Millan M H, Millan M J, Herz A
Neurosci Lett. 1982 Apr 26;29(3):269-73. doi: 10.1016/0304-3940(82)90328-7.
The present study examines the role of brain networks of noradrenaline (NA) in the control of pituitary secretion of beta-endorphin into systemic plasma. The blocker of NA synthesis, FLA-63, elicited a pronounced elevation in levels of beta-endorphin immunoreactivity (beta-EI) in systemic plasma and depleted the anterior but not the neurointermediate lobe content of beta-EI. This finding suggests the existence of a noradrenergic mechanism tonically inhibiting the secretion of adenohypophyseal pools of beta-EI into plasma. Selective destruction of the ventral noradrenergic bundle diminished the NA content of the hypothalamus but not the cortex, and produced an increase in plasma levels of beta-EI. Lesions of the locus coeruleus, the primary origin of the dorsal noradrenergic bundle, in contrast, decreased NA levels in the cortex but not the hypothalamus and failed to modify beta-EI levels in plasma. the ventral bundle may, thus, via a hypothalamic site of action, be the noradrenergic pathway inhibiting the secretion of beta-EI into the circulation.
本研究探讨去甲肾上腺素（NA）脑网络在控制垂体向全身血浆分泌β-内啡肽中的作用。NA合成阻滞剂FLA - 63引起全身血浆中β-内啡肽免疫反应性（β-EI）水平显著升高，并使垂体前叶β-EI含量减少，但神经中间叶β-EI含量未减少。这一发现表明存在一种去甲肾上腺素能机制，该机制持续性抑制腺垂体池中β-EI向血浆的分泌。选择性破坏腹侧去甲肾上腺素能束可降低下丘脑而非皮质的NA含量，并使血浆中β-EI水平升高。相反，蓝斑（背侧去甲肾上腺素能束的主要起源）损伤可降低皮质而非下丘脑的NA水平，且未能改变血浆中β-EI水平。因此，腹侧束可能通过下丘脑作用位点，成为抑制β-EI分泌入循环的去甲肾上腺素能途径。
