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The Journal of Neurophysiology Vol. 86 No. 3 September 2001, pp. 1202-1210
Copyright ©2001 by the American Physiological Society
1Neurosciences, Ottawa Health Research Institute, University of Ottawa, Ottawa, Ontario K1Y 4E9, Canada; and 2National Institute on Drug Abuse, Intramural Research Program, Baltimore, Maryland 21224
Oz, Murat,
Miloslav Kolaj, and
Leo P. Renaud.
Electrophysiological Evidence for Vasopressin V1
Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn
Neurons. J. Neurophysiol. 86: 1202-1210, 2001. Prominent arginine-vasopressin (AVP) binding and AVP
V1 type receptors are expressed early in the
developing rat spinal cord. We sought to characterize their influence
on neural excitability by using patch-clamp techniques to record
AVP-induced responses from a population of motoneurons and interneurons
in neonatal (5-18 days) rat spinal cord slices. Data were obtained
from 58 thoracolumbar
(T7-L5) motoneurons and
166 local interneurons. A majority (>90%) of neurons responded to
bath applied AVP (10 nM to 3 µM) and (Phe2,
Orn8)-vasotocin, a V1
receptor agonist, but not V2 or oxytocin receptor agonists. In voltage-clamp, postsynaptic responses in motoneurons were
characterized by slowly rising, prolonged (7-10 min) and tetrodotoxin-resistant inward currents associated with a 25% reduction in a membrane potassium conductance that reversed near 
100 mV. In
interneurons, net AVP-induced inward currents displayed three patterns:
decreasing membrane conductance with reversal near 100 mV, i.e.,
similar to that in motoneurons (24 cells); increasing conductance with
reversal near 40 mV (21 cells); small reduction in conductance with
no reversal within the current range tested (41 cells). A presynaptic
component recorded in most neurons was evident as an increase in the
frequency but not amplitude (in motoneurons) of inhibitory and
excitatory postsynaptic currents (IPSCs and EPSCs), in large part
due to AVP-induced firing in inhibitory (mainly glycinergic) and
excitatory (glutamatergic) neurons synapsing on the recorded cells. An
increase in frequency but not amplitude of miniature IPSCs and EPSCs
also indicated an AVP enhancement of neurotransmitter release from axon
terminals of inhibitory and excitatory interneurons. These observations provide support for a broad presynaptic and postsynaptic distribution of AVP V1 type receptors and indicate that their
activation can enhance the excitability of a majority of neurons in
neonatal ventral spinal cord.
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