FUNCTIONAL-PROPERTIES OF PERIGENICULATE INHIBITION OF DORSAL LATERAL GENICULATE-NUCLEUS THALAMOCORTICAL NEURONS IN-VITRO

Citation
Mv. Sanchezvives et Da. Mccormick, FUNCTIONAL-PROPERTIES OF PERIGENICULATE INHIBITION OF DORSAL LATERAL GENICULATE-NUCLEUS THALAMOCORTICAL NEURONS IN-VITRO, The Journal of neuroscience, 17(22), 1997, pp. 8880-8893
Citations number
54
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
17
Issue
22
Year of publication
1997
Pages
8880 - 8893
Database
ISI
SICI code
0270-6474(1997)17:22<8880:FOPIOD>2.0.ZU;2-C
Abstract
The properties of the inhibitory influence of neurons in the perigenic ulate (PGN) nucleus on thalamocortical cells were examined with intrac ellular recordings in the ferret geniculate slice maintained in vitro. Activation of PGN neurons with the local application of glutamate cau sed IPSPs in thalamocortical neurons that were mediated by both GABA(A ) and GABA(B) receptors, as well as the activation of spindle waves. W ith low intensity stimulation of the PGN, local application of bicucul line to the dorsal lateral geniculate nucleus (LGNd) strongly inhibite d evoked and spindle-associated IPSPs, indicating that these are large ly mediated by GABA(A) receptors. The generation of GABA(B) receptor-m ediated IPSPs in thalamocortical cells that were large enough to gener ate rebound low threshold Ca2+ spikes required substantially increased activation of the PGN with glutamate. The activation of synchronous b icuculline-induced slowed oscillations in thalamocortical neurons requ ired the block of GABA(A) receptors in the LGNd as well as in the PGN. These results indicate that bursts of action potentials in PGN neuron s can result in the activation of both GABA(A) and GABA(B) receptors i n thalamocortical neurons, with the strong activation of GABA(B) recep tors requiring an intense, simultaneous discharge of a number of PGN n eurons, Functionally, these results sug gest that PGN neurons inhibit thalamocortical cells preferentially through the activation of GABA(A) receptors, although the strong activation of GABA(B) receptors may oc cur under pathological conditions and contribute to the generation of abnormal, synchronous slow oscillations.