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DOI 10.1016/0006-8993(92)90082-k

Медицинская библиотека · Brain research · 1992

Functional neurolobectomy induced by controlled compression of the pituitary stalk.

Dohanics J, Hoffman G E, Smith M S, Verbalis J G

СтатьяПоддержка службы здравоохранения СШАПеревод пока не подготовлен

Аннотация

Degeneration of magnocellular nerve terminals in the neurohypophysis was induced by compressing the pituitary stalk of anesthetized rats for 30 s using a triangle-shaped wire. Immediately after stalk compression (SC), rats exhibited markedly increased water intake characteristic of diabetes insipidus, followed by a triphasic pattern of fluid intake. In SC rats, arginine vasopressin (AVP) and oxytocin (OT) contents of the neurointermediate lobe (NIL) of the pituitary gland were significantly reduced to approximately 2.5% and approximately 10% of sham-operated controls, respectively. In contrast, OT, but not AVP, content of the stalk-median eminence (SME) of SC rats was significantly increased. Histological examination of the pituitaries showed substantial degeneration of the neural lobe with very scarce AVP-neurophysin and OT-neurophysin immunoreactivity, while both the anterior and the intermediate lobes appeared to be intact. Plasma AVP and OT responses to infusion of hypertonic NaCl were significantly blunted in SC rats compared to sham-operated controls. However, two days after surgery the secretory patterns of LH in SC rats were similar to those in the controls. These results indicate that controlled compression of the pituitary stalk results in selective degeneration of the neural lobe without causing permanent ischemic damage to the anterior pituitary, and produces marked sustained functional deficits in pituitary AVP and OT secretion. Consequently, SC provides an alternative means to achieve selective neurolobectomy in rats.

Для цитирования: Dohanics J, Hoffman G E, Smith M S, Verbalis J G. Functional neurolobectomy induced by controlled compression of the pituitary stalk.. Brain research. 1992. DOI: 10.1016/0006-8993(92)90082-k.

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