title: Functional properties of perigeniculate inhibition of dorsal lateral geniculate nucleus thalamocortical neurons in vitro.
abstract: The properties of the inhibitory influence of neurons in the perigeniculate (PGN) nucleus on thalamocortical cells were examined with intracellular recordings in the ferret geniculate slice maintained in vitro. Activation of PGN neurons with the local application of glutamate caused IPSPs in thalamocortical neurons that were mediated by both GABAA and GABAB receptors, as well as the activation of spindle waves. With low intensity stimulation of the PGN, local application of bicuculline to the dorsal lateral geniculate nucleus (LGNd) strongly inhibited evoked and spindle-associated IPSPs, indicating that these are largely mediated by GABAA receptors. The generation of GABAB receptor-mediated IPSPs in thalamocortical cells that were large enough to generate rebound low threshold Ca2+ spikes required substantially increased activation of the PGN with glutamate. The activation of synchronous bicuculline-induced slowed oscillations in thalamocortical neurons required the block of GABAA receptors in the LGNd as well as in the PGN. These results indicate that bursts of action potentials in PGN neurons can result in the activation of both GABAA and GABAB receptors in thalamocortical neurons, with the strong activation of GABAB receptors requiring an intense, simultaneous discharge of a number of PGN neurons. Functionally, these results suggest that PGN neurons inhibit thalamocortical cells preferentially through the activation of GABAA receptors, although the strong activation of GABAB receptors may occur under pathological conditions and contribute to the generation of abnormal, synchronous slow oscillations.
authors.affiliation: Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
authors.forename: M V
authors.initials: MV
authors.lastname: Sanchez-Vives
authors.forename: D A
authors.initials: DA
authors.lastname: McCormick
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D001418:Baclofen / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology* / Q000502:physiology; D003292:Convulsants / Q000494:pharmacology; D004594:Electrophysiology; D005260:Female; D005289:Ferrets; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005829:Geniculate Bodies / Q000166:cytology* / Q000502:physiology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009433:Neural Inhibition / Q000502:physiology*; D009434:Neural Pathways; D009474:Neurons / Q000737:chemistry / Q000502:physiology; D009943:Organophosphorus Compounds / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000502:physiology; D018080:Receptors, GABA-B / Q000502:physiology; D017661:Receptors, Presynaptic / Q000502:physiology; D013787:Thalamic Nuclei / Q000166:cytology* / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D000086:Acetazolamide; D000927:Anticonvulsants; D001418:Baclofen; D001640:Bicuculline; D003292:Convulsants; D018755:GABA Agonists; D018756:GABA Antagonists; D009943:Organophosphorus Compounds; D010852:Picrotoxin; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D017661:Receptors, Presynaptic; D005680:gamma-Aminobutyric Acid; C066430:CGP 35348