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.

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