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 n
eurons of the perigeniculate nucleus (PGN) onto other PGN neurons was
examined with intracellular recordings in vitro. Intracellular recordi
ngs from PGN neurons during the generation of spindle waves revealed b
arrages of EPSPs and IPSPs. The excitation of local regions of the PGN
with the local application of glutamate resulted in activation of IPS
Ps in neighboring PGN neurons. These IPSPs displayed an average revers
al potential of -77 mV and were blocked by application of bicuculline
methiodide or picrotoxin, indicating that they are mediated by GABA(A)
receptors. In the presence of GABA(A) receptor blockade, the activati
on of PGN neurons with glutamate could result in slow IPSPs that were
mediated by GABA(B) receptors in a subset (40%) of cells. Similarly, a
pplication of specific agonists muscimol and baclofen demonstrated tha
t PGN neurons possess both functional GABA(A) and GABA(B) receptors. E
xamination of the axon arbors of biocytin-filled PGN neurons often rev
ealed the presence of beaded axon collaterals within the PGN, suggesti
ng that this may be an anatomical substrate for PGN to PGN inhibition.
Functionally, activation of inhibition between PGN neurons could resu
lt in a shortening or a complete abolition of the low threshold Ca2+ s
pike or an inhibition of tonic discharge. We suggest that the mutual i
nhibition between PGN neurons forms a mechanism by which the excitabil
ity of these cells is tightly controlled. The activation of a point wi
thin 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'' me
chanism for thalamic function.