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The Journal of Neurophysiology Vol. 83 No. 2 February 2000, pp. 705-711
Copyright ©2000 by the American Physiological Society
1Netherlands Institute for Brain Research, 1105 AZ Amsterdam, The Netherlands; 2Neurosciences, Loeb Research Institute, Ottawa Civic Hospital and University of Ottawa, Ottawa, Ontario K1Y 4E9, Canada; and 3Department of Anatomy and Embryology, Academic Medical Centre, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
Hermes, M.L.H.J.,
J. M. Ruijter,
A. Klop,
R. M. Buijs, and
L. P. Renaud.
Vasopressin Increases GABAergic Inhibition of Rat Hypothalamic
Paraventricular Nucleus Neurons In Vitro. J. Neurophysiol. 83: 705-711, 2000. This investigation
used an in vitro hypothalamic brain slice preparation and whole cell
and perforated-patch recording to examine the response of magnocellular
neurons in hypothalamic paraventricular nucleus (PVN) to bath
applications of vasopressin (VP; 100-500 nM). In 22/38 cells,
responses were characterized by an increase in the frequency of
bicuculline-sensitive inhibitory postsynaptic potentials or currents
with no detectable influence on excitatory postsynaptic events.
Perforated-patch recordings confirmed that VP did not have an effect on
intrinsic membrane properties of magnocellular PVN neurons
(n = 17). Analysis of intrinsic membrane properties
obtained with perforated-patch recording (n = 23)
demonstrated that all of nine VP-sensitive neurons showed a rebound
depolarization after transient membrane hyperpolarization from rest. By
contrast, 12/14 nonresponding neurons displayed a delayed return to
resting membrane potentials. Recordings of reversed inhibitory
postsynaptic currents with chloride-loaded electrodes showed that
responses to VP persisted in media containing glutamate receptor
antagonists but were abolished in the presence of tetrodotoxin. In
addition, responses were mimicked by vasotocin [Phe2,
Orn8], a selective V1a receptor agonist, and
blocked by
[
-Mercapto-,-cyclopentamethylenepropionyl1,O-Me-Tyr2,
Arg8]-VP (Manning compound), a V1a/OT receptor
antagonist. Neither [deamino-Cys1,Val4,D-Arg8]-VP,
a selective V2 receptor agonist, nor oxytocin were
effective. Collectively, the results imply that VP acts at
V1a receptors to excite GABAergic neurons that are
presynaptic to a population of magnocellular PVN neurons the identity
of which features a unique rebound depolarization. Endogenous sources
of VP may be VP-synthesizing neurons in suprachiasmatic nucleus, known
to project toward the perinuclear regions of PVN, and/or the
magnocellular neurons within PVN.
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