Origin of Insulin-Receptive Nerve Terminals in Rat Median Eminence*

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Abstract
The origin of insulin-receptive axon terminals in the rat median eminence was determined by combining surgical and chemical ablation techniques and the in vivo radioautographic approach, in which labeling of the median eminence with blood-borne [125I]insulin served as a quantifiable marker for the presence of receptive axonal elements. Whereas unilateral deafferentation of the median eminence from the ipsilateral brain produced as much as a 50% ipsilateral loss of insulinbinding sites, transection of axonal projections to median eminence from neurons located lateral to the ventromedial hypothalamic nucleus produced no detectable loss in insulin-binding capacity. Unilateral electrocoagulation of various regions of the medial basal hypothalamus indicated that insulin-receptive axon terminals arise primarily from neurons in and about the hypothalamic arcuate nucleus and from the posterior ventrolateral subdivision of the hypothalamic ventromedial nucleus. A primary site of origin from the arcuate nucleus was confirmed in rats treated neonatally with monosodium L-glutamate, which, in addition to a selective destruction of arcuate neurons, produced a profound reduction in the insulin-specific binding capacity of the median eminence. The results of this study indicate that insulin-binding axon terminals arise from a unique class of tuberoinfundibular neuron with hormone-receptive capacity. These neurons may function to mediate direct interaction of circulating insulin with central autonomical, behavioral, and neuroendocrine systems. (Endocrinology113: 1393, 1983)

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