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Received for publication August 9, 2004.
Revised December 17, 2004.
Accepted for publication December 17, 2004.
We postulated that differential sensitivity to ethanol of synaptic GABAA somatic and dendritic IPSCs in hippocampal CA1 pyramidal neurons (Weiner et al., 1997) could be due to differences in the extent of GABAB receptor activity at GABAergic synapses in these two subfields of the hippocampus. Our present results show that dendritic (distally evoked) GABA IPSCs contain a larger GABAB IPSC component of the total GABA IPSC than the somatic (proximately evoked) subfield. The inhibition of GABAB receptors by pretreatment of hippocampal slices with CGP-52432, a selective GABAB receptor antagonist, changes the basal ethanol-insensitive, distally evoked GABAA IPSCs to become more sensitive to ethanol. In addition, paired-pulse stimulation of the proximal and distal subfields of hippocampal pyramidal neurons shows that ethanol alone increases the probability of GABA release at proximal but not distal regions. Changes by ethanol on the probability of GABA release are only seen at distal locations during GABAB blockade. Finally, when the modulation of presynaptic GABAB receptors is minimized by the local application of GABA (10 mM) directly onto somatic or dendritic GABAergic synaptic regions, a postsynaptic GABAB receptor appears to exert significant negative (inhibiting) influence on the effects of ethanol on GABAA IPSCs in the distal subfields of CA1 pyramidal neurons. Together, our data suggest that differences in both presynaptic and postsynaptic GABAB receptor activity at these GABAergic synapses may modulate the differential ethanol sensitivity of proximal and distal GABAA IPSCs in hippocampal CA1 pyramidal neurons.
Key words:
Ethanol, GABA-A receptor, GABA-B receptor, Hippocampal slice, Synaptic transmission, Whole-cell recording
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