The antinociceptive effect of ABT-594 was prevented, but not reversed, by the noncompetitive neuronal nicotinic acetylcholine receptor antagonist mecamylamine 5 micromol/kg, i.p. (erowid.org)
Nitric oxide sy2
The anti-fibrillatory action of carbamylcholine was prevented by the nicotinic receptor antagonist mecamylamine, inhibitors of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by the nitric oxide (NO) donor sodium nitroprusside. (ox.ac.uk)
Developmental expression of neuronal nitric oxide synthase in P/Q-type voltage-gated calcium ion channel mutant mice, leaner and tottering. (tamu.edu)
Antagonist3
In contrast, the antinociceptive effect of ABT-594 was not prevented by hexamethonium 10 micromol/kg, i.p., a neuronal nicotinic acetylcholine receptor antagonist that does not readily enter the central nervous system, nor by naltrexone 0.8 micromol/kg, an opioid receptor antagonist. (erowid.org)
Yet, in all groups, epibatidine-induced strip contractions were similarly inhibited by mecamylamine and hexamethonium (ganglionic nicotinic receptor antagonists), SR 16584 (α3β4 neuronal nicotinic receptor antagonist), atracurium and tubocurarine (neuromuscular nicotinic receptor antagonists), and atropine (muscarinic receptor antagonist), indicating that nicotinic receptors (particularly α3β4 subtypes), neuromuscular and muscarinic receptors play roles in bladder contractility. (jefferson.edu)
The effect of CCh on VFT was abolished by a muscarinic (atropine, 0.1 μmol l(-1) , n = 6) or a nicotinic receptor antagonist (mecamylamine, 10 μmol l(-1) , n = 6). (ox.ac.uk)
Antagonists1
This effect cannot be prevented by systemic injection of either α7-nAChR (nicotinic ACh receptor)-selective [methyllycaconitine (MLA)] or β2*-nAChR-selective [mecamylamine (MEC)] antagonists but is prevented by coinjection of MLA and MEC. (barrowneuro.org)
Synaptic2
Thus, ACh modulates network dynamics in a biphasic fashion, probably by inhibiting excitatory synaptic transmission and facilitating neuronal excitability through muscarinic signaling pathways. (springer.com)
Collectively, these findings demonstrate that systemic nicotine acting via either α7- or β2*-nAChRs increases presynaptic and postsynaptic glutamatergic function, and consequently initiates glutamatergic synaptic plasticity, which may be an important, early neuronal adaptation in nicotine reward and reinforcement. (barrowneuro.org)
Currents2
With whole-cell recording from single neurons, we found that ACh inhibited excitatory postsynaptic currents (EPSCs) while elevating neuronal firing in a dose-dependent manner. (springer.com)
Here, we report that single, systemic exposure in rats to nicotine (0.17 mg/kg free base) increases the ratio of DA neuronal currents mediated by AMPA relative to NMDA receptors (AMPA/NMDA ratio) assessed 24 h later, based on slice-patch recording. (barrowneuro.org)
It inhibits neuronal dopamine reuptake, in addition to being a weak blocker of serotonin and norepinephrine reuptake. (medscape.com)
Cultured neuronal1
Here, we investigated how ACh influences reverberatory activity in cultured neuronal networks. (springer.com)
Activity1
However, understanding exactly how such molecular and cellular actions of ACh translate into modulation of the network activity of neuronal ensembles in vivo has been challenging, in part due to the vast complexity of native circuits. (springer.com)
Transmission1
After systemic exposure to nicotine, glutamatergic (but not GABAergic) transmission onto rat VTA DA neuronal inputs is enhanced. (barrowneuro.org)
Effects2
ABT-594 [5-2R-azetidinylmethoxy-2-chloropyridine], a novel neuronal nicotinic acetylcholine receptor agonist, produced significant antinociceptive effects in mice against both acute noxious thermal stimulation--the hot-plate and cold-plate tests--and persistent visceral irritation--the abdominal constriction writhing assay maximally-effective dose in each test 0.62 micromol/kg, i.p. (erowid.org)
These data indicate that ABT-594 is a centrally acting neuronal nicotinic acetylcholine receptor agonist with potent antinociceptive and anxiolytic-like effects in mice. (erowid.org)
Nicotinic receptor modulator1
Professor Bartlett said varenicline acted as a neuronal nicotinic receptor modulator (nAChR) and similar results were observed with other such drugs including mecamylamine and cytisine. (sciencedaily.com)
NAChRs3
Although molecular biology provides new insights into the subunit compositions and the stoichiometries of insect neuronal nicotinic acetylcholine receptors (nAChRs), our knowledge about the phosphorylation/dephosphorylation mechanisms of native neuronal nAChRs is limited. (aspetjournals.org)
In neuronal nAChRs, the binding site is located at the interface of an α and a β subunit or between two α subunits in the case of α 7 receptors. (wikipedia.org)
A paradigmatic case is constituted by the epilepsies caused by altered neuronal nicotinic acetylcholine receptors (nAChRs), which exert complex physiological functions in mature as well as developing brain. (unimib.it)
NNRs3
A nicotinic channel blocker, TC-5214, is being investigated as potential augmentation therapy for resistant hypertension in a phase 2 exploratory study, according to an announcement by Targacept (Winston-Salem, North Carolina), a company spun off from R.J. Reynolds Tobacco Co. in 2000 to develop drugs based on its understanding of neuronal nicotinic receptors (NNRs). (medscape.com)
[ 20 ] Targacept researchers identified the S -(+) enantiomer (TC-5214) as more effective than R -(-)-mecamylamine (TC-5213) at low concentrations (micromolar range) in inhibiting the low-sensitivity isoforms of human α4β2 NNRs. (medscape.com)
We found that in reduced concentrations ( micromolar array), TC-5214 [S-(+)-mecamylamine] was far better as compared to TC-5213 [R-(:)* mecamylamine] throughout inhibiting the particular Mark vii alpha dog Some try out Two NNRs. (pdpksignaling.com)
Hydrochloride2
[ 18 ] TC-5214 is the S -(+) enantiomer of mecamylamine hydrochloride, a drug initially developed for its ganglion-blocking activity and introduced in the United States in the mid-1950s for the treatment of severe hypertension. (medscape.com)
Targacept acquired the commercial rights to mecamylamine hydrochloride in 2002 and it is currently available as a 2.5-mg tablet (Inversine®) for the management of moderately severe to severe essential hypertension and uncomplicated malignant hypertension . (medscape.com)
Nicotine3
These protective effects of nicotine were fully reversed by inhibition of neuronal nicotinic receptors by mecamylamine. (nih.gov)
7. Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells. (nih.gov)
9. Wheel running during chronic nicotine exposure is protective against mecamylamine-precipitated withdrawal and up-regulates hippocampal α7 nACh receptors in mice. (nih.gov)
Receptors3
muscle-type nicotinic receptors and neuronal-type nicotinic receptors. (wikipedia.org)
In both muscle-type and neuronal-type receptors, the subunits are very similar to one another, especially in the hydrophobic regions. (wikipedia.org)
The stereoselectivity involving mecamylamine enantiomers at HS and also Mark vii alpha dog 4 experiment with Two receptors demonstrates that TC-5214 will be the chosen stereoisomer pertaining to discerning activation of HS, whilst it is more efficient inside quelling LS receptor perform. (pdpksignaling.com)
Concentrations1
The function of the nAChR channels expressed by BEC was demonstrated by biphasic increase in the concentrations of intracellular calcium ([Ca++]i) in response to activation of the channel by Nic and fluctuations of [Ca++]i due to channel blockade by mecamylamine (Mec). (nih.gov)
Exposure1
Importantly, concomitant exposure to SS and the nAChR antagonist mecamylamine during gestation blocked the development of BPD. (nih.gov)
Cells2
B ) Peak current density elicited by 0 mV pulse in nematocytes (n = 5), neurons (n = 6), and non-neuronal cells (n = 3). (elifesciences.org)
The present investigation examines a hypothesis that OP compound inhibiting the EC-hydrolase(s) dysregulates the EC-signaling system, triggering apoptosis in neuronal cells. (inrae.fr)
Development1
[5] This change in NKCC1 presence seems to be responsible for altering responses to the neurotransmitters GABA and glycine from excitatory to inhibitory, which was suggested to be important for early neuronal development. (epiphanyasd.com)