GAMMA-AMINOBUTYRIC-ACID TYPE-B RECEPTOR-DEPENDENT BURST-FIRING IN THALAMIC NEURONS - A DYNAMIC CLAMP STUDY

Citation
D. Ulrich et Jr. Huguenard, GAMMA-AMINOBUTYRIC-ACID TYPE-B RECEPTOR-DEPENDENT BURST-FIRING IN THALAMIC NEURONS - A DYNAMIC CLAMP STUDY, Proceedings of the National Academy of Sciences of the United Statesof America, 93(23), 1996, pp. 13245-13249
Citations number
34
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
93
Issue
23
Year of publication
1996
Pages
13245 - 13249
Database
ISI
SICI code
0027-8424(1996)93:23<13245:GTRBIT>2.0.ZU;2-J
Abstract
Synchronized network responses in thalamus depend on phasic inhibition originating in the thalamic reticular nucleus (nRt) and are mediated by the neurotransmitter gamma-aminobutyric acid (GABA), A suggested ro le for intra-nRt connectivity in inhibitory phasing remains controvers ial, Recently, functional GABA type B (GABA(B)) receptors were demonst rated on nRt cells, and the slow time course of the GABA(B) synaptic r esponse seems ideally suited to deinactivate low-threshold calcium cha nnels. This promotes burst firing, a characteristic feature of synchro nized responses. Here we investigate GABA(B)-mediated rebound burst fi ring in thalamic cells, Whole-cell current-clamp recordings were obtai ned from nRt cells and somatosensory thalamocortical relay cells in ra t brain slices. Synthetic GABA(B) inhibitory postsynaptic potentials, generated by a hybrid computer-neuron synapse (dynamic clamp), trigger ed rebound low-threshold calcium spikes in both cell types when peak i nhibitory postsynaptic potential hyperpolarization was greater than -9 2 mV. The threshold inhibitory postsynaptic potential conductance for rebound burst generation was comparable in nRt (7 nS) and thalamocorti cal (5 nS) cells, However, burst onset in nRt (1 s) was considerably d elayed compared with thalamocortical (0.6 s) cells. Thus, GABA(B) inhi bitory postsynaptic potentials can elicit low-threshold calcium spikes in both relay and nRt neurons, but the resultant oscillation frequenc y would be faster for thalamocortical-nRt networks (3 Hz) than for nRt -nRt networks (1-2 Hz), We conclude, therefore, that fast (> 2 Hz) GAB A(B)-dependent thalamic oscillations are maintained primarily by recip rocal connections between excitatory and inhibitory cells. These findi ngs further indicate that when oscillatory neural networks contain bot h recurrent and reciprocal inhibition, then distinct population freque ncies may result when one or the other type of inhibition is favored.