Reversal of the delta-9-tetrahydrocannabinol inhibitory effect on prolactin secretion by rostral deafferentation of the medial basal hypothalamus.
Reversal of the delta-9-tetrahydrocannabinol inhibitory effect on prolactin secretion by rostral deafferentation of the medial basal hypothalamus.
复制标题
通过内侧基底下丘脑的喙部传入神经阻滞逆转 delta-9-四氢大麻酚对催乳素分泌的抑制作用。
DOI：
10.1159/000124646
复制
发表时间：
1986
影响因子：
4.1
通讯作者：
Tyrey,L
中科院分区：
文献类型：
--
作者：
Tyrey,L
在交叉后额叶横断下丘脑吻侧的雌性大鼠中，研究了内侧基底下丘脑（MBH）吻侧传入阻滞对δ-9-四氢大麻酚（THC）引起的血清催乳素（PRL）浓度变化的影响。在其他动物的同一平面上切割下丘脑背侧，以控制外科手术或背侧脑损伤的可能影响。所有动物在立体定位手术后28-35天进行卵巢切除术，以消除组间卵巢功能差异的潜在混杂效应。将未损伤的大鼠卵巢切除以提供THC抑制活性的阳性对照组。卵巢切除术后至少4周，在110分钟实验期的中点用THC（0.5或1.0 mg/kg体重）或载体静脉内处理动物，在此期间通过留置的心房插管以10分钟间隔获得血液样品。血清催乳素浓度测定放射免疫法和切割位置确认组织学。当给予卵巢切除的动物而没有脑损伤时，THC在30分钟内从平均治疗水平抑制血清PRL浓度（p < 0.05），并且PRL水平在治疗后采样期的剩余时间内保持抑制。单独使用溶剂处理无效。交叉后平面切割未横切下丘脑吻侧的动物同样显示出对THC给药的PRL抑制（p < 0.05）。相反，对具有完全至脑底部的视交叉后切口的动物施用THC产生迅速的PRL升高，其在治疗后10分钟达到峰值（p < 0.05），然后下降至但不显著低于治疗前的平均PRL水平。用1 mg THC/kg体重处理后的PRL升高（5倍）大于用0.5 mg/kg体重处理后的PRL升高（p < 0.01）。仅用溶剂处理不会增加血清PRL。这些结果表明，将视交叉上区与MBH分离的吻侧下丘脑的横切导致THC对血清PRL浓度的急性作用的明显逆转，因为通常在THC给药后对未损伤大鼠的持续PRL抑制被转换为突然的，尽管是短暂的PRL升高，而没有随后抑制低于预处理水平的证据。虽然THC诱导的PRL升高的机制仍然未知，但在MBH吻侧传入阻滞的动物中没有PRL抑制表明THC不会通过直接促进正中隆起神经末梢释放PRL抑制因子来抑制PRL分泌。
The effect of rostral deafferentation of the medial basal hypothalamus (MBH) on delta-9-tetrahydrocannabinol (THC)-induced changes in serum prolactin (PRL) concentrations was investigated in female rats having retrochias-matic frontal cuts that transected the rostral hypothalamus. Cuts dorsal to the hypothalamus were produced in the same plane in other animals in order to control for possible effects of the surgical procedure or dorsal brain damage. All animals were ovariectomized 28–35 days after stereotaxic surgery to obviate potential confounding effects of differences in ovarian function between groups. Unlesioned rats were ovariectomized to provide a positive control group for THC inhibitory activity. At least 4 weeks after ovariectomy, animals were treated intravenously with THC (0.5 or 1.0 mg/kg body weight) or vehicle at the midpoint of a 110-min experimental period during which blood samples were obtained at 10-min intervals via indwelling atrial cannulae. Serum PRL concentrations were determined by radioimmunoassay and cut locations were confirmed histologically. When administered to ovariectomized animals without brain lesions, THC suppressed serum PRL concentrations from the average treatment level within 30 min (p < 0.05), and PRL levels remained suppressed for the remainder of the posttreatment sampling period. Treatment with the vehicle alone was without effect. Animals with retrochiasmatic plane cuts that did not transect the rostral hypothalamus similarly displayed PRL suppression in response to THC administration (p < 0.05). In contrast, THC administration to animals having retrochiasmatic cuts complete to the base of the brain produced a prompt PRL rise which peaked 10 min after treatment (p < 0.05) and then declined to, but not significantly below, the average pretreatment PRL level. The PRL rise (5-fold) following treatment with 1 mg THC/kg body weight was greater than that which followed treatment with 0.5 mg/kg body weight (p < 0.01). Serum PRL was not increased by treatment with the vehicle alone. These results indicate that transections of the rostral hypothalamus which separated the suprachiasmatic region from the MBH resulted in an apparent reversal of the acute effect of THC on serum PRL concentrations in that the sustained PRL inhibition that typically followed THC administration to unlesioned rats was converted to an abrupt, albeit brief PRL rise without evidence of subsequent suppression below pretreatment levels. While the mechanism of the THC-induced PRL rise remains unknown, the absence of PRL suppression in animals with rostral deafferentation of the MBH suggests that THC does not inhibit PRL secretion by directly promoting the release of PRL-inhibiting factor from median eminence nerve terminals.