Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The subcellular localization and functional significance of neuronal nicotinic acetylcholine receptor alpha4-subunits were investigated in the rat hypothalamic supraoptic nucleus. A high level of alpha4 mRNA expression was found in the magnocellular neurons in the supraoptic nucleus. Strong immunoreactitivy for alpha4 in neurons of the supraoptic nucleus was detected in the rough endoplasmic reticulum and cytoplasmic matrix, although it was very weak in the Golgi apparatus, except for the transport vesicles. Immunoreactivity for alpha4 was detected in both the pre-synaptic axon terminals and post-synaptic axon terminals. A high level of signals for vasopressin mRNA was detected in the supraoptic nucleus after the animals were injected s.c. with nicotine. These findings suggest that alpha4-containing subtypes are synthesized in the rough endoplasmic reticulum and transported to the plasma membrane and serve as pre- and post-synaptic nicotinic acetylcholine receptors. Nicotine may up-regulate vasopressin gene expression in the supraoptic nucleus, acting through nicotinic acetylcholine receptors.
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PMID:Neuronal nicotinic acetylcholine receptor in the hypothalamus: morphological diversity and neuroendocrine regulations. 938 62

Strong immunoreactivity for neuronal nicotinic acetylcholine receptor alpha4 subunit was detected in neurons of the supraoptic nucleus (SON). At the ultrastructural level, immunoreactivity for alpha4 was detected in the post-synaptic membranes as well as in the cytoplasmic matrices in the magnocellular neurons. Nicotine (1-10 microM) increased cytosolic Ca2+ concentrations ([Ca2+]i) in isolated arginine-vasopressin (AVP)-containing neurons in the rat SON. Nicotine (10 microM) was less potent in increasing [Ca2+]i in AVP-containing neurons than noradrenaline (1 microM), a known neurotransmitter in the SON. The nicotine-induced [Ca2+]i increase in AVP-containing neurons was markedly reduced when pre-treated with a protein kinase A (PKA) blocker, H89 (40 microM). These findings suggest that nicotine, a known neurotransmitter in the SON, activates AVP-containing neurons via nicotinic acetylcholine receptor which is linked to stimulation of cAMP-PKA-regulated Ca2+ signaling pathway.
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PMID:Nicotine increases cytosolic Ca2+ in vasopressin neurons. 952 22