HISTOCHEMICAL AND PHARMACOLOGICAL ANALYSIS OF NORADRENERGIC PROJECTIONS TO THE PARAVENTRICULAR HYPOTHALAMUS IN RELATION TO FEEDING STIMULATION
HISTOCHEMICAL AND PHARMACOLOGICAL ANALYSIS OF NORADRENERGIC PROJECTIONS TO THE PARAVENTRICULAR HYPOTHALAMUS IN RELATION TO FEEDING STIMULATION
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DOI：
10.1016/0006-8993(80)91037-9
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发表时间：
1980-01-01
期刊：
影响因子：
2.9
通讯作者：
BROWN, LL
中科院分区：
文献类型：
--
作者：
LEIBOWITZ, SF;BROWN, LL
采用中脑损毁、荧光组织化学和脑插管相结合的方法，分析去甲肾上腺素能投射到下丘脑室旁核(PVN)及其在刺激摄食行为中的作用。中央被盖束(CTT)的背侧成分穿过桥脑背侧，然后通过被盖内侧辐射(TR)投射到腹侧被盖，正好位于内侧丘系的背侧，它显然含有重要的去甲肾上腺素能轴突，支配PVN并介导去甲肾上腺素能刺激摄食行为。损毁被盖背侧电解或6-羟基多巴胺[6-羟基多巴胺]后，PVN内的儿茶酚胺曲张(最显著的是小细胞区内细小而中等大小的圆形精索静脉曲张)减少，PVN注射突触前药物三羟环丙胺和地地帕明引起的摄食反应显著减弱或丧失，以及注射去甲肾上腺素引起的相同反应增强。如果背侧CTT和内侧TR纤维只受到部分损伤，PVN的这些药理和神经化学变化就会减轻。如果病变立即落在这些纤维的背部而不损害它们，这些变化根本不会发生。腹侧被盖的特定病变，不仅没有破坏CTT和TR轴突的背侧，而是损害了CTT的腹侧成分，不仅没有破坏抗抑郁药物的作用，而且实际上增强了它们在PVN中的作用。切断背侧CTT和内侧TR纤维的旋转腹侧延伸的腹内侧损害与背侧损害在更背尾水平损害这一投射具有相同的行为后果。损毁其他儿茶酚胺投射对下丘脑室旁核刺激进食功能影响不大。
Midbrain lesions, fluorescence histochemistry and brain cannulation were used in combination to analyze noradrenergic projections to the paraventricular nucleus of the [rat] hypothalamus (PVN) and their function in stimulating feeding behavior. The dorsal component of the central tegmental tract (CTT), which ascends through the dorsal pons and then projects through the medial tegmental radiations (TR) into the ventral tegmentum just dorsal to the medial lemniscus, apparently contains the crucial noradrenergic axons which innervate the PVN and mediate noradrenergic stimulation of feeding behavior. Dorsal tegmental electrolytic or 6-OHDA [6-hydroxydopamine] lesions which damaged specifically these fibers invariably caused a reduction of catecholamine varicosities within the PVN (most notably, fine and moderate-size, rounded varicosites within the parvocellular area), a strong reduction or loss of the feeding response elicited by PVN injection of the presynaptically-acting drugs tranylcypromine and desipramine, and a potentiation of the same response produced by injected norepinephrine. These pharmacological and neurochemical changes in the PVN were reduced in magnitude if the dorsal CTT and medial TR fibers received only partial damage. These changes did not occur at all if the lesion fell immediately dorsal to these fibers without damaging them. Specific lesions in the ventral tegmentum, which failed to damage the dorsal CTT and TR axons but damaged the ventral component of the CTT, not only failed to disrupt the action of the antidepressant agents but actually potentiated their effectiveness in the PVN. Ventromedial lesions which severed the rostroventral extension of the dorsal CTT and medial TR fibers had the same behavioral consequences as the dorsal lesions which damaged this projection at a more dorsocaudal level. Damage to other catecholamine projections had little effect on PVN function in stimulating eating.