MohanKumar P S, MohanKumar S M, Quadri S K, Voogt J L
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, USA.
J Neuroendocrinol. 2001 Mar;13(3):261-9. doi: 10.1046/j.1365-2826.2001.00621.x.
The purpose of this study was to investigate the age-related changes in the responsiveness of tuberoinfundibular dopamine (TIDA) neurones to chronic hypoprolactinemia induced by treatment with bromocriptine, a dopamine receptor agonist. In one experiment, TIDA neuronal activity after acute hypoprolactinemia or exogenous prolactin was monitored by measuring tyrosine hydroxylase (TH) activity in the stalk median eminence of middle-aged cycling female rats (10-12 months), old constant oestrous rats (18-20 months) and old pseudopregnant rats (22-24 months). In another experiment, middle-aged cycling (10-12 months) rats were treated with bromocriptine for 6 or 12 months. TH activity was measured in the stalk median eminence, TH mRNA levels were measured in the arcuate nucleus and dopamine concentrations were measured in the arcuate nucleus and median eminence. Responsiveness of TIDA neurones to exogenous prolactin and to the withdrawal of bromocriptine in these rats was also tested. While the TIDA neurones in all three age groups responded to acute hypoprolactinemia by showing a reduction in TH activity, older rats failed to respond to exogenous prolactin administration. In contrast, chronic hypoprolactinemia for 12 months enabled the rats to retain TIDA neuronal responsiveness to exogenous prolactin. It also decreased TIDA neuronal function as measured by dopamine concentrations in the median eminence, TH activity in the stalk median eminence and TH mRNA in the arcuate nucleus of ageing rats. The restoration of the responsiveness of these neurones to prolactin stimulation in older rats demonstrates for the first time that hypoprolactinemia produced by chronic bromocriptine treatment indeed provides a neuroprotective effect on TIDA neurones. These results indicate that maintaining a low level of neuronal activity by lowering prolactin levels may be a contributing factor in retaining the plasticity of TIDA neurones.
本研究的目的是调查结节漏斗多巴胺（TIDA）神经元对由多巴胺受体激动剂溴隐亭治疗诱导的慢性低催乳素血症反应性的年龄相关变化。在一项实验中，通过测量中年发情周期雌性大鼠（10 - 12个月）、老年持续发情大鼠（18 - 20个月）和老年假孕大鼠（22 - 24个月）的正中隆起柄部的酪氨酸羟化酶（TH）活性，监测急性低催乳素血症或外源性催乳素后的TIDA神经元活动。在另一项实验中，对中年发情周期（10 - 12个月）的大鼠用溴隐亭治疗6或12个月。测量正中隆起柄部的TH活性，测量弓状核中的TH mRNA水平，并测量弓状核和正中隆起中的多巴胺浓度。还测试了这些大鼠中TIDA神经元对外源性催乳素和溴隐亭撤药的反应性。虽然所有三个年龄组的TIDA神经元都通过显示TH活性降低来对急性低催乳素血症作出反应，但老年大鼠对外源性催乳素给药无反应。相反，12个月的慢性低催乳素血症使大鼠能够保留TIDA神经元对外源性催乳素的反应性。它还降低了TIDA神经元功能，这通过老年大鼠正中隆起中的多巴胺浓度、正中隆起柄部的TH活性和弓状核中的TH mRNA来衡量。老年大鼠中这些神经元对催乳素刺激反应性的恢复首次证明，慢性溴隐亭治疗产生的低催乳素血症确实对TIDA神经元具有神经保护作用。这些结果表明，通过降低催乳素水平来维持低水平的神经元活动可能是保留TIDA神经元可塑性的一个促成因素。
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