GABA(B) receptors couple to potassium and calcium channels on identified lateral perforant pathway projection neurons.
Activation of presynaptic GABA(B) receptors inhibits neurotransmitter release at most cortical synapses, at least in part because of inhibition of voltage-gated calcium channels. One synapse where this is not the case is the lateral perforant pathway synapse onto dentate granule cells in the hippocampus. The current study was conducted to determine whether the neurons that make these synapses express GABA(B) receptors that can couple to ion channels. Perforant pathway projection neurons were labeled by injecting retrograde tracer into the dorsal hippocampus. The GABA(B) receptor agonist baclofen (10 microM) activated inwardly rectifying potassium channels and inhibited currents mediated by voltage-gated calcium channels in retrogradely labeled neurons in layer II of the lateral entorhinal cortex. These effects were reversed by coapplication of the selective GABA(B) receptor antagonist CGP 55845A (1 microM). Equivalent effects were produced by 100 microM adenosine, which inhibits neurotransmitter release at lateral perforant pathway synapses. The effects of baclofen and adenosine on inward currents were largely occlusive. These results suggest that the absence of GABA(B) receptor-mediated presynaptic inhibition at lateral perforant pathway synapses is not simply due to a failure to express these receptors and imply that GABA(B) receptors can either be selectively localized or regulated at terminal versus somatodendritic domains.
Wang
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Department of Pharmacology and Toxicology, Medical College of Georgia, and Medical Research Service, Veterans Administration Medical Center, Augusta, Georgia 30912-2300, USA.
Lambert
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NA
D000241:Adenosine / Q000494:pharmacology; D000700:Analgesics / Q000494:pharmacology; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D004594:Electrophysiology; D018728:Entorhinal Cortex / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000737:chemistry / Q000502:physiology; D019580:Perforant Pathway / Q000737:chemistry* / Q000166:cytology* / Q000502:physiology; D010721:Phosphinic Acids / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D011412:Propanolamines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018080:Receptors, GABA-B / Q000502:physiology*; D013569:Synapses / Q000737:chemistry / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D000700:Analgesics; D015220:Calcium Channels; D018755:GABA Agonists; D018756:GABA Antagonists; D010721:Phosphinic Acids; D015221:Potassium Channels; D011412:Propanolamines; D018080:Receptors, GABA-B; C085075:CGP 55845A; D001418:Baclofen; D000241:Adenosine