Brog J S, Zahm D S
Department of Anatomy and Neurobiology, St Louis University School of Medicine, MO 63104, USA.
Neuroscience. 1995 Mar;65(1):71-86. doi: 10.1016/0306-4522(94)00460-m.
It was previously reported that following striatal dopamine depletion or pharmacological blockade of dopamine neurotransmission, neurotensin immunoreactivity is elicited in at least two distinct subpopulations of striatal neurons (Neuroscience Vol. 46, pp. 335-350, 1992). Recently it was shown that Fos immunoreactivity, interpreted as an indicator of enhanced neuronal activity, is appreciably co-localized in only one of the subpopulations of neurotensin-immunoreactive neurons observed following blockade of the dopamine D2 receptor (Neuroscience Vol. 57, pp. 649-660, 1993). In the present study, similar methods were used to determine the degree of co-localization of Fos and neurotensin immunoreactivity in striatal neurons in response to the dopamine-depleting effects of 6-hydroxydopamine lesions and reserpine administration. It was observed that following these treatments, a subpopulation of neurons at the small end of the medium size range exhibited light neurotensin immunoreactivity and frequent co-localization with Fos immunoreactivity. This population was predominant after reserpine administration in the dorsolateral quadrant of the striatum. Another subpopulation comprised larger neurons that exhibited intense neurotensin immunoreactivity in perikarya and proximal processes that was rarely co-localized with Fos immunoreactivity. This type of neuron was observed following all the drug treatments but was present almost to the exclusion of the smaller type of cells three days following ventral midbrain 6-hydroxydopamine lesions, being mainly located in the dorsomedial and ventrolateral portions of the striatum. The present data support the results of the preceding studies in being consistent with the existence of two subpopulations of striatal neurons that accumulate neurotensin following dopamine depletion. The possibility is considered that one subpopulation accumulates neurotensin in response to co-ordinate increases in neuronal activity and neurotensin synthesis, and the other as a result of decreased release.
先前有报道称，在纹状体多巴胺耗竭或多巴胺神经传递的药理学阻断之后，至少在纹状体神经元的两个不同亚群中会引发神经降压素免疫反应性（《神经科学》第46卷，第335 - 350页，1992年）。最近有研究表明，被解释为神经元活动增强指标的Fos免疫反应性，仅在多巴胺D2受体阻断后观察到的神经降压素免疫反应性神经元亚群之一中明显共定位（《神经科学》第57卷，第649 - 660页，1993年）。在本研究中，使用了类似的方法来确定纹状体神经元中Fos和神经降压素免疫反应性的共定位程度，以应对6 - 羟基多巴胺损伤和利血平给药所产生的多巴胺耗竭效应。观察到在这些处理之后，中等大小范围较小一端的神经元亚群表现出轻度的神经降压素免疫反应性，并频繁与Fos免疫反应性共定位。在利血平给药后，该群体在纹状体背外侧象限中占主导。另一个亚群由较大的神经元组成，这些神经元在胞体和近端突起中表现出强烈的神经降压素免疫反应性，很少与Fos免疫反应性共定位。在所有药物处理后都观察到了这种类型的神经元，但在腹侧中脑6 - 羟基多巴胺损伤三天后，几乎完全是这种较大类型的细胞，主要位于纹状体的背内侧和腹外侧部分。本研究数据支持了先前研究的结果，即与多巴胺耗竭后积累神经降压素的纹状体神经元两个亚群的存在相一致。研究考虑了一种可能性，即一个亚群因神经元活动和神经降压素合成的协同增加而积累神经降压素，另一个亚群则是由于释放减少所致。
