Premium
Hypothyroidism impairs long‐term potentiation in sympathetic ganglia: Electrophysiologic and molecular studies
Author(s) -
Alzoubi K.H.,
Bedawi A.S.,
Aleisa A.M.,
Alkadhi K.A.
Publication year - 2004
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20268
Subject(s) - long term potentiation , synaptic plasticity , medicine , endocrinology , neurotransmission , superior cervical ganglion , biology , calmodulin , stimulation , neuroscience , chemistry , calcium , receptor
Electrophysiologic and molecular techniques were used to study the effect of adult‐onset hypothyroidism on synaptic plasticity in the superior cervical sympathetic ganglion. Ganglia excised from adult thyroidectomized and sham‐operated rats were subjected to a brief high‐frequency stimulation of the preganglionic nerve to express long‐term potentiation (gLTP). Western blotting was carried out to determine the protein levels of key signaling molecules that may be involved in the expression of gLTP. Input/output relationship in ganglia from hypothyroid rats indicated a normal basal synaptic transmission, whereas activity‐dependent types of synaptic plasticity, posttetanic potentiation (PTP) and gLTP, were impaired. Immunoblot analysis showed that both calcium/calmodulin kinase II (CaMKII) and phosphorylated CaMKII (P‐CaMKII) levels were reduced markedly in hypothyroid rat ganglia compared to those from euthyroid controls. Additionally, protein levels of nitric oxide synthase‐1, heme oxygenase‐2, calmodulin, protein kinase C (PKC), and calcineurin were also reduced in hypothyroid rat ganglia. The results indicate that abnormally low basal levels of signaling molecules may be responsible for hypothyroidism‐induced impairment of gLTP in superior cervical ganglia. In addition, the results indicate that synaptic plasticity in sympathetic ganglia may involve a molecular sequence of events similar to that proposed for LTP in the hippocampus. © 2004 Wiley‐Liss, Inc.