Mesencephalic trigeminal neurons are primary sensory neurons which hav
e cell somata located within the brain stem. In spite of the presence
of synaptic terminals on and around the cell somata, applications of a
variety of neurotransmitter substances in earlier studies have failed
to demonstrate responses. Using intracellular recording in a brain sl
ice preparation, we have observed prominent depolarizations and decrea
ses in input resistance in response to applications of gamma-aminobuty
ric acid (GABA) in most recorded mesencephalic trigeminal neurons. Tho
se cells failing to respond were located deeply within the slice, and
the low responsiveness was shown to be related to uptake of GABA in th
e slice. The responses were direct, since they remained during perfusi
on with a low calcium, high magnesium solution that blocks synaptic tr
ansmission. The responses were mimicked by the GABA(A) receptor agonis
t isoguvacine, and blocked by GABA(A) receptor antagonists. The GABA(B
) receptor agonist baclofen evoked no changes in membrane potential or
input resistance in neurons exhibiting depolarizations with GABA appl
ication. Tests of neuronal excitability during GABA applications indic
ated that the excitatory effects of the depolarization prevail over th
e depressant effects of the increase in membrane conductance. In situ
hybridization histochemistry indicated that the GABA(A) receptors in M
e5 cells are comprised of alpha(2), beta(2), and gamma(2) subunits. (C
) 1997 Elsevier Science B.V.