Disease relevance of Methylarecaidin

• Rather than improving the chorea, arecoline tended to exacerbate the choreic movements [1].
• Roles of keratinocyte inflammation in oral cancer: regulating the prostaglandin E2, interleukin-6 and TNF-alpha production of oral epithelial cells by areca nut extract and arecoline [2].
• Memory improvement without toxicity during chronic, low dose intravenous arecoline in Alzheimer's disease [3].
• The vasodilation that occurs after beta-2 adrenoceptor stimulation with salbutamol, as well as the negative chronotropic action induced by the muscarinic receptor stimulant arecoline, were inhibited 4 days after vaccination with two combined diphtheria-pertussis-tetanus whole-cell vaccines and their plain pertussis product [4].
• Oxotremorine was more potent than arecoline in increasing the mechanical phasic activity, without inducing a sustained contracture [5].

Psychiatry related information on Methylarecaidin

• Arecoline, a cholinergic muscarinic receptor agonist, induced rapid eye movement sleep significantly more rapidly in patients with primary affective illness in remission than in normal control subjects matched for age and sex [6].
• Human serial learning: enhancement with arecholine and choline impairment with scopolamine [7].
• Multiple-dose arecoline infusions in Alzheimer's disease [8].
• The cholinergic rapid eye movement (REM) induction test using arecoline hydrobromide, a cholinergic muscarinic receptor agonist, was studied in patients with affective disorder and in normal controls to determine whether or not depression is associated with enhanced induction of REM sleep by muscarinic agonists [9].
• Twelve patients with dementia of the Alzheimer type received two-hour infusions of placebo and the muscarinic cholinergic agonist arecoline hydrobromide at rates of 1, 2, and 4 mg/h in a double-blind, randomized fashion [8].

High impact information on Methylarecaidin

• AN extract (100-800 microg/ml) and arecoline (0.1-0.8 mM) also stimulated ERK1/ERK2 phosphorylation with a maximal stimulation at 5-10 min of exposure [10].
• In addition, U0126 and PD98059 (50 microM) also decreased AN extract- and arecoline-associated PGE2 and IL-6 production in GK and KB cells [10].
• We observed the induction of c-Fos mRNA expression in human gingival keratinocyte (GK) and KB carcinoma cells by areca nut (AN) extract and arecoline [10].
• However, U0126 by itself arrested the cells in G0/G1 phase, but was not able to prevent AN- and arecoline-induced cell death or apoptosis [10].
• To test the hypothesis that depression and REM sleep share common cholinergic mechanisms the authors administered arecoline 25 min after completion of the first REM period to 14 patients with remitted bipolar affective disorder, 15 normal controls, and 5 subjects with a personal or family history of affective disorder [11].

Chemical compound and disease context of Methylarecaidin

• Electroconvulsive shock reduces the cataleptogenic effect of both haloperidol and arecoline in rats [12].
• This impairment was not attenuated by any post-training dose of arecoline; however, immediate post-training injections of both epinephrine (at 0.05 mg/kg) and glucose (at 100 mg/kg) significantly reduced the amnesia [13].
• To investigate further the postsynaptic cholinergic responsivity in Alzheimer's disease, patients were studied with arecoline and nicotine [14].
• Atropine microinjected bilaterally into the PRF attenuated the cataleptogenic effect of eserine and arecoline i.p. We suggest that the PRF is a site at which systemically given cholinergic drugs act to produce catalepsy [15].
• Dexetimide strongly antagonized the bradycardia as well as the increase in bladder pressure induced by pilocarpine, carbachol, oxotremorine, arecoline, acetyl-beta-methylcholine and acetylcholine, whereas pirenzepine was much less effective [16].

Biological context of Methylarecaidin

• Arecoline did produce significant alterations of blood pressure, heart rate, and body temperature, probably by central cholinergic stimulation [1].
• Clinical pharmacokinetics of arecoline in subjects with Alzheimer's disease [17].
• CONCLUSIONS: Because optimal dose variation is due to differing plasma kinetics, the plasma arecoline level measured at a single infusion rate can be used to choose the optimal dose for memory enhancement in patients with Alzheimer's disease [17].
• The present finding of twin concordance in response to arecoline suggests genetic variation in sensitivity of CNS muscarinic cholinergic receptors [18].
• Exposure to arecoline (> 0.2 mM) for 24 h induced G(2)/M cell cycle arrest of OMF and KB cells [19].

Anatomical context of Methylarecaidin

• Areca nut (AN) and arecoline may inhibit the growth of oral mucosal fibroblasts (OMF) and keratinocytes [19].
• Arecoline- and AN-conditioned medium decreased phytohemagglutinin-mediated CD4+ and CD8+ T cell activation [2].
• High levels of signaling through GAR-3 inhibit pharyngeal muscle relaxation and impair feeding--but do not block muscle repolarization--when worms are exposed to arecoline, a muscarinic agonist [20].
• Arecoline increased incorporation in these two fractions by up to 400% but did not increase incorporation into the myelin, mitochondrial, or cytosolic fractions [21].
• Pituitary stalk transection led to diminished plasma ACTH and corticosterone responses to arecoline [22].

Associations of Methylarecaidin with other chemical compounds

• Atropine (a muscarinic chilinergic blocker), arecoline (a muscarinic stimulator) and nicotine (a nicotinic cholinergic stimulating drug) did not affect basal prolactin levels [23].
• Extracts of betel quid and arecaidine (a metabolite of arecoline present in Betel nut) were negative [24].
• The muscarinic agonists oxotremorine, pilocarpine, arecoline, and carbachol also compete effectively for the L-[3H]QNB binding site [25].
• Pretreatment of rat brain cortical slices with arecoline in vitro resulted in a dose-dependent inhibition of carbachol-stimulated [3H]inositol monophosphate accumulation [26].
• This hypothesis was confirmed by the dose-dependent ability of arecoline to cause hypothalamic CRH secretion in vitro, an effect antagonized by atropine, and its failure to elicit ACTH and corticosterone secretion by dispersed anterior pituicytes and adrenocortical cells in culture, respectively [22].

Gene context of Methylarecaidin

• In addition, arecoline was found to inhibit MMP-2 secretion and production at the concentration level of 40 microg/ml [27].
• Arecoline was found to elevate TIMP-1 expression at the concentration level under 20 microg/ml in a dose-dependent manner [27].
• Nicotine and arecoline therefore significantly increased IL-1 alpha and -1 beta secretions and the surface expression of ICAM-1 in KB CCL17 cells [28].
• However, incubation of cells for 72 hrs in the presence of nicotine and/or arecoline treatments and antibody against IL-1 alpha or IL-1 beta significantly increased cell growth as compared with the antibody free one [29].
• The regulation of COX-2 expression induced by arecoline is critically dependent on the cellular GSH concentration [30].

Analytical, diagnostic and therapeutic context of Methylarecaidin

• METHODS: Plasma arecoline concentrations were measured during and after high-dose (i.e., 5 mg intravenously over 30 minutes) and up to 2 weeks of continuous multiple-dose steady-state intravenous infusions of arecoline in 15 subjects with mild to moderate Alzheimer's disease [17].
• Five groups of subjects underwent EEG sleep recordings, arecoline rapid eye movement (REM) induction response testing, and Schedule for Affective Disorders and Schizophrenia (SADS) interview [31].
• Quantitative autoradiography indicated regionally selective increases in brain [14C]AA and [14C]DA incorporation in response to arecoline [32].
• The vasodilation after beta 2-adrenoceptor stimulation with salbutamol as well as the negative chronotropic action induced by the muscarinic receptor stimulant arecoline were inhibited 4 days after vaccination [33].
• 2. Animals were inoculated intratracheally with bovine parainfluenza-3 virus or control medium 7 days after treatment with capsaicin (50 mg kg-1, s.c.). Four days after inoculation, tracheal contractions were measured to increasing concentrations of substance P, histamine and the cholinoceptor agonist, arecoline [34].

References