Acute and chronic restraint stress: effects on [I]-galanin binding in normotensive and hypertensive rat brain

The neuropeptide galanin (GAL) has been implicated in the neural response to a number of stressors including restraint; however, the effect of restraint stress on GAL receptor density in the central nervous system (CNS) has not been investigated. Normotensive (Wistar-Kyoto; WKY) and hypertensive (spontaneously hypertensive; SHR) rats were subjected to a daily 60-min restraint stress paradigm for 0 (control), 1, 3, 5 or 10 consecutive days, and the density of [¹²⁵I]-GAL binding sites following exposure to restraint was compared between strains using quantitative autoradiography. Significant differences in basal (no stress) levels of GAL receptor density between WKY and SHR were detected in regions such as the central nucleus of the amygdala (Ce) and ventromedial hypothalamus (VMH) (P<0.05). In WKY, restraint stress (1 day) induced significant decreases in GAL receptor density in forebrain regions such as the Ce (−41%) and medial nucleus of the amygdala (−41%) (P<0.05). Chronic restraint (10 days) did not induce significant decreases in these nuclei in WKY, indicating that forebrain neurons containing GAL receptors in WKY possessed a functional ability to adapt to repeated restraint. In addition, restraint stress induced significant decreases in GAL receptor density in SHR in regions such as the lateral parabrachial nucleus (−43%; 5 days of restraint) and hypoglossal nucleus (−18% for entire restraint period) (P<0.05). In conclusion, restraint stress resulted in region- and strain-specific alterations in GAL receptor density, some of which may contribute to the altered stress response previously observed in hypertensive rats. The results clearly support the hypothesis that neuropeptides such as GAL are an integral component of the neural response to psychological stress, although the functional significance of the changes in GAL receptor density described in this study awaits elucidation.