Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Studies involving the electrophoretic administration of antagonists of ACh (atropine, DHbetaE) and cholinesterase inhibitors (neostigmine, physostigmine) to MGN neurones indicate that ACh is an excitatory transmitter in the feline MGN, most probably released from fibres which originate in or traverse the mesencephalon.2. Auditory afferents to the MGN, cortico-geniculate fibres and the excitatory fibres which mediate ;spontaneous' firing of MGN neurones are unlikely to be cholinergic.3. Almost all geniculo-cortical relay cells are excited by ACh, this excitation being mediated by receptors which have both muscarinic and nicotinic properties. The excitation of relay cells by ACh is sometimes preceded or followed by a depression of firing which is resistant to atropine and DHbetaE, but the significance of this depression is unknown.4. The firing of many unidentified MGN neurones is depressed by ACh in the absence of any excitation, and this depression is blocked by both atropine and DHbetaE, and potentiated by anticholinesterases. This type of depression by ACh may be related to cholinergic inhibition, but this possibility has yet to be investigated.
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PMID:Cholinergic and non-cholinergic transmission in the medial geniculate nucleus of the cat. 434 15

1. The whole-cell configuration of the patch-clamp technique was used to study the modulation of giant depolarizing potentials (GDPs) by nicotinic acetylcholine receptors (nAChRs) in CA3 hippocampal neurons in slices from postnatal day (P) 2-6 rats. 2. Bath application of nicotine increased GDP frequency in a concentration-dependent manner. For example, nicotine (0.5-1 microM) enhanced GDP frequency from 0.05 +/- 0.04 to 0.17 +/- 0.04 Hz. This effect was prevented by the broad-spectrum nicotinic receptor antagonist dihydro-beta-erythtroidine (DHbetaE, 50 microM) and partially antagonized by methyllycaconitine (MLA, 50 nM) a competitive antagonist of alpha7 nAChRs. GDP frequency was also enhanced by AR-17779 (100 microM), a selective agonist of alpha7 nAChRs. 3. The GABA(A) receptor antagonist bicuculline (10 microM) and the non-NMDA glutamate receptor antagonist DNQX (20 microM) blocked GDPs and prevented the effects of nicotine on GDPs. In the presence of DNQX, nicotine increased GABA-mediated synaptic noise, indicating that this drug may have a direct effect on GABAergic interneurons. 4. Bath application of edrophonium (20 microM), a cholinesterase inhibitor, in the presence of atropine (1 microM), increased GDP frequency, indicating that nAChRs can be activated by ACh released from the septo-hippocampal fibres. This effect was prevented by DHbetaE (50 microM). 5. In the majority of neurons tested, MLA (50 nM) and DHbetaE (50 microM) reduced the frequency of GDPs with different efficacy: a reduction of 98 +/- 11 and 61 +/- 29 % was observed with DHbetaE and MLA, respectively. In a subset of cells (40 % in the case of MLA and 17 % in the case of DHbetaE) these drugs induced a twofold increase in GDP frequency. 6. It is suggested that, during development, nAChRs modulate the release of GABA, assessed as GDPs, through distinct nAChRs. The rise of intracellular calcium via nAChRs would further strengthen GABA-mediated oscillatory activity. This can be crucial for consolidation of synaptic contacts and for the fine-tuning of the developing hippocampus.
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PMID:Regulation of GABA release by nicotinic acetylcholine receptors in the neonatal rat hippocampus. 1157 59