The effects of acute phencyclidine treatment on neuropeptide Y (NPY) neuronal system in the rat arcuate nucleus studied by immunocytochemistry and in situ hybridization.
K Fukui, Y Kawashima, H Iizumi, H Utsumi, T Nakajima
Journal of neural transmission (Vienna, Austria : 1996) January 1, 1996 DOI: 10.1007/bf01276415 (opens in new tab) via PubMed
Summary
AI-generated from the abstractAcute treatment with the dissociative drug phencyclidine (PCP) increased the expression of neuropeptide Y (NPY) in the arcuate nucleus of the rat hypothalamus. NPY-immunoreactive cell bodies appeared in treated rats but not in controls, and NPY mRNA signals were higher in treated animals. These findings suggest that glutamatergic neurons may partly regulate the NPY system in this brain region.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Intervention | Phencyclidine (PCP) |
| Duration | Acute treatment |
| Key finding | Acute PCP treatment increased NPY-immunoreactive perikarya and NPY mRNA in the arcuate nucleus of the rat hypothalamus, suggesting glutamatergic control of the NPY system. |
Abstract
Phencyclidine (PCP) is a dissociative drug and an antagonist of N-methyl-D-aspartate (NMDA) receptor. The effects of PCP treatment on neuropeptide Y (NPY) system in the arcuate nucleus of the rat hypothalamus were examined both by immunocytochemistry and in situ hybridization. In acute PCP-treated rats, the NPY-immunoreactive perikarya appeared in the arcuate nucleus but no perikarya were detected in controls, without colchicine pretreatment. The signals of NPY mRNA by in situ hybridization increased in the PCP-treated rats than those of controls. These results suggest that the NPY system in the arcuate nucleus might be partly controlled by glutamatergic neurons.