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Volume 17, Number 22,
Issue of November 15, 1997
pp. 8894-8908
Inhibitory Interactions between Perigeniculate GABAergic
Neurons
Received June 17, 1997; revised Aug. 4, 1997; accepted Aug. 28, 1997.
Maria V. Sanchez-Vives1,
Thierry Bal2, and
David A. McCormick1
1 Section of Neurobiology, Yale University School of
Medicine, New Haven, Connecticut 06510, and 2 Institut
Alfred Fessard, Centre National de la Recherche Scientifique, Avenue de
la Terrasse, Gif Sur Yvette, Cedex 91198, France
Perigeniculate neurons form an interactive sheet of cells that
inhibit one another as well as thalamocortical neurons in the dorsal
lateral geniculate nucleus (LGNd). The inhibitory influence of the
GABAergic neurons of the perigeniculate nucleus (PGN) onto other PGN
neurons was examined with intracellular recordings in vitro. Intracellular recordings from PGN neurons during the
generation of spindle waves revealed barrages of EPSPs and IPSPs. The
excitation of local regions of the PGN with the local application of
glutamate resulted in activation of IPSPs in neighboring PGN neurons.
These IPSPs displayed an average reversal potential of 77 mV and were blocked by application of bicuculline methiodide or picrotoxin, indicating that they are mediated by GABAA receptors. In
the presence of GABAA receptor blockade, the activation of
PGN neurons with glutamate could result in slow IPSPs that were
mediated by GABAB receptors in a subset (40%) of cells.
Similarly, application of specific agonists muscimol and baclofen
demonstrated that PGN neurons possess both functional GABAA
and GABAB receptors. Examination of the axon arbors of
biocytin-filled PGN neurons often revealed the presence of beaded axon
collaterals within the PGN, suggesting that this may be an anatomical
substrate for PGN to PGN inhibition.
Functionally, activation of inhibition between PGN neurons could result
in a shortening or a complete abolition of the low threshold
Ca2+ spike or an inhibition of tonic discharge. We
suggest that the mutual inhibition between PGN neurons forms a
mechanism by which the excitability of these cells is tightly
controlled. The activation of a point within the PGN may result in the
inhibition of neighboring PGN neurons. This may be reflected in the
LGNd as a center of inhibition surrounded by an annulus of
disinhibition, thus forming a "center-surround" mechanism for
thalamic function.
Key words:
inhibition;
thalamus;
thalamic reticular nucleus;
GABAergic;
oscillations;
sleep;
epilepsy
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