Lesions of the ventral noradrenergic (norepinephrinergic) bundle affect brain and pituitary pools of endorphins and the response of these to stress in rats.

Abstract

The present study examines the interrelationship of the ventral noradrenergic (norepinephrinergic) bundle (VB) with brain and hypophyseal pools of endorphins. As compared to sham-operated rats, selective destruction of the VB depressed hypothalamic levels of norepinephrine and abolished the fall in these levels evoked by acute foot shock stress. Stress elevated plasma levels of beta-endorphin immunoreactivity (beta-EI) and both basal and poststress circulating levels of beta-EI were significantly greater in lesioned as compared to sham animals on days 4 and 10, but not 28, postsurgery. At each time, stress depleted the anterior and neurointermediate lobe content of beta-EI in both sham-operated and lesioned rats. These data indicate that stress mobilizes beta-EI from the pituitary into plasma and that the VB may inhibit the tonic and stress-elicited secretion of beta-EI into the circulation. In lesioned rats, a transient depression in basal levels of beta-EI in the septum and in those of met-enkephalin immunoreactivity (M-EI) in periventricular midbrain tissue was seen. Stress selectively depleted the beta-EI as compared to the M-EI content of discrete brain regions, including the septum and this periventricular tissue, in sham-operated animals. Lesioned rats also responded to stress with a fall in beta-EI levels and, in contrast to sham rats, with a decrease in the M-EI levels of the hypothalamus and periventricular tissue. These data demonstrate that the VB does not mediate the activation of brain beta-EI elicited by stress and suggest the existence of an interaction of the VB with certain brain pools of beta-EI and M-EI both tonically and under stress.