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Lateral Geniculate ◽  
Dependent Form ◽  
Dorsal Lateral Geniculate ◽  
Feedback Connections ◽  
Spike Firing ◽  
Stimulation Of

The thalamic reticular nucleus (TRN) modulates thalamocortical transmission through inhibition. In mouse, TRN terminals in the dorsal lateral geniculate nucleus (dLGN) form synapses with relay neurons but not interneurons. Stimulation of TRN terminals in dLGN leads to a frequency-dependent form of inhibition, with higher rates of stimulation leading to a greater suppression of spike firing. Thus, TRN inhibition appears more dynamic than previously recognized, having a graded rather than an all-or-none impact on thalamocortical transmission.

scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

Limbic seizures increase pronociceptin mRNA levels in the thalamic reticular nucleus

Neuroreport ◽  
1999 ◽  
Vol 10 (3) ◽  
pp. 541-546 ◽  
Author(s):  
Gianni Bregola ◽  
Sanzio Candeletti ◽  
Patrizia Romualdi ◽  
Michele Simonato
Keyword(s):  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Mrna Levels ◽  
Limbic Seizures
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