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GABA A receptor‐mediated IPSCs in rat thalamic sensory nuclei: patterns of discharge and tonic modulation by GABA B autoreceptors
Author(s) -
Feuvre Y.,
Fricker D.,
Leresche N.
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.091bl.x
Subject(s) - baclofen , gabaa receptor , inhibitory postsynaptic potential , gabab receptor , chemistry , neuroscience , electrophysiology , biophysics , agonist , receptor , biology , biochemistry
1 The patterns of discharge of spontaneous GABA A ‐mediated inhibitory postsynaptic currents (sIPSCs), originating from the nucleus reticularis thalami (NRT), and their modulation by GABAg autoreceptors, were studied in rat thalamocortical (TO) neurones using whole‐cell voltage‐clamp recordings in brain slices. 2 sIPSCs were recorded in all ventro‐basal (VB) and dorsal lateral geniculate (LGN) neurones. In VB neurones, in the presence of tetraethylammonium (TEA, 5 mm), these sIPSCs can occur in bursts at frequencies of either 0.1 or 1–2 Hz. In the presence of tetrodotoxin (TTX), these bursting activities are replaced by the continuous discharge of miniature IPSCs (mIPSCs), recorded in the absence of TEA, at a frequency of 4 Hz. The kinetic properties of mIPSCs were similar in VB and LGN TC neurones. 3 In VB TC neurones the GABA B receptor agonist (±)‐baclofen, at a concentration of 0.05 μ m , decreased the mIPSC frequency by 22% without affecting their amplitude distribution. Increasing the (±)‐baclofen concentration to 1 and 10 μ m caused similar reductions (41 and 47%, respectively) in the mIPSCs frequency: these values were significantly different from the one observed with 0.05 μ m (±)‐baclofen. In LGN TC neurones, where mIPSCs originate from both NRT and local interneurone terminals, 1 μ m (±)‐baclofen produced a 66% reduction in the mIPSC frequency. 4 The GABA B receptor antagonist CGP55845A (50 n m ) not only blocked the baclofen‐mediated decrease in mIPSC frequency, but also produced a 52% increase in the mIPSC frequency compared with control in three out of seven neurones. Application of CGP55845A (50–500 n m ) alone produced a 77 % increase in the mIPSC frequency in three out of nine VB neurones, and in the LGN, CGP55845A (100 n m ) produced a 53% increase in four out of nine neurones. CGP55845A (100 n m ) also reversibly increased the amplitude of evoked GABA A IPSCs by 74 and 57 % in three out of three VB and three out of five LGN neurones, respectively. 5 Application of GABA (1.5–5 μ m ) decreased the mIPSC frequency in VB TC neurones by a similar extent (48%) as 1–10 μ m (±)‐baclofen. 6 In the presence of 100 μ m Cd 2+ , (±)‐baclofen still decreased the mIPSC frequency by about 40%, indicating that the effect of presynaptic GABA B receptor activation on spontaneous GABA release did not occur through a reduction of voltage‐dependent Ca 2+ currents. 7 Cd 2+ (100 μ m ) decreased the amplitude of both mIPSCs and isoguvacine‐induced current by 30 and 19%, respectively, indicating an effect of this divalent cation on postsynaptic GABA A receptors. 8 We conclude that GABA B autoreceptors are present on the GABAergic terminals within the thalamic sensory nuclei and that these receptors can be tonically activated by the ambient GABA.