生物谷報(bào)道：5月8日,，美國(guó)麻省理工大學(xué)研究人員在Neuron雜志上報(bào)告說(shuō)，大麻素受體拮抗劑類減肥藥物可能會(huì)危害兒童大腦發(fā)育,。
大麻素受體拮抗劑由于能通過(guò)阻斷大腦組織中大麻素受體來(lái)降低人的食欲,，因而被開發(fā)成一種新的減肥藥物，如法國(guó)塞諾菲－安萬(wàn)特制藥集團(tuán)研發(fā)的新型減肥藥利莫納班,。
通常說(shuō)的大麻藥物是從植物大麻中提取而來(lái),，大麻中含有的特殊活躍化合物統(tǒng)稱為大麻素。人體內(nèi)也會(huì)產(chǎn)生大麻素,，被稱為內(nèi)源性大麻素,。內(nèi)源性大麻素可以幫助調(diào)節(jié)人體食物攝入、能量?jī)?chǔ)存和消耗,。
研究人員通過(guò)老鼠實(shí)驗(yàn)發(fā)現(xiàn),，大麻素受體拮抗劑在降低人的食欲的同時(shí)，可能也會(huì)抑制兒童神經(jīng)系統(tǒng)發(fā)育時(shí)所必需的大腦適應(yīng)性重塑,。
大腦有根據(jù)環(huán)境調(diào)整神經(jīng)功能的能力,，這對(duì)于兒童和動(dòng)物幼崽的大腦發(fā)育特別重要。例如,，把新生老鼠一只眼睛蒙上,，即便是一天，大腦中大部分的神經(jīng)鍵也會(huì)轉(zhuǎn)向另一只未被蒙上的眼睛,，這就是幼鼠大腦的適應(yīng)性重塑功能,。然而，當(dāng)實(shí)驗(yàn)幼鼠被注射大麻素受體拮抗劑后,，研究人員發(fā)現(xiàn)神經(jīng)鍵無(wú)法轉(zhuǎn)向大腦的特定區(qū)域,，大腦適應(yīng)性重塑能力消失了。
生物谷推薦原始出處：
Neuron,，Vol 58, 340-345, 08 May 2008,，Cheng-Hang Liu, Mark F. Bear
Cannabinoid Receptor Blockade Reveals Parallel Plasticity Mechanisms in Different Layers of Mouse Visual Cortex
Cheng-Hang Liu,1 Arnold J. Heynen,1 Marshall G. Hussain Shuler,1 and Mark F. Bear1,
1 Howard Hughes Medical Institute, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
Corresponding author
Mark F. Bear
[email protected]
Summary
The ocular dominance (OD) shift that occurs in visual cortex after brief monocular deprivation (MD) is a classic model of experience-dependent cortical plasticity. It has been suggested that OD plasticity in layer 2/3 of visual cortex precedes and is necessary for plasticity in the thalamocortical input layer 4. Here, we show in mouse visual cortex that rapid OD plasticity occurs simultaneously in layers 2/3 and 4. Remarkably, pharmacological blockade of cannabinoid receptors completely prevents the OD shift in layer 2/3, leaving plasticity intact in layer 4. Thus, experience-dependent cortical modifications in layers 2/3 and 4 can occur in parallel, via distinct mechanisms. These findings simplify the mechanistic description of plasticity in layer 4, force a revision in the interpretation of previous studies in which laminar differences in OD plasticity mechanisms were unrecognized, and have important implications for the therapeutic use of cannabinoid receptor antagonists in humans.
