所長招聘セミナー

Vasopressin (VP, the antidiuretic hormone) is released when plasma osmolality is elevated to increase renal water reabsorption. This hormone is also released in response to hyperthermia, to counter the impact of evaporative fluid loss during thermoregulatory cooling. Although the responsiveness of VP neurons to these stimuli depends in part on afferent signals originating from neurons in the preoptic area of the hypothalamus, recent studies in our laboratory have shown that these cells are also intrinsically sensitive to changes in osmolality and temperature. Both types of stimuli cause the activation of a cation permeable conductance in these cells. The inward current that results from this effect leads to membrane depolarization which contributes to the enhancement of action potential discharge under these conditions. These responses are absent in VP neurons obtained from Trpv1-knockout (Trpv1-KO) mice. These animals also show impaired VP release in response to hypertonicity and hyperthermia in vivo, indicating that expression of the Trpv1 gene is required for normal homeostatic VP release. Finally, the electrophysiological responses observed in VP neurons obtained from wild type mice are blocked by inhibitors of Trpv1, indicating that the transduction channel comprises at least one subunit encoded by the Trpv1 gene. These studies indicate that osmosensory transduction and thermosensory transduction can be performed by single neurons, and that both sensory mechanisms depend on a channel comprising Trpv1-like protein.