Elevated substance P (NK-1) receptor immunoreactivity in the cerebellum of seizure prone gerbil

In the present study, we performed a comparative analysis of the distribution of substance P (SP) receptor (NK-1) immunoreactivity in order to determine the characteristics of the SP system in the cerebelli of rat and gerbils. In the rat cerebellar cortex, only a few Purkinje cells exhibited weak NK...

Full description

Saved in:
Bibliographic Details
Published in:Neuropeptides (Edinburgh) 2005-02, Vol.39 (1), p.9-14
Main Authors: Kim, Duk-Soo, Yoo, Ki-Yeon, Hwang, In-Koo, Jung, Ju-Young, Won, Moo Ho, Seo, Je Hoon, Kang, Tae-Cheon
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In the present study, we performed a comparative analysis of the distribution of substance P (SP) receptor (NK-1) immunoreactivity in order to determine the characteristics of the SP system in the cerebelli of rat and gerbils. In the rat cerebellar cortex, only a few Purkinje cells exhibited weak NK-1 receptor immunoreactivity. Similar to the case of rat, NK-1 receptor immunoreactivity in the cerebellar cortex of seizure resistant (SR) gerbils was rarely detected. In contrast, in the cerebellar cortex of seizure sensitive (SS) gerbils, dendrites and cell bodies of Purkinje cell showed strong NK-1 receptor immunoreactivity. Similar to the cerebellar cortex, little NK-1 receptor immunoreactivity in deep cerebellar nuclei was observed in the rat. In SR gerbils, however, deep cerebellar nuclei showed weak NK-1 receptor immunoreactivity. NK-1 receptor immunoreactivity in the deep cerebellar nuclei of SS gerbils was markedly increased, as compared with SR gerbils. Based on the present data, we suggest that the SP system of cerebellar circuit in gerbil are different from rat, and over-expression of NK-1 receptor immunoreactivity in Purkinje cells of SS gerbils may be relevant to Purkinje cell loss induced by seizure activity.
ISSN:0143-4179
1532-2785
DOI:10.1016/j.npep.2004.09.009