Menani J V, Beltz T G, Johnson A K
Department of Psychology, University of Iowa, Iowa City 52242-1407, USA.
Brain Res. 1995 Oct 16;695(2):250-2. doi: 10.1016/0006-8993(95)00872-n.
This study investigated the effects of bilateral injections of the local anesthetic, lidocaine, into the lateral parabrachial nucleus (LPBN) on the dipsogenic and pressor responses induced by intracerebroventricular (i.c.v.) injection of angiotensin II (ANG II). Centrally injected ANG II (50 ng/1 microliters) induced water intake (10.2 +/- 0.8 ml/h) and pressor responses (22 +/- 1 mmHg). Prior bilateral injection of 10% lidocaine (200 nl) into the LPBN increased the water intake (14.2 +/- 1.4 ml/h), but did not change the pressor response (17 +/- 1 mmHg) to i.c.v. ANG II. Lidocaine alone injected into the LPBN also induced a pressor response (23 +/- 3 mmHg). These results showing that bilateral LPBN injection of lidocaine increase water intake induced by i.c.v. ANG II are consistent with electrolytic and neurotoxic lesion studies and suggest that the LPBN is associated with inhibitory mechanisms controlling water intake induced by ANG II. These results also provide evidence that it is feasible to reversibly anesthetize this brain area to facilitate fluid-related ingestive behavior.
本研究调查了向外侧臂旁核（LPBN）双侧注射局部麻醉剂利多卡因，对脑室内（i.c.v.）注射血管紧张素II（ANG II）所诱导的饮水和升压反应的影响。脑室内注射ANG II（50 ng/1微升）可诱导饮水（10.2±0.8毫升/小时）和升压反应（22±1毫米汞柱）。事先向LPBN双侧注射10%利多卡因（200纳升）可增加饮水（14.2±1.4毫升/小时），但对脑室内注射ANG II的升压反应（17±1毫米汞柱）无影响。单独向LPBN注射利多卡因也可诱导升压反应（23±3毫米汞柱）。这些结果表明，向LPBN双侧注射利多卡因可增加脑室内注射ANG II所诱导的饮水，这与电解和神经毒性损伤研究结果一致，并提示LPBN与控制ANG II诱导饮水的抑制机制有关。这些结果还提供了证据，表明可逆性麻醉该脑区以促进与液体相关的摄食行为是可行的。
