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Nicotine prevents disruption of the late phase LTP‐related molecular cascade in adult‐onset hypothyroidism
Author(s) -
Alzoubi K.H.,
Aleisa A.M.,
Alkadhi K.A.
Publication year - 2007
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20306
Subject(s) - creb , long term potentiation , nicotine , adenylyl cyclase , medicine , endocrinology , protein kinase a , hippocampus , brain derived neurotrophic factor , stimulation , chemistry , cyclic adenosine monophosphate , neurotrophic factors , calmodulin , kinase , biology , receptor , calcium , transcription factor , biochemistry , gene
We have shown previously that chronic nicotine treatment reverses adult‐onset hypothyroidism‐induced impairment of late‐phase long‐term potentiation (L‐LTP) in area CA1 of the hippocampus. In the present study, basal and stimulated levels of signaling molecules essential for the expression of L‐LTP were determined in area CA1. Immunoblots analysis showed that chronic nicotine treatment of hypothyroid rats prevented the reduction in the basal protein levels of adenylyl cyclase I (ACI), mitogen‐activated protein kinases [MAPKp44/42 (ERK1/2)], calcium‐calmodulin‐dependent protein kinase IV (CaMKIV), and cyclic‐AMP response element binding protein [CREB; phosphorylated (P‐) and total]. A significant increase in the levels of P‐CREB, P‐MAPKp44, P‐MAPKp42 and brain derived neurotrophic factor (BDNF) was seen 4 h after multiple train high frequency stimulation (MHFS) in nicotine‐treated hypothyroid and control animals, but not in hypothyroid animals. The levels of total CREB, total MAPKp44, total MAPKp42, and CaMKIV were elevated in all groups 4 h after MHFS. These findings suggest that prevention of the reduced basal level of CaMKIV, MAPKp44/42, and CREB by nicotine along with the regained ability of MHFS to induce MAPKp44/42 and CREB phosphorylation in nicotine treated hypothyroid animals may be responsible for the reversal of L‐LTP impairment by chronic nicotine treatment in this disease model. © 2007 Wiley‐Liss, Inc.