The Journal of Neurophysiology Vol. 86 No. 3 September 2001, pp. 1202-1210
Copyright ©2001 by the American Physiological Society

Electrophysiological Evidence for Vasopressin V₁ Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

 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.