Effects of arginine vasopressin on firing activity and thermosensitivity of rat PO/AH area neurons

Abstract

It is well known that the preoptic–anterior hypothalamus (PO/AH), containing temperature-sensitive and -insensitive neurons plays an important role in precise thermoregulatory responses. Previous in vivo studies suggest that the arginine vasopressin (AVP) is an important endogenous mediator in thermoregulation, since AVP and V1a vasopressin receptor antagonist can induce hypothermia and hyperthermia, respectively. In the present study, intracellular electrophysiological activity was recorded from temperature-sensitive and -insensitive neurons in rat PO/AH tissue slices, using a whole-cell patch clamp. By monitoring neuron’s changes of firing activity and thermosensitivity when perfused with AVP or V1a vasopressin receptor antagonist, we found that AVP increased the spontaneous firing rate in 65% of warm-sensitive neurons and decreased it in nearly 50% of cold-sensitive and temperature-insensitive neurons. These changes are due to the AVP enhancing the rise rate of depolarization prepotential in warm-sensitive neurons and reducing it in the other neurons. Moreover, AVP increased the thermosensitivity of warm-sensitive neurons while it decreased thermosensitivity of cold-sensitive and temperature-insensitive neurons. V1a vasopressin receptor participated in these responses. Since excited warm-sensitive neurons or inhibited cold-sensitive and temperature-insensitive neurons promote heat loss or suppress heat production and retention. These results that AVP excites warm-sensitive neurons and inhibits cold-sensitive and temperature-insensitive neurons suggest a probable mechanism of AVP-induced hypothermia.