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 β-endorphin immunoreactivity (β-EI) and both basal and poststress circulating levels of β-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 β-EI in both sham-operated and lesioned rats. These data indicate that stress mobilizes β-EI from the pituitary into plasma and that the VB may inhibit the tonic and stress-elicited secretion of β-EI into the circulation. In lesioned rats, a transient depression in basal levels of β-EI in the septum and in those of met-enkephalin immunoreactivity (M-EI) in periventricular midbrain tissue was seen. Stress selectively depleted the β-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 β-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 β-EI elicited by stress and suggest the existence of an interaction of the VB with certain brain pools of β-EI and M-EI both tonically and under stress.