TY - JOUR AU - Slézia, Andrea AU - Hangya, Balázs AU - Ulbert, István AU - Acsády, László TI - Phase advancement and nucleus-specific timing of thalamocortical activity during slow cortical oscillation JF - JOURNAL OF NEUROSCIENCE J2 - J NEUROSCI VL - 31 PY - 2011 IS - 2 SP - 607 EP - 617 PG - 11 SN - 0270-6474 DO - 10.1523/JNEUROSCI.3375-10.2011 UR - https://m2.mtmt.hu/api/publication/1536705 ID - 1536705 AB - The exact timing of cortical afferent activity is instrumental for the correct coding and retrieval of internal and external stimuli. Thalamocortical inputs represent the most significant subcortical pathway to the cortex, but the precise timing and temporal variability of thalamocortical activity is not known. To examine this question, we studied the phase of thalamic action potentials relative to cortical oscillations and established correlations among phase, the nuclear location of the thalamocortical neurons, and the frequency of cortical activity. The phase of thalamic action potentials depended on the exact frequency of the slow cortical oscillation both on long (minutes) and short (single wave) time scales. Faster waves were accompanied by phase advancement in both cases. Thalamocortical neurons located in different nuclei fired at significantly different phases of the slow waves but were active at a similar phase of spindle oscillations. Different thalamic nuclei displayed distinct burst patterns. Bursts with a higher number of action potentials displayed progressive phase advancement in a nucleus-specific manner. Thalamic neurons located along nuclear borders were characterized by mixed burst and phase properties. Our data demonstrate that the temporal relationship between cortical and thalamic activity is not fixed but displays dynamic changes during oscillatory activity. The timing depends on the precise location and exact activity of thalamocortical cells and the ongoing cortical network pattern. This variability of thalamic output and its coupling to cortical activity can enable thalamocortical neurons to actively participate in the coding and retrieval of cortical signals. LA - English DB - MTMT ER - TY - JOUR AU - Wanaverbecq, N AU - Bodor, Ágnes AU - Bokor, Hajnalka AU - Slézia, Andrea AU - Luthi, A AU - Acsády, László TI - Contrasting the functional properties of GABAergic axon terminals with single and multiple synapses in the thalamus JF - JOURNAL OF NEUROSCIENCE J2 - J NEUROSCI VL - 28 PY - 2008 IS - 46 SP - 11848 EP - 11861 PG - 14 SN - 0270-6474 DO - 10.1523/JNEUROSCI.3183-08.2008 UR - https://m2.mtmt.hu/api/publication/109948 ID - 109948 N1 - Megjegyzés-21502962 Megjegyzés-10069677 FU: Wellcome Trust [084651]; Hungarian Scientific Research Fund [OTKA : 49100, 64184, 75676]; Institut du Cerveau et de la Moelle epiniere ; : Synapsis Foundation ; Schuller-Stiftung ; Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation ; Swiss National : Science Foundation [3100A0_116006] FX: This work was supported by the Wellcome Trust ( L. A. is in receipt of : a Wellcome Trust International Senior Research Fellowship and a project : Grant 084651), the Hungarian Scientific Research Fund (OTKA 49100, : 64184, and 75676), the Institut du Cerveau et de la Moelle epiniere, : the Synapsis Foundation, the Schuller-Stiftung, the Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation, an anonymous : foundation, and the Swiss National Science Foundation ( No. : 3100A0_116006). N.W. and A. L. performed the experimental portions of : this work at the Biozentrum, University of Basel, Basel, Switzerland. : We thank Dr. Balazs Hangya for his help in the statistical analysis, : and Krisztina Faddi and Gyo. zo. Goda for their excellent technical : assistance. Wethank Prof. Zoltan Nusser, Dr. Szabolcs Kali, Dr. Lisa : Mapelli, and Fabio Longordo for their comments on this manuscript and : Prof. Peter Somogyi for providing us the anti-GABA antiserum. Megjegyzés-20982799 FU: Wellcome Trust [084651]; Hungarian Scientific Research Fund [OTKA : 49100, 64184, 75676]; Institut du Cerveau et de la Moelle epiniere ; : Synapsis Foundation ; Schuller-Stiftung ; Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation ; Swiss National : Science Foundation [3100A0_116006] FX: This work was supported by the Wellcome Trust ( L. A. is in receipt of : a Wellcome Trust International Senior Research Fellowship and a project : Grant 084651), the Hungarian Scientific Research Fund (OTKA 49100, : 64184, and 75676), the Institut du Cerveau et de la Moelle epiniere, : the Synapsis Foundation, the Schuller-Stiftung, the Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation, an anonymous : foundation, and the Swiss National Science Foundation ( No. : 3100A0_116006). N.W. and A. L. performed the experimental portions of : this work at the Biozentrum, University of Basel, Basel, Switzerland. : We thank Dr. Balazs Hangya for his help in the statistical analysis, : and Krisztina Faddi and Gyo. zo. Goda for their excellent technical : assistance. Wethank Prof. Zoltan Nusser, Dr. Szabolcs Kali, Dr. Lisa : Mapelli, and Fabio Longordo for their comments on this manuscript and : Prof. Peter Somogyi for providing us the anti-GABA antiserum. Megjegyzés-20982816 FU: Wellcome Trust [084651]; Hungarian Scientific Research Fund [OTKA : 49100, 64184, 75676]; Institut du Cerveau et de la Moelle epiniere ; : Synapsis Foundation ; Schuller-Stiftung ; Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation ; Swiss National : Science Foundation [3100A0_116006] FX: This work was supported by the Wellcome Trust ( L. A. is in receipt of : a Wellcome Trust International Senior Research Fellowship and a project : Grant 084651), the Hungarian Scientific Research Fund (OTKA 49100, : 64184, and 75676), the Institut du Cerveau et de la Moelle epiniere, : the Synapsis Foundation, the Schuller-Stiftung, the Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation, an anonymous : foundation, and the Swiss National Science Foundation ( No. : 3100A0_116006). N.W. and A. L. performed the experimental portions of : this work at the Biozentrum, University of Basel, Basel, Switzerland. : We thank Dr. Balazs Hangya for his help in the statistical analysis, : and Krisztina Faddi and Gyo. zo. Goda for their excellent technical : assistance. Wethank Prof. Zoltan Nusser, Dr. Szabolcs Kali, Dr. Lisa : Mapelli, and Fabio Longordo for their comments on this manuscript and : Prof. Peter Somogyi for providing us the anti-GABA antiserum. Megjegyzés-10022519 FU: Wellcome Trust [084651]; Hungarian Scientific Research Fund [OTKA : 49100, 64184, 75676]; Institut du Cerveau et de la Moelle epiniere ; : Synapsis Foundation ; Schuller-Stiftung ; Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation ; Swiss National : Science Foundation [3100A0_116006] FX: This work was supported by the Wellcome Trust ( L. A. is in receipt of : a Wellcome Trust International Senior Research Fellowship and a project : Grant 084651), the Hungarian Scientific Research Fund (OTKA 49100, : 64184, and 75676), the Institut du Cerveau et de la Moelle epiniere, : the Synapsis Foundation, the Schuller-Stiftung, the Schweizerische : Mobiliarversicherungsgesellschaft, the MBF Foundation, an anonymous : foundation, and the Swiss National Science Foundation ( No. : 3100A0_116006). N.W. and A. L. performed the experimental portions of : this work at the Biozentrum, University of Basel, Basel, Switzerland. : We thank Dr. Balazs Hangya for his help in the statistical analysis, : and Krisztina Faddi and Gyo. zo. Goda for their excellent technical : assistance. Wethank Prof. Zoltan Nusser, Dr. Szabolcs Kali, Dr. Lisa : Mapelli, and Fabio Longordo for their comments on this manuscript and : Prof. Peter Somogyi for providing us the anti-GABA antiserum. Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :29 Export Date: 1 August 2019 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :29 Export Date: 21 August 2019 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :30 Export Date: 6 March 2020 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :30 Export Date: 9 March 2020 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :30 Export Date: 24 May 2020 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :31 Export Date: 22 March 2021 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :31 Export Date: 1 April 2021 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :32 Export Date: 12 April 2021 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 Department of Neurovegetative Physiology, Centre de Recherche de Neurobiologie-Neurophysiologie de Marseille (CRN2M), University of Aix-Marseille II-III, 13397 Marseille Cedex 20, France Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary Département de Biologie Cellulaire et de Morphologie, University of Lausanne, 1005 Lausanne, Switzerland Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, H-1083 Budapest, Hungary Cited By :32 Export Date: 20 April 2021 CODEN: JNRSD Correspondence Address: Acsády, L.; Institute of Experimental Medicine, Szigony u. 43, H-1083 Budapest, Hungary; email: acsady@koki.hu Chemicals/CAS: gamma-Aminobutyric Acid, 56-12-2 AB - Diverse sources of GABAergic inhibition are a major feature of cortical networks, but distinct inhibitory input systems have not been systematically characterized in the thalamus. Here, we contrasted the properties of two independent GABAergic pathways in the posterior thalamic nucleus of rat, one input from the reticular thalamic nucleus (nRT), and one "extrareticular" input from the anterior pretectal nucleus (APT). The vast majority of nRT-thalamic terminals formed single synapses per postsynaptic target and innervated thin distal dendrites of relay cells. In contrast, single APT-thalamic terminals formed synaptic contacts exclusively via multiple, closely spaced synapses on thick relay cell dendrites. Quantal analysis demonstrated that the two inputs displayed comparable quantal amplitudes, release probabilities, and multiple release sites. The morphological and physiological data together indicated multiple, single-site contacts for nRT and multisite contacts for APT axons. The contrasting synaptic arrangements of the two pathways were paralleled by different short-term plasticities. The multisite APT-thalamic pathway showed larger charge transfer during 50-100 Hz stimulation compared with the nRT pathway and a greater persistent inhibition accruing during stimulation trains. Our results demonstrate that the two inhibitory systems are morpho-functionally distinct and suggest and that multisite GABAergic terminals are tailored for maintained synaptic inhibition even at high presynaptic firing rates. These data explain the efficacy of extrareticular inhibition in timing relay cell activity in sensory and motor thalamic nuclei. Finally, based on the classic nomenclature and the difference between reticular and extrareticular terminals, we define a novel, multisite GABAergic terminal type (F3) in the thalamus. LA - English DB - MTMT ER - TY - JOUR AU - Lu, J AU - Helton, TD AU - Blanpied, TA AU - Rácz, Bence AU - Newpher, TM AU - Weinberg, RJ AU - Ehlers, MD TI - Postsynaptic positioning of endocytic zones and AMPA receptor cycling by physical coupling of dynamin-3 to homer JF - NEURON J2 - NEURON VL - 55 PY - 2007 IS - 6 SP - 874 EP - 889 PG - 16 SN - 0896-6273 DO - 10.1016/j.neuron.2007.06.041 UR - https://m2.mtmt.hu/api/publication/1204243 ID - 1204243 AB - Endocytosis; of AMPA receptors and other postsynaptic cargo occurs at endocytic zones (EZs), stably positioned sites of clathrin adjacent to the postsynaptic density (PSD). The tight localization of postsynaptic endocytosis is thought to control spine composition and regulate synaptic transmission. However, the mechanisms that situate the EZ near the PSD and the role of spine endocytosis in synaptic transmission are unknown. Here, we report that a physical link between dynamin-3 and the postsynaptic adaptor Homer positions the EZ near the PSD. Disruption of dynamin-3 or its interaction with Homer uncouples the PSD from the EZ, resulting in synapses lacking postsynaptic clathrin. Loss of the EZ leads to a loss of synaptic AMPA receptors and reduced excitatory synaptic transmission that corresponds with impaired synaptic recycling. Thus, a physical link between the PSD and the EZ ensures localized endocytosis and recycling by recapturing and maintaining a proximate pool of cycling AMPA receptors. LA - English DB - MTMT ER - TY - JOUR AU - Bokor, Hajnalka AU - Frére, SG AU - Eyre, Mark David AU - Slézia, Andrea AU - Ulbert, István AU - Lüthi, A AU - Acsády, László TI - Selective GABAergic control of higher-order thalamic relays JF - NEURON J2 - NEURON VL - 45 PY - 2005 IS - 6 SP - 929 EP - 940 PG - 12 SN - 0896-6273 DO - 10.1016/j.neuron.2005.01.048 UR - https://m2.mtmt.hu/api/publication/109610 ID - 109610 LA - English DB - MTMT ER - TY - JOUR AU - Hajnik, Tünde AU - Lai, YY AU - Siegel, JM TI - Atonia-related regions in the rodent pons and medulla JF - JOURNAL OF NEUROPHYSIOLOGY J2 - J NEUROPHYSIOL VL - 84 PY - 2000 IS - 4 SP - 1942 EP - 1948 PG - 7 SN - 0022-3077 UR - https://m2.mtmt.hu/api/publication/1865302 ID - 1865302 N1 - : FN Thomson Reuters Web of Knowledge AB - Electrical stimulation of circumscribed areas of the pontine and medullary reticular formation inhibits muscle tone in cats. In this report, we present an analysis of the anatomical distribution of atonia-inducing stimulation sites in the brain stem of the rat. Muscle atonia could be elicited by electrical stimulation of the nuclei reticularis pontis oralis and caudalis in the pons as well as the nuclei gigantocellularis, gigantocellularis alpha, gigantocellularis ventralis, and paragigantocellularis dorsalis in the medulla of decerebrate rats. This inhibitory effect on muscle tone was a function of the intensity and frequency of the electrical stimulation. Average latencies of muscle-tone suppressions elicited by electrical stimulation of the pontine reticular formation were 11.02 +/- 2.54 and 20.49 +/- 3.39 (SD) ms in the neck and in the hindlimb muscles, respectively. Following medullary stimulation, these latencies were 11.29 +/- 2.44 ms in the neck and 18.87 +/- 2.64 ms in the hindlimb muscles. Microinjection of N-methyl-D-aspartate (NMDA, 7 mM/0.1 ml) agonists into the pontine and medullary inhibitory sites produced muscle-tone facilitation, whereas quisqualate (10 mM/ 0.1 ml) injection induced an inhibition of muscle tone. NMDA-induced muscle tone change had a latency of 31.8 +/- 35.3 s from the pons and 10.5 +/- 0.7 s from the medulla and a duration of 146.7 +/- 95.2 s from the pons and 55.5 +/- 40.4 s from the medulla. The latency of quisqualate (QU)-induced reduction of neck muscle tone was 30.1 +/- 37.9 s after pontine and 39.5 +/- 21.8 s after medullary injection. The duration of muscle-tone suppression induced by QU injection into the pons and medulla was 111.5 +/- 119.2 and 169.2 +/- 145.3 s. Smaller rats (8 wk old) had a higher percentage of sites producing muscle-tone inhibition than larger rats (16 wk old), indicating an age-related change in the function of brain stem inhibitory systems. The anatomical distribution of atonia-related sites in the rat has both similarities and differences with the distribution found in the cat, which can be explained by the distinct anatomical organization of the brain stem in these two species. LA - English DB - MTMT ER - TY - JOUR AU - LERESCHE, N AU - LIGHTOWLER, S AU - Soltesz, Ivan AU - JASSIKGERSCHENFELD, D AU - CRUNELLI, V TI - LOW-FREQUENCY OSCILLATORY ACTIVITIES INTRINSIC TO RAT AND CAT THALAMOCORTICAL CELLS JF - JOURNAL OF PHYSIOLOGY-LONDON J2 - J PHYSIOL-LONDON VL - 441 PY - 1991 SP - 155 EP - 174 PG - 20 SN - 0022-3751 UR - https://m2.mtmt.hu/api/publication/2941590 ID - 2941590 AB - 1. Low-frequency membrane potential oscillations recorded intracellularly from thalamocortical (TC) cells of the rat and cat dorsal lateral geniculate nucleus (dLGN) and of the rat ventrobasal nucleus (VB) maintained in vitro were investigated. On the basis of their electrophysiological and pharmacological properties, four types of activity were distinguished and named: the pacemaker oscillations, the spindle-like oscillations, the 'very slow' oscillations and the 'N-methyl-D-aspartate' (NMDA) oscillations. 2. The pacemaker oscillations (95 out of 173 cells) consisted of rhythmic, large-amplitude (10-30 mV) depolarizations which occurred at a frequency of 1.8 +/- 0.3 Hz (range, 0.5-2.9 Hz) and could often give rise to single or a burst of action potentials. Pacemaker oscillations were observed when the membrane potential was moved negative to -55 and positive to -80 mV, but in a given cell the upper and lower limits of this voltage range were separated by only 13.1 +/- 0.5 mV. Above -45 mV tonic firing consisting of single action potentials was seen in the cells showing this or the other types of low-frequency oscillations. 3. The spindle-like oscillations were observed in thirty-nine (out of 173) TC cells and consisted of rhythmic (2.1 +/- 0.3 Hz), large-amplitude depolarizations (and often associated burst firing) similar to the pacemaker oscillations but occurring in discrete periods every 5-25 s and lasting for 1.5-28 s. The spindle-like oscillations were observed when the membrane potential was moved negative to -55 and positive to -80 mV and in two cells they were transformed into continuous pacemaker oscillations by depolarization of the membrane potential to -60 mV. 4. Pacemaker and spindle-like oscillations were unaffected by tetrodotoxin (TTX) or by selective blockade of NMDA, non-NMDA, GABA(A), GABA(B), nicotinic, muscarinic, alpha- and beta-noradrenergic receptors. 5. The 'very slow' oscillations consisted of a TTX-insensitive, slow hyperpolarization-depolarization sequence (5-15 mV in amplitude) which lasted up to 90 s and was observed in nine dLGN cells and in two VB cells. The pacemaker and the spindle-like oscillations were recorded in one cell each which also showed the 'very slow' oscillations. 6. The 'NMDA' oscillations were observed only in a 'Mg2+-free' medium (0 mM-Mg2+, 2-4 mM-Ca2+; 64 out of 72 cells) and consisted of large-amplitude (10-25 mV) depolarizations that did not occur at regular intervals and were intermixed with smaller depolarizations present on the baseline and on the failing phase of the larger ones. The 'NMDA' oscillations were voltage dependent (observed in the range from -60 to -85 mV), insensitive to TTX and had a frequency of 1-4 Hz. Application of selective NMDA receptor antagonists reversibly transformed the NMDA into the pacemaker or the spindle-like oscillations while blockade of non-NMDA receptors as well as the other receptors mentioned above (paragraph 4) had no effect on the 'NMDA' oscillations. 7. The pacemaker, the spindle-like and the 'very slow' oscillations were never observed in electrophysiologically identified rat and cat dLGN interneurones (n = 12). Similarly, in a 'Mg2+-free' medium, interneurones in the dLGN and cells in the ventral lateral geniculate nucleus did not show the 'NMDA' oscillations but only slow, small-amplitude (< 4 mV) depolarizations that were reversibly abolished by DL-2-amino-5-phosphono-valeric acid (25-mu-M). 8. These results indicate that (i) single TC cells in different thalamic nuclei of different species are capable of four types of low-frequency oscillatory activity that do not require the evoked rhythmic recruitment of other neurones and (ii) activation of the NMDA receptors by spontaneously released excitatory amino acid brings about the transformation of the pacemaker and the spindle-like oscillations into the 'NMDA' oscillations. LA - English DB - MTMT ER - TY - JOUR AU - Somogyi, Péter Pál AU - Hodgson, Anthony J AU - Chubb, Ian W AU - Penke, Botond AU - Erdei, Anna TI - Antisera to γ-aminobutyric acid : II. immunocytochemical application to the central nervous system JF - JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY J2 - J HISTOCHEM CYTOCHEM VL - 33 PY - 1985 IS - 3 SP - 240 EP - 248 PG - 9 SN - 0022-1554 DO - 10.1177/33.3.2579123 UR - https://m2.mtmt.hu/api/publication/103037 ID - 103037 LA - English DB - MTMT ER -