Differential potencies of cocaine and its metabolites, cocaethylene and benzoylecgonine, in suppressing the functional expression of somatostatin and neuropeptide Y producing neurons in cultures of fetal cortical cells.
Differential potencies of cocaine and its metabolites, cocaethylene and benzoylecgonine, in suppressing the functional expression of somatostatin and neuropeptide Y producing neurons in cultures of fetal cortical cells.
复制标题
可卡因及其代谢物可卡乙烯和苯甲酰爱康宁在抑制胎儿皮质细胞培养物中生长抑素和产生神经肽 Y 的神经元的功能表达方面的不同功效。
DOI：
10.1016/s0006-2952(97)00202-5
复制
发表时间：
1997
影响因子：
5.8
通讯作者：
Barnea,A
中科院分区：
文献类型：
--
作者：
Aguila-Mansilla,N;Little,BB;Ho,RH;Barnea,A
Using aggregate cultures derived from 17-day-old fetal rat cortex, we addressed the question: Does cocaine alter the functional expression of neuropeptide Y (NPY) and somatostatin (SRIF) neurons and, if so, are cocaethylene (CE) and benzoylecgonine (BZE) as active as cocaine? NPY/SRIF production in response to brain-derived neurotrophic factor (BDNF) or phorbol-12-myristate-13-acetate (PMA) was used as a functional criterion. A 5-day exposure to cocaine did not affect basal or stimulated (BDNF or PMA) production of NPY but it markedly suppressed BDNF- or PMA-stimulated production of SRIF. Exposure to CE led to a drastic suppression of basal as well as stimulated (BDNF or PMA) production of both NPY and SRIF. These effects of cocaine and CE were concentration dependent (1–100 μM). BZE did not alter any of these functional parameters. Next, we evaluated the fate of cocaine, CE, and BZE in the culture medium. Cocaine was converted to BZE, whereas BZE was not converted to cocaine. CE was converted to cocaine and BZE, with substantial amounts of cocaine and CE remaining in the medium after 72 hr (≈ 20% each). In summary, cocaine, CE, and BZE exhibited differential potencies in suppressing the expression of cultured NPY and SRIF neurons: CE was more potent than cocaine and BZE was inactive. SRIF neurons were more susceptible than NPY neurons to the effects of cocaine. The higher potency of CE may be due to a property of the compound and/or to CE serving as a source for a slow, continuous formation of cocaine by the brain cells themselves.
登录
查看更多内容
脑源性神经营养因子对培养的大脑皮层神经元中神经肽表达的调节
影响因子：
4.7
作者：
H. Nawa;Y. Bessho;J. Carnahan;S. Nakanishi;K. Mizuno
通讯作者：
K. Mizuno
体外发育过程中中脑神经元原代培养物中[3H]多巴胺摄取位点和[3H]可卡因识别位点的表征
影响因子：
4.7
作者：
M. Grilli;A. Wright;I. Hanbauer
通讯作者：
I. Hanbauer
可卡因、去甲可卡因和可卡乙烯对大鼠脑中毒蕈碱受体刺激的磷酸肌醇代谢的抑制作用。
DOI：
10.1016/0165-3806(94)90057-4
发表时间：
1994
期刊：
Brain research. Developmental brain research
影响因子：
--
作者：
X. Tan;L. Costa
通讯作者：
L. Costa
致命病例中可卡因和苯甲酰爱康宁的脑浓度。
影响因子：
1.6
作者：
V. Spiehler;D. Reed
通讯作者：
D. Reed
急性和慢性可卡因给药对大鼠脑内生长抑素水平和结合的影响
影响因子：
2.9
作者：
M. N. Rodríguez;E. Arilla
通讯作者：
E. Arilla