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Protein binding: 10–33%: Metabolism: ..
Methamphetamine toxicity is inhibited by a variety of drug treatments, including: 1) DA synthesis inhibitor alpha-methyl-para-tyrosine; 2) DA receptor antagonists; 3) NMDA receptor antagonists, e.g., MK-801; 4) DA and serotonergic reuptake inhibitors protecting against DA and serotonin toxicity respectively (195). Even though most studies have found that serotonergic and DA reuptake inhibitors specifically protect these two sites, certain reuptake blockers (such as benztropine) do not (195). On the other hand, mazindol, a non-specific blocker, protects against both DA and serotonergic neurotoxicity. Ali et al. (1994) have further demonstrated in mice that a major factor for neurotoxicity is hyperthermia which is highly correlated with the degree of long-term DA depletion (21). Furthermore, haloperidol, diazepam and MK-801, all of which can reduce methamphetamine-induced hyperthermia, protect rats against DA depletion (4). They also demonstrated that reducing the ambient temperature (4°C) reduced neurotoxicity to the same levels found when phenobarbital, diazepam and MK-801 were present to protect the cell. Tolerance to methamphetamine induced by increasing doses also reduces the hyperthermic response and as well protects against neurotoxicity (89, 188).
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One of the hallmarks of amphetamine-induced neurotoxicity is the loss of DA uptake sites in the striatum and accumbens. These studies of transporters after chronic amphetamine have reported decreases in the range of 30–40% (158). Recently, Silvia et al. (198) addressed the functional significance of changes in transporters on amphetamine's behavioral effects. After seven days of infusion of transporter RNA antisense ODN into the SN/VTA nuclei, mazindol binding was reduced 32% in the caudate. Administration of 2 mg/kg of amphetamine at this time resulted in robust contralateral turning (an increase of 400%); in contrast, 10 mg/kg of cocaine induced no changes in the turning response. The lack of turning response to cocaine after transporter reduction contrasts with the substantial cocaine-induced contralateral turning after unilateral SN/VTA D ODN to reduce D autoreceptors in the striatum (199). Thus, the amphetamine-induced loss of DA uptake sites could have two consequences: 1) a protective mechanism reducing further neurotoxicity, and 2) reverse tolerance to subsequent amphetamine administration, perhaps resulting in adverse symptoms such as paranoid psychosis (see also the discussion on neurotoxicity in the habenular interpeduncular track and its possible relationship to augmentation amphetamine-induced adverse effects).