1 In the present study in vitro electrophysiology and receptor autorad
iography were used to determine whether rat vagal afferent neurones po
ssess dopamine D-2 receptors. 2 Dopamine (10-300 mu M) elicited a temp
erature- and concentration-dependent depolarization of the rat isolate
d nodose ganglion preparation. When applied to the tissue 15 min prior
to agonist, raclopride (10 mu M), clozapine (10 mu M) or a mixture of
raclopride and clozapine (10 mu M each) all produced a threefold para
llel shift to the right of the dopamine concentration-response curve.
In contrast, SCH 23390 (100 nM), phentolamine and propranolol (1 mu M
each) failed to antagonize the dopamine-mediated depolarization. 3 [I-
125]-NCQ 298 (0.5 nM), a D-2 selective radioligand, bound topographica
lly to sections of rat brainstem. Densitometric quantification of auto
radiograms revealed 93.8 +/- 0.5% specific binding of this salicylamid
e radioligand, as determined by raclopride (10 mu M, n = 10 animals).
Binding was highest in the nucleus tractus solitarius (NTS), particula
rly the medial and gelatinous subnuclei. In addition, specific binding
was also observed in the interpolar spinal trigeminal nucleus and the
inferior olive. 4 Unilateral nodose ganglionectomy caused a 36.6 +/-
3.0% reduction in specific binding in the denervated NTS compared to t
he contralateral NTS. Furthermore, the loss of binding was confined to
the dorsal aspect of the medial subnucleus of the NTS. Sham surgery h
ad no effect on the binding of [I-125]-NCQ 298 in rat brainstem. 5 The
present data provide evidence for the presence of functionally releva
nt dopamine D-2 receptors on both the soma and central terminals of ra
t vagal afferent neurones. In addition, the majority of D-2 receptors
in the rat NTS appear to be located postsynaptically with respect to v
agal terminals, and are presumably located either on ascending glossop
haryngeal terminals, descending terminals from higher brain regions or
on neuronal cell bodies within the NTS.