Tag: Cholinergic system

Recent preclinical studies have observed that ivermectin enhances the release of dopamine in the dorsal striatum of the brain, although not through a direct mechanism. This finding challenges the conventional understanding of the antiparasitic drug's effects and raises new questions about its potential neurological impact, including whether ivermectin increases dopamine levels in humans.

According to preclinical studies, activating muscarinic M1 receptors has shown to improve cognitive performance and synaptic plasticity. This critical effect is central to understanding **what happens when M1 receptors are stimulated**, revealing their importance in enhancing brain function and their potential as therapeutic targets for neurodegenerative diseases.

According to preclinical studies, the atypical antipsychotic olanzapine can produce a significant, dose-dependent increase in extracellular acetylcholine (ACh) release in brain regions such as the hippocampus. This effect runs counter to the drug's known anticholinergic properties, presenting a pharmacological paradox that explains both its therapeutic benefits and some side effects.

While many antipsychotics are associated with pupil dilation (mydriasis) due to anticholinergic effects, certain older and atypical antipsychotic medications have been linked to miosis, or constricted pupils. This less common phenomenon often occurs in the context of overdose or is driven by specific receptor interactions.

Scientific studies have long established that gabapentin does not directly increase acetylcholine release in the brain. The relationship between this medication and the body's cholinergic system is more complex, involving indirect signaling pathways rather than a simple boosting of the neurotransmitter.

Studies have shown that some medications can contribute to an anticholinergic burden, but it is important to distinguish between drug classes based on their primary action. The answer to, '**Is atenolol an anticholinergic drug?**' is a definitive no, as it belongs to a completely different class of medications called beta-blockers.

Discovered in 1914, acetylcholine (ACh) was the very first neurotransmitter to be identified [1.5.3]. Understanding **what is the mechanism of action of acetylcholine?** is fundamental to grasping how our nervous system controls everything from muscle movement to memory [1.5.3, 1.5.5].

In September 2024, the FDA approved xanomeline-trospium (Cobenfy) for the treatment of schizophrenia, representing the first new class of antipsychotic medication to market in decades that does not primarily target dopamine receptors. Understanding **how does xanomeline affect the brain?** requires exploring its innovative mechanism centered on the brain's cholinergic system, a fundamental pathway for cognition and behavior.

Research indicates that while choline is an essential nutrient for health, excessive intake from supplements can cause headaches and other side effects. This occurs primarily when consumption exceeds recommended upper intake levels.

Muscarinic antagonists have been used as bronchodilators for centuries, with early forms including the inhalation of smoke from certain plants like *Datura stramonium*. Today, modern derivatives are used to treat respiratory conditions by explaining precisely how do muscarinic antagonists cause bronchodilation through a targeted biochemical process.