Chihara K, Kato Y, Ogo S, Imura H
Neuroendocrinology. 1975;18(2):192-203. doi: 10.1159/000122398.
The effect of pretreatment with alpha-methyl-p-tyrosine (alpha-MT) on the basal levels of plasma growth hormone (GH) and the responses to chlorpromazine (CPZ) were investigated in urethane-anesthetized rats with either complete hypothalamic deafferentation (c.d.), hypothalamic ablation (H.A.) or sham operation (Sham). Basal GH levels were high in C.D. rats, intermediate in H.A. rats, and low in Sham rats without any pretreatment. Pretreatment with alpha-MT caused a significant increase in basal GH levels in both C.D. and Sham rats, but not in H.A. rats. GH release following the intravenous injection of CPZ, which was observed in C.D. and Sham rats without alpha-MT pretreatment, was blunted by treatment with alpha-MT. In H.A. rats CPZ failed to stimulate the secretion of GH regardless of alpha-MT pretreatment. Neither the injection of L-DOPA nor DL-DOPS affected basal GH levels in non-alpha-MT pretreated C.D. rats. However, plasma GH levels significantly decreased following the injection of L-DOPA, but not DL-DOPS, in C.D. rats pretreated with alpha-MT. These findings suggest that the injection of CPZ causes an enhancement of GH release by inhibiting the catecholaminergic (dopaminergic) mechanism, which is active within the basal medial hypothalamus (BMH) and plays an inhibitory role in GH secretion. They also suggest that the extrahypothalamic inhibitory neural pathway, which is connected to the BMH and is interrupted by hypothalamic deafferentation, is not catecholaminergic.
在氨基甲酸乙酯麻醉的大鼠中,研究了用α-甲基-对酪氨酸(α-MT)预处理对血浆生长激素(GH)基础水平以及对氯丙嗪(CPZ)反应的影响,这些大鼠分别接受了完全下丘脑去传入(c.d.)、下丘脑切除(H.A.)或假手术(Sham)。在未进行任何预处理的情况下,c.d.大鼠的基础GH水平高,H.A.大鼠的基础GH水平中等,Sham大鼠的基础GH水平低。用α-MT预处理导致c.d.大鼠和Sham大鼠的基础GH水平显著升高,但H.A.大鼠未出现这种情况。静脉注射CPZ后观察到的GH释放,在未用α-MT预处理的c.d.大鼠和Sham大鼠中存在,但在用α-MT处理后受到抑制。在H.A.大鼠中,无论是否用α-MT预处理,CPZ都未能刺激GH分泌。在未用α-MT预处理的c.d.大鼠中,注射左旋多巴(L-DOPA)和DL-DOPS均未影响基础GH水平。然而,在用α-MT预处理的c.d.大鼠中,注射L-DOPA后血浆GH水平显著降低,但注射DL-DOPS后未降低。这些发现表明,注射CPZ通过抑制儿茶酚胺能(多巴胺能)机制导致GH释放增强,该机制在下丘脑基底内侧(BMH)内活跃,并且在GH分泌中起抑制作用。它们还表明,与BMH相连且因下丘脑去传入而中断的下丘脑外抑制性神经通路不是儿茶酚胺能的。