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 V 1a 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 V 1a 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. V 1a 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.