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Hippocampus acetylcholine

The effect of allethrin (a Type I pyrethroid), cyhalothrin, and deltamethrin (Type II pyrethroids) on neurotransmitter release from the hippocampus (acetylcholine, glutamate, and GABA release) and striatum (dopamine release) has recently been investigated using ex vivo microdialysis in freely moving rats exhibiting the symptoms of pyrethroid poisoning [94-97]. Deltamethrin increased the release... [Pg.65]

Dronabinol (tetrahydrocannabinol), the active principle from cannabis and synthetic cannabinoids, nabilone and levonantradol are effective in treating nausea and vomiting in cancer chemotherapy. The mode of action is unclear but appears to involve cannabinoid CBi receptors. Cannabinoids have been shown to reduce acetylcholine release in the cortex and hippocampus, and have been suggested to inhibit medullary activity by a cortical action. Inhibition of prostaglandin synthesis and release of endorphins may also be involved in the antiemetic effect. A review of trials of dronabinol, nabilone or levonantradol concluded that while the cannabinoids were superior to placebo or dopamine receptor antagonists in controlling emesis... [Pg.461]

The pathologic hallmarks of the disease in the brain include neurofibrillary tangles and neuritic plaques made up of various proteins, which result in a shortage of the neurotransmitter acetylcholine. These are primarily located in brain regions involved in learning, memory, and emotional behaviors such as the cerebral cortex, hippocampus, basal forebrain, and amygdala.11... [Pg.515]

Cunha, R. A., Johansson, B., Fredholm, B. B., Ribeiro, J. A. Sebastiao, A. M. (1995). Adenosine A2A receptors stimulate acetylcholine release from nerve terminals of the rat hippocampus. Neurosci. Lett. 196 (1-2), 41-4. [Pg.355]

Fredholm, B. B. (1990a). Adenosine Al-receptor-mediated inhibition of evoked acetylcholine release in the rat hippocampus does not depend on protein kinase C. Acta Physiol. Scand. 140 (2), 245-55. [Pg.355]

Fredholm, B. B. (1990b). Differential sensitivity to blockade by 4-aminopyridine of presynaptic receptors regulating [3H]acetylcholine release from rat hippocampus. J. Neurochem. 54 (4), 1386-90. [Pg.355]

Dani, J.A., Radcliffe, K.A., Pidoplichko, V.I. Variations in desensitization of nicotinic acetylcholine receptors from hippocampus and midbrain dopamine areas. Eur. J. Pharmacol. 393 31, 2000. [Pg.32]

Revuelta, A. V., Moroni, F., Cheney, D. L., and Costa, E. (1978) Effect of cannabinoids on the turnover rate of acetylcholine in rat hippocampus, striatum and cortex. Naunyn Schmie-debergs Arch. Pharmacol., 304 107-110. [Pg.213]

Hossain MM, Suzuki T, Sato I, Takewaki T, Suzuki K, Kobayashi H (2004) The modulatory effect of pyrethroids on acetylcholine release in the hippocampus of freely moving rats. Neurotoxicology 25 825-833... [Pg.72]

In almost all tissues where 5-HT4 receptors are present, 5-HT or any other agonists increase intracellular cAMP synthesis [12], as has been shown for hippocampus, atrium, esophagus, intestinal tissue and adrenal cortex. A number of processes can be triggered by an increase in intracellular cAMP. For instance in the intestine, an increase in intracellular cAMP concentrations following activation of 5-HT4 receptors can trigger a relaxation of the smooth muscle. However, activation of 5-HT4 receptors present on intestinal inter- and motor-neurons leads to a facilitation of acetylcholine release and, thereby, to increased contractions of intestinal smooth muscle [13]. [Pg.197]

Reid, R.T., Lloyd, G.K., and Rao, T.S., Pharmacological characterization of nicotine-induced acetylcholine release in the rat hippocampus in vivo evidence for a permissive dopamine synapse, Br. J. Pharmacol., 127, 1486, 1999. [Pg.238]

Several indirect neurochemical effects of methyixanthines contribute to their effects. Micromolar concentrations of caffeine enhance release of acetylcholine (Pedata et al. 1984). However, this effect is biphasic, augmenting release at 50 pM, but decreasing it at 0.5 pM. This effect is also modulatory, affecting stimulated, but not basal, release. Caffeine enhances acetylcholine release in the hippocampus, which is due to adenosine Al receptor subtypes (Carter et al. 1995). Conversely, chronic caffeine reduces the excitatory effect of acetylcholine in the cerebral cortex (Lin and Phillis... [Pg.99]

Opioids dose-dependently reduce the release of acetylcholine in several brain areas, including the hippocampus, striatum, and cerebral cortex... [Pg.305]

Carter AJ, O Connor WT, Carter MJ, Ungerstedt U. (1995). Caffeine enhances acetylcholine release in the hippocampus in vivo by a selective interaction with adenosine A1 receptors. J Pharmacol Exp Ther. 273(2) 637-42. [Pg.448]

Lapchak PA, Araujo DM, Collier B. (1989). Regulation of endogenous acetylcholine release from mammalian brain slices by opiate receptors hippocampus, striatum, and cerebral cortex of guinea-pig and rat. Neuroscience. 31(2) 313-25. [Pg.525]

Gessa GL, Casu MA, Carta G, Mascia MS. (1998). Cannabinoids decrease acetylcholine release in the medial-prefrontal cortex and hippocampus, reversal by SR 141716A. Eur J Pharmacol. 355(2-3) 119-24. [Pg.559]


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See also in sourсe #XX -- [ Pg.32 ]




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