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

Comparing GABAergic cell populations in the thalamic reticular nucleus of normal and genetic absence epilepsy rats from Strasbourg (GAERS)

2013 ◽  
Vol 34 (11) ◽  
pp. 1991-2000 ◽  
Author(s):  
Safiye Çavdar ◽  
Hüsniye Hacıoğlu Bay ◽  
Özlem Kirazlı ◽  
Yusuf Özgür Çakmak ◽  
Filiz Onat
Keyword(s):  
Absence Epilepsy ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Cell Populations

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

No loss in total neuron number in the thalamic reticular nucleus and neocortex in the genetic absence epilepsy rats from Strasbourg

1996 ◽  
Vol 26 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Anne Sabers ◽  
Arne Møller ◽  
Jørgen Scheel-Krüger ◽  
Agnete Mouritzen Dam
Keyword(s):  
Absence Epilepsy ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Neuron Number

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 Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms

Brain ◽  
2019 ◽  
Vol 143 (1) ◽  
pp. 161-174 ◽  
Author(s):  
Qing-Long Miao ◽  
Stefan Herlitze ◽  
Melanie D Mark ◽  
Jeffrey L Noebels
Keyword(s):  
Developmental Plasticity ◽  
Absence Epilepsy ◽  
Adult Brain ◽  
Burst Firing ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Adult Onset ◽  
Childhood Absence Epilepsy ◽  
Loss Of Function ◽  
Relay Neurons

Abstract Inborn errors of CACNA1A-encoded P/Q-type calcium channels impair synaptic transmission, producing early and lifelong neurological deficits, including childhood absence epilepsy, ataxia and dystonia. Whether these impairments owe their pathologies to defective channel function during the critical period for thalamic network stabilization in immature brain remains unclear. Here we show that mice with tamoxifen-induced adult-onset ablation of P/Q channel alpha subunit (iKOp/q) display identical patterns of dysfunction, replicating the inborn loss-of-function phenotypes and, therefore demonstrate that these neurological defects do not rely upon developmental abnormality. Unexpectedly, unlike the inborn model, the adult-onset pattern of excitability changes believed to be pathogenic within the thalamic network is non-canonical. Specifically, adult ablation of P/Q channels does not promote Cacna1g-mediated burst firing or T-type calcium current (IT) in the thalamocortical relay neurons; however, burst firing in thalamocortical relay neurons remains essential as iKOp/q mice generated on a Cacna1g deleted background show substantially diminished seizure generation. Moreover, in thalamic reticular nucleus neurons, burst firing is impaired accompanied by attenuated IT. Interestingly, inborn deletion of thalamic reticular nucleus-enriched, human childhood absence epilepsy-linked gene Cacna1h in iKOp/q mice reduces thalamic reticular nucleus burst firing and promotes rather than reduces seizure, indicating an epileptogenic role for loss-of-function Cacna1h gene variants reported in human childhood absence epilepsy cases. Together, our results demonstrate that P/Q channels remain critical for maintaining normal thalamocortical oscillations and motor control in the adult brain, and suggest that the developmental plasticity of membrane currents regulating pathological rhythmicity is both degenerate and age-dependent.

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.

Sign in / Sign up

Export Citation Format

Share Document