The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 51-56
Copyright ©2000 by the American Physiological Society
Sexually Dimorphic Regulation of NK-1 Receptor-Mediated
Electrophysiological Responses in Vagal Primary Afferent Neurons
Eun Joo
Oh,1
Loren P.
Thompson,2 and
Daniel
Weinreich1
1Department of Pharmacology and Experimental
Therapeutics and 2Department of Obstetrics,
Gynecology, and Reproductive Science, University of Maryland School of
Medicine, Baltimore, Maryland 21201
Oh, Eun Joo,
Loren P. Thompson, and
Daniel Weinreich.
Sexually Dimorphic Regulation of NK-1 Receptor-Mediated
Electrophysiological Responses in Vagal Primary Afferent Neurons. J. Neurophysiol. 84: 51-56, 2000. Neurons can display sexual dimorphism in receptor expression,
neurotransmitter release, and synaptic plasticity. We have detected sexual dimorphism in functional tachykinin receptors in vagal afferents
(nodose ganglion neurons, NGNs) by studying the effects of hormonal
variation on the depolarizing actions of substance P (SP) in female
guinea pig NGNs. Using conventional "sharp" microelectrode recording plus measurement of serum 17
-estradiol values, we examined SP responses in NGNs isolated from 1) ovariectomized females
(OVX), 2) OVX females treated with 17-estradiol (OVX + E2), 3) pregnant females, and 4) males. Depending
on various manipulations, 19-41% female NGNs were depolarized
(16 ± 1.1 mV, mean ± SE) by 100 nM SP acting
through NK-1 receptors. The NGNs of OVX + E2 females (41%, 15/37;
17 ± 2.1 mV) and pregnant females (41%, 32/79; 16 ± 1.7 mV) were more likely to respond to SP than those of control males
(P < 0.001). The percentage of SP-sensitive NGNs from
OVX females (19%, 21/109; 15 ± 1.9 mV) was not significantly
different (P = 0.361) from that of control males (13%,
11/83; 13 ± 2.0 mV). The serum 17-estradiol values for OVX + E2, pregnant, and OVX females were 23.9 ± 3.3 pg/ml
(n = 8), 16.0 ± 2.4 pg/ml (n = 4), and 3.9 ± 0.3 pg/ml (n = 8), respectively.
These data indicate that there is a gender difference in NK-1 receptor
expression in guinea pig nodose neurons, and they suggest that estrogen
may modulate SP responsiveness in these neurons.
