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Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
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Drug dependence, abuse, and addiction are complex phenomena that can precipitate various abnormal states. Physical dependence refers to a state of pharmacological adaptation to a drug. This adaptation often results in tolerance—a reduced response to the drug after repeated administrations. When the drug use is abruptly stopped, withdrawal symptoms occur due to the body's need to readjust from the pharmacologically induced imbalance. However, tolerance and withdrawal symptoms do not necessarily...
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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
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Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

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Published on: January 22, 2016

Nucleus accumbens invulnerability to methamphetamine neurotoxicity.

Donald M Kuhn, Mariana Angoa-Pérez, David M Thomas

    ILAR Journal
    |February 6, 2013
    PubMed
    Summary

    Methamphetamine damages dopamine (DA) neurons, particularly in the caudate-putamen (CPu), causing persistent structural and functional problems. While the nucleus accumbens (NAc) shows some recovery, altered DA homeostasis can increase Meth toxicity in this region.

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    Area of Science:

    • Neuroscience
    • Neuropharmacology
    • Toxicology

    Background:

    • Methamphetamine (Meth) is a potent neurotoxin impacting the central nervous system.
    • Long-term Meth abuse leads to persistent structural abnormalities and functional deficits.
    • Dopamine (DA) neuronal systems are primary targets of Meth-induced neurotoxicity.

    Purpose of the Study:

    • To review the neurotoxic effects of Methamphetamine, focusing on the dopamine system.
    • To elucidate the differential impact of Meth on brain regions like the caudate-putamen (CPu) and nucleus accumbens (NAc).
    • To discuss the role of animal models in understanding Meth neurotoxicity and developing therapies.

    Main Methods:

    • Review of postmortem brain tissue analyses from human Meth addicts.
    • Analysis of noninvasive imaging studies in intact human brains.
    • Synthesis of findings from animal models of Methamphetamine abuse.

    Main Results:

    • Meth causes heterogeneous and persistent damage to DA nerve endings in the CPu, with greater deficits in ventral and lateral aspects.
    • The NAc is initially spared but can become vulnerable with altered DA homeostasis, leading to increased CPu toxicity.
    • While CPu DA deficits are persistent, the NAc exhibits partial recovery, indicating different neuroplasticity.

    Conclusions:

    • Methamphetamine-induced neurotoxicity disproportionately affects specific DA pathways.
    • Alterations in DA homeostasis can expand Meth's neurotoxic effects to normally resistant brain regions like the NAc.
    • Understanding regional differences in neurotoxicity and recovery is crucial for therapeutic development.