Hemorrhage activates catecholaminergic neurons sensitive to GABA in the nucleus of the solitary tract with ascending projections to the subfornical organ in rats.

The activity of neurons in the region of the nucleus of the solitary tract (NTS) that were antidromically identified by electrical stimulation of the rat subfornical organ (SFO) was tested for a response to microiontophoretic application of gamma-aminobutyric acid (GABA), hemorrhage (10 ml/kg b.w.t.), or local administration of the chemical neurotoxin, 6-hydroxydopamine (6-OHDA), into the SFO stimulation site. Microiontophoretically (MIPh) applied GABA caused a decrease excitability in 22 out of 24 neurons tested, and the inhibition was blocked by MIPh-applied bicuculline, a GABAA antagonist, but not by phaclofen, a GABAB antagonist. Of these neurons that responded to GABA, 17 displayed an increase in neural firing in response to hemorrhage, while 5 were unresponsive. The occurrence of both antidromic spikes and post-stimulus inhibition of 9 out of 13 neurons tested was completely abolished by the injection of 6-OHDA into the SFO. These results suggest that neurons in the region of the NTS, which carry peripheral baroreceptor information to the SFO, receive GABAergic inhibitory inputs via a GABAA receptor mechanism, and imply that part of these neurons are catecholaminergic.