Electrophysiological evidence for vasopressin v1 receptors on motoneurons,
inhibitory and excitatory premotor and other ventral horn neurons in neonatal rat spinal
cord.
Oz , Murat, Miloslav Kolaj and Leo P Renaud .
1 Neurosciences, Ottawa Health Research Institute, University of Ottawa, Ottawa,
Ontario, Canada K1Y 4E9 and 2 National Institute on Drug Abuse, Intramural Research
Program, 5500 Nathan Shock Dr. Baltimore, MD, 21224
APStracts 8:0237J, 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 (T 7–L 5) motoneurons and 166
local interneurons. A majority (> 90%) of neurons responded to bath applied AVP (10
nM – 3 ?M) 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 minutes) and tetrodotoxin-resistant
inward currents associated with a 25% reduction in a membrane potassium conductance
that reversed near ?100mV. 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, 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.
Received 26 February 2001; accepted in final form 30 May 2001
APS Manuscript Number J153-1.
Article publication pending Am J Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 31 July 2001