User:Miniroovigilante/Acetylcholine

amphetamine releases dopamine into the synapse by reversing DAT .............. the dat reversal depends on the activation and increased PKC activity, alpha-7 nicotinic [pre/post?] receptor activation, alpha1b, beta-3[?], Ca2+-channel activity (excitotoxic stimului-induced DA release], increased glutamate and EAA activity and release, stimulating Nitric oxide formation, enhancing certain NMDA-current-pro-excitotoxic activity and processes................ect.

Protein kinase C alpha-7 [pre/post] alpha-1b adrenergic [pre/post] D2 pre/post D3 pre/post D4 [subtypes?] ? --> decreased/altered NMDA/glutamate activity...? 5ht2a [activation/activity adequate] M1/2/3/4/5 ? beta-2 adrenergic ?

dynorphin enkephalin PPOMC---> a/b/g-MSH melanocortin, Proopiomelanocortin, beta-endorphin, sigma 1, sigma 2 ? M4

 DONT LOOK AT THIS TABLE I MADE IT UP ALL BY MYSELF ITS WRONG Muscarinic Acetylcholine antagonists:  -  binding profiles / selectivities --- ? not sure, only have a few references, and i probably mixed up the Ki and nM values, since I don't actually know what they represent quantitatively-wise.

not finished,

Anti-nicotinic properties of anticholinergic antiparkinson drugs. The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain, pharmacological evidence is lacking. This study describes the anti-nicotinic properties of the clinically used anticholinergic antiparkinson drugs, benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl. Nicotine-induced convulsion and arecoline-induced tremor in mice were effectively prevented by these drugs. The concentrations of benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl affording 50% prevention of nicotine-induced convulsion (ED50 values) were 7.4, 4.6, 7.8, 4.9, 3.1 and 3.3 mg kg(-1), respectively. The classical muscarinic receptor antagonist atropine had potent anti-muscarinic effects but very weak anti-nicotinic activity. The classical nicotinic receptor antagonist mecamylamine had potent anti-nicotinic activity but no anti-muscarinic effects. The pattern of shift of the dose-response curve for nicotine-induced convulsion in mice was determined in the presence of increasing concentrations of the anticholinergic antiparkinson drugs. These drugs were found to increase the ED50 (0.49 mg kg(-1)) of nicotine-induced convulsion in a dose-related manner. The maximum effect of nicotine and the slope of nicotine dose-response curve were not significantly influenced by either low or high doses of benztropine, procyclidine or trihexylphenidyl, which suggests competitive action. Biperiden, caramiphen and ethopropazine, at low doses which significantly increased the ED50 of nicotine, did not affect the maximum effect of nicotine or the slope of the nicotine dose-response curve; at higher doses, however, they reduced the maximum effect and the slope, which suggests that these drugs have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice. The experiments demonstrate that the anticholinergic antiparkinson drugs and mecamylamine effectively antagonize nicotine-induced convulsion, but atropine does not; some of these drugs have competitive properties whereas others seem to have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice.

Postsynaptic Action of Brain-Derived Neurotrophic Factor Attenuates 7 Nicotinic Acetylcholine Receptor-Mediated Responses in Hippocampal Interneurons

Relationship of brain-derived neurotrophic factor and its receptor TrkB to altered inhibitory prefrontal circuitry in schizophrenia. http://www.ncbi.nlm.nih.gov/pubmed/15647480