Immunohistochemical localization of the beta 2 and beta 3 subunits of the GABAA receptor in the basolateral amygdala of the rat and monkey.
Immunohistochemical localization of the beta 2 and beta 3 subunits of the GABAA receptor in the basolateral amygdala of the rat and monkey.
复制标题
大鼠和猴子基底外侧杏仁核中 GABAA 受体 β 2 和 β 3 亚基的免疫组织化学定位。
DOI：
10.1016/0306-4522(96)00269-2
复制
发表时间：
1996
期刊：
影响因子：
3.3
通讯作者：
Mascagni,F
中科院分区：
文献类型：
--
作者：
McDonald,AJ;Mascagni,F
The basolateral amygdala has a strong intrinsic inhibitory system mediated by GABAAreceptors and is the main site of the anxiolytic actions of benzodiazepines. In an effort to identify the anatomical susbstrates for these transmitter and drug actions, immunohistochemical techniques were used to analyse the neuronal localization of the β2 and β3 receptor subunits of the GABAA–benzodiazepine receptor complex in the rat and monkey basolateral amygdala. The overall pattern of GABAA–benzodiazepine receptor immunoreactivity was very similar in both species. The density of the immunoreactivity in the neuropil varied in different nuclei of the basolateral amygdaloid complex. In both species the neuropil of the lateral nucleus exhibited the most robust staining. Immunoreactivity was also seen in neuronal perikarya and dendrites where it was localized to the cytoplasm and/or surface membrane. The cell type with the strongest immunoreactivity was a subpopulation of small non-pyramidal neurons that had numerous thin dendrites. Other larger non-pyramidal neurons were also stained. Pyramidal neurons in the rat and monkey basolateral amygdala exhibited light to moderate perikaryal staining that varied in different nuclei. The results of this study indicate that the pattern of GABAA–benzodiazepine receptor immunoreactivity in the neuropil of the rat and monkey basolateral amygdala closely resembled the distribution of benzodiazepine receptors localized in previous radioligand autoradiographic studies. The finding of intense immunoreactivity in subpopulations of non-pyramidal neurons suggests the existence of disinhibitory mechanisms which may be important for the activation of basolateral amygdaloid projection neurons.
