GABAA receptor-mediated IPSCs in rat thalamic sensory nuclei: patterns of discharge and tonic modulation by GABAB autoreceptors

• Published in: The Journal of physiology 1997-07, Vol.502 (Pt 1), p.91-104
• Main Authors: Feuvre, Y., Fricker, D., Leresche, N.
• Format: Article
• Language: English
• Subjects: Animals; Autoreceptors - physiology; Baclofen - pharmacology; Cadmium - pharmacology; GABA Agonists - pharmacology; GABA Antagonists - pharmacology; gamma-Aminobutyric Acid - pharmacology; Geniculate Bodies - chemistry; Geniculate Bodies - cytology; Geniculate Bodies - physiology; Interneurons - chemistry; Interneurons - physiology; Isonicotinic Acids - pharmacology; Male; Membrane Potentials - drug effects; Membrane Potentials - physiology; Organ Culture Techniques; Patch-Clamp Techniques; Phosphinic Acids - pharmacology; Presynaptic Terminals - chemistry; Presynaptic Terminals - drug effects; Presynaptic Terminals - physiology; Propanolamines - pharmacology; Rats; Rats, Wistar; Receptors, GABA-A - physiology; Receptors, GABA-B - physiology; Tetrodotoxin - pharmacology; Thalamic Nuclei - chemistry; Thalamic Nuclei - cytology; Thalamic Nuclei - physiology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1997.091bl.x

1. The patterns of discharge of spontaneous GABAA-mediated inhibitory postsynaptic currents (sIPSCs), originating from the nucleus reticularis thalami (NRT), and their modulation by GABAB autoreceptors, were studied in rat thalamocortical (TC) 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 GABAB receptor agonist (+/-)-baclofen, at a concentration of 0.05 microM, decreased the mIPSC frequency by 22% without affecting their amplitude distribution. Increasing the (+/-)-baclofen concentration to 1 and 10 microM caused similar reductions (41 and 47%, respectively) in the mIPSCs frequency: these values were significantly different from the one observed with 0.05 microM (+/-)-baclofen. In LGN TC neurones, where mIPSCs originate from both NRT and local interneurone terminals, 1 microM (+/-)-baclofen produced a 66% reduction in the mIPSC frequency. 4. The GABAB receptor antagonist CGP55845A (50 nM) 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 nM) alone produced a 77% increase in the mIPSC frequency in three out of nine VB neurones, and in the LGN, CGP55845A (100 nM) produced a 53% increase in four out of nine neurones. CGP55845A (100 nM) also reversibly increased the amplitude of evoked GABAA 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 microM) decreased the mIPSC frequency in VB TC neurones by a similar extent (48%) as 1-10 microM (+/-)-baclofen. 6. In the presence of 100 microM Cd2+, (+/-)-baclofen still decreased the mIPSC frequency by about 40%, indicating that the effect of presynaptic GABAB receptor activation on spontaneous GABA release did not occur through a reduction of voltage-dependent Ca2+ currents. 7. Cd2+ (100 microM) decreased the amplitude of both mIPSCs and isoguvacine-in