Wahlestedt C, Pich E M, Koob G F, Yee F, Heilig M
Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.
Science. 1993 Jan 22;259(5094):528-31. doi: 10.1126/science.8380941.
The function of neuropeptide Y, one of the most abundant peptide transmitters of the mammalian brain, remains unclear because of a lack of specific receptor antagonists. An antisense oligodeoxynucleotide corresponding to the NH2-terminus of the rat Y1 receptor was constructed and added to cultures of rat cortical neurons. This treatment resulted in a reduced density of Y1 (but not Y2) receptors and diminished the decrease in adenosine 3',5'-monophosphate (cAMP) usually seen after Y1 receptor activation. Repeated injection of the same oligodeoxynucleotide into the lateral cerebral ventricle of rats was followed by a similar reduction of cortical Y1 (but not Y2) receptors. Such antisense-treated animals displayed behavioral signs of anxiety. Thus, specific inhibition of neurotransmitter receptor expression can be accomplished in the living brain and demonstrates that altered central neuropeptide Y transmission produces an anxiety-like state.
神经肽Y是哺乳动物脑中含量最为丰富的肽类递质之一,由于缺乏特异性受体拮抗剂,其功能尚不清楚。构建了一种与大鼠Y1受体NH2末端对应的反义寡脱氧核苷酸,并将其添加到大鼠皮质神经元培养物中。这种处理导致Y1(而非Y2)受体密度降低,并减弱了通常在Y1受体激活后出现的3',5'-环磷酸腺苷(cAMP)的减少。将相同的寡脱氧核苷酸反复注射到大鼠侧脑室后,皮质Y1(而非Y2)受体也出现类似程度的减少。经这种反义处理的动物表现出焦虑的行为迹象。因此,在活体脑中可以实现对神经递质受体表达的特异性抑制,这表明中枢神经肽Y传递的改变会产生类似焦虑的状态。