Significance of the Thalamic Reticular Nucleus GABAergic Neurons in Normal and Pathological Activity of the Brain

Abstract

The relationship between neurons of the thalamic reticular nucleus (TRN) and relay neurons of the thalamic nuclei was studied. Activation of the TRN neurons was shown to abate activity of relay neurons. This evidence was obtained by stimulation of the TRN and the neocortex and, by introduction of small doses of nembutal as well. Suppression of the relay neuronal activity by the TRN neurons is supposed to occur monosynaptically. It has been also revealed that neuronal activity of the TRN enhances in a clonic phase of seizures generated by stimulation of the hippocampus and as soon as the electroencephalographic seizure reactions disappear. The suppression of limbic motor seizures is obviously related to the process of potentiation in GABAergic synapses of thalamocortical networks. Thus, stimulation of the TRN appears to be a rather valuable methodical tool that can open up prospects in the development of new “anticonvulsive” strategies in the treated of temporal lobe epilepsy.

Share and Cite:

Z. Nanobashvili, A. Surmava, I. Bilanishvili, M. Barbaqadze, M. Mariamidze and N. Khizanishvili, "Significance of the Thalamic Reticular Nucleus GABAergic Neurons in Normal and Pathological Activity of the Brain," Journal of Behavioral and Brain Science, Vol. 2 No. 4, 2012, pp. 436-444. doi: 10.4236/jbbs.2012.24051.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] R. Davis, “Cerebellar Stimulation for Cerebral Palsy Spastisity, Function and Seizures,” Archive of Medical Research, Vol. 31, No. 2, 2000, pp. 290-299. doi:10.1016/S0188-4409(00)00065-5
[2] G. Weiss, J. Lewis and R. Jimenes-Riverac, “Antikindlig Effects of Locus Coeruleus Stimulation: Mediation by Ascending Noradrenergic Projections,” Experimental Neurology, Vol. 108, No. 1, 1990, pp. 136-140. doi:10.1016/0014-4886(90)90020-S
[3] V. Magdaleno-Madrigal, A. Valdés-Cruz, D. Martinez- Vargas, et al., “Effect of Electrical Stimulation of the Solitary Tract on the Development of Electrical Kindling in the Cat,” Epilepsia, Vol. 43, No. 9, 2002, pp. 964-969. doi:10.1046/j.1528-1157.2002.05702.x
[4] F. Velasco, M. Velasco and A. Velasco, “Effect of Chronic Electrical Stimulation of the Centromedian Thalamic Nuclei on Various Intractable Seizure Patyerns: 1. Clinical Seizures and Paroxysmal EEG Activity,” Epilepsia, Vol. 34, No. 6, 1993, pp. 1052-1064. doi:10.1111/j.1528-1157.1993.tb02134.x
[5] S. Chanel, M. Westerveld and S. Spenser, “Long-Term Outcome of Vagus Nerve Stimulation for Refractory Partial Epilepsy,” Epilepsy and Behavior, Vol. 4, No. 3, 2003, pp. 302-309. doi:10.1016/S1525-5050(03)00109-4
[6] S. Mraovitch and Y. Calando, “Interactions between Limbic, Thalamo-Striatal-Cortical and Central Autonomic Pathways during Epileptic Seizure Progression,” Journal of Comparative Neurology, Vol. 411, No. 1, 1999, pp. 145-161. doi:10.1002/(SICI)1096-9861(19990816)411:1<145::AID-CNE11>3.0.CO;2-1
[7] G. Avanzini, M. de Curtis, C. Marescaux F. Panzica, R. Spreafico and M. Vergnes, “Role of the Thalamic Reticular Nucleus in the Generation of Rhythmic Thalamo- Cortical Activities Subserving Spike and Waves,” Journal of Neural Transmition, Vol. 35, 1992, pp. 85-95.
[8] D. Contreras and M. Steriade, “Cellular Basis of EEG Slow Rhythms: A Study of Dynamic Corticothalamic Relationships,” Journal of Neuroscience, Vol. 15, No. 1, 1995, pp. 604-622.
[9] C. Cox, J. Huguenard and D. Prince, “Nucleus Reticularis Neurons Mediate Diverse Inhibitory Effects in Thalamus,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 94, No. 16, 1997, pp. 8854- 8859. doi:10.1073/pnas.94.16.8854
[10] C. Houser, J. Vaughn, R. Barber and E. Roberts, “GABA Neurons Are the Major Cell Type of the Nucleus Reticularis Thalami,” Brain Research, Vol. 200, No. 2-3, 1980, pp. 341-354. doi:10.1016/0006-8993(80)90925-7
[11] U. Kim, M. Sanchez-Vives and D. McCormick, “Functional Dynamics of GABA-Ergic Inhibition in the Thalamus,” Science, Vol. 278, No. 5335, 1997, pp. 130-134. doi:10.1126/science.278.5335.130
[12] D. McCormick, “Neurotransmitter Actions in the Thalamus and Cerebral Cortex and Their Role in Neuromodulation of Thalamocortical Activity,” Progress in Neurobiology, Vol. 39, No. 4, 1992, pp. 337-388. doi:10.1016/0301-0082(92)90012-4
[13] Z. Nanobashvili, T. Chachua, A. Nanobashvili, I. Bilanishvili and O. Lindvall and Z. Kokaia, “Suppression of Limbic Motor Seizures by Electrical Stimulation in Thalamic Reticular Nucleus,” Experimental Neurology, Vol. 181, No. 1, 2003, pp. 224-230. doi:10.1016/S0014-4886(03)00045-1
[14] M. Steriade, “Grouping of Brain Rhythms in Corticothalamic Systems,” Neuroscience, Vol. 137, No. 4, 2006, pp. 1087-1106.
[15] J. McNamara, D. Bonhous and C. Shin, “The Kindling Model of Epilepsy,” In: P. Schwartzkroin, Ed., Epilepsy: Models, Mechanisms and Concepts, Cambridge University Press, Cambridge. 1993, pp. 27-47. doi:10.1017/CBO9780511663314.003
[16] D. Purpura and B. Cohen, “Intracellular Recording from Thalamic Neurons during Recruiting Responses,” Journal of Neurophysiology, Vol. 25, No. 5, 1962, pp. 621-630.
[17] T. Frigiesi, “Intracellular Recordings from Neurons in Dorsolateral Thalamic Reticular Nucleus during Capsular, Basal Ganglia and Midline Thalamic Stimulation,” Brain Research, Vol. 48, No. 1972, pp. 157-164. doi:10.1016/0006-8993(72)90176-X
[18] S. David, S. Muruyama, X. Machne and K. Unna, “Evidence Supporting Cholinergic Transmission at the Lateral Geniculate Body of the Cat,” International Journal of Neuropharmacology, Vol. 2, No. 2-3, 1963, pp. 113-119. doi:10.1016/0028-3908(63)90014-5
[19] I. Schlag, “A Study of the Action of Nembutal on Diencephalon and Mesencephalic Unit Activity,” Archive of International Physiology and Biochemistry, Vol. 64, No. 3, 1956, pp. 470-477. doi:10.3109/13813455609150221
[20] C. Richards, “On the Mechanisms of Barbiturate Anaesthesia,” Journal of Physiology, Vol. 227, No. 3, 1972, pp. 749- 758.
[21] M. Larsen and M. Major, “The Effect of Hexobarbital on the Duration of the Recurrent IPSP in the Cat Motoneurons,” Brain Research, Vol. 21, No. 2, 1970, pp. 309-316. doi:10.1016/0006-8993(70)90377-X
[22] R. Nicol, “The Effects of Anaesthesia on Synaptic Excitation and Inhibition in the Olfactory Bulb,” Journal of Physiology, Vol. 233, No. 3, 1972, pp. 803-812.
[23] J. Eccles, D. Faber and H. Taborikova, “The Action of a Parallel Fiber Volley on the Antidromic Invasion of Purkinje Cells of Cat Cerebellum,” Brain Research, Vol. 25, No. 2, 1971, pp. 335-342. doi:10.1016/0006-8993(71)90442-2
[24] F. Serkov, I. Yanovski and A. Talnov, “Effect of Pentobarbital, Chloralose, and Urethane on Inhibitory Postsynaptic Potentials of Cortical Neurons,” Neurophysiology, Vol. 6, No. 4, 1974, pp. 339-346.
[25] W. Singer and U. Drager, “Postsynaptic Potentials in Relay Neurons of the Cat Lateral Geniculate Nucleus after Stimulation of the Mesencephalic Reticular Formation,” Brain Research, Vol. 41, No. 1, 1972, pp. 214-221. doi:10.1016/0006-8993(72)90632-4
[26] R. Dingledine and I. Kelly, “Brain Stem Stimulation and the Acetylcholine Evoked Inhibition of Neurons in the Feline Nucleus Reticularis Thalami,” Journal of Physiology, Vol. 271, No. 1, 1977, pp. 135-147.
[27] N. Nauta and G. Koupers, “Some Ascending Pathways in the Brain Stem Reticular Formation,” In: H. H. Jasper, L. D. Proctor, R. S. Knighton, W. C. Noshay and R. N. Costello, Eds., Reticular Formation of the Brain, Boston. 1954, pp. 3-30.
[28] C. S. Sherrington, “The Integrative Activity of the Nervous System,” Yale University Press, New Haven and London, 1966.
[29] Y. Komatsu, “Age-Dependent Long-Term Potentiation of Inhibitory Synaptic Transmission in Rat Visual Cortex,” Journal of Neuroscience, Vol. 14, No. 11, 1994, pp. 6488- 6499.
[30] T. Labakhua, G. Bekaya and V. Okudzhava, “Post-Tetanic Potentiation of Inhibitory Postsynaptic Potentials in the Motor Cortex of the Cat,” Doklady Akademii Nauk SSSR, Vol. 259, No. 4, 1981, pp. 1013-1015. (in Russion).
[31] G. Grabauskas and R. Bradly, “Potentiation of GABAergic Synaptic Transmission in the Rostral Nucleus of the Solitary Tract,” Neuroscience, Vol. 94, No. 4, 1999, pp. 1173-1182. doi:10.1016/S0306-4522(99)00379-6
[32] H. Korn, Y. Oda and D. Faber, “Long-Term Potentiation of Inhibitory Circuits and Synapses in the Central Nervous System,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 89, No. 1, 1992, pp. 440-443. doi:10.1073/pnas.89.1.440
[33] L. Novak and J. Bullier, “Axons, but Not Cell Bodyes, Are Activated by Electrical Stimulation in Cortical Gray Matter 1. Evidence from Chronaxy Measurement,” Experimental Brain Research, Vol. 118, No. 4, 1998, pp. 477-488. doi:10.1007/s002210050304

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.