How Does Ambien Work?
Neurons and Neurotransmitters
The brain's functions, including sensation, emotions, muscle control and cognition, are all governed by small cells called neurons. Neurons represent a complicated network of interconnected cells that communicate with each other using chemical signals called neurotransmitters. These neurotransmitters are secreted by neurons into spaces called neurons, where they can bind to special proteins called receptors, which are designed to bind to specific neurotransmitters. When a neurotransmitter binds to a receptor, it causes a signal to be sent to the other neurons in the synapse. Often there are many different kinds of receptors for a neurotransmitter, with each receptor being specific to certain kinds of neurons. Ambien works by specifically binding to certain receptors, altering the brain's activity.
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- The brain's functions, including sensation, emotions, muscle control and cognition, are all governed by small cells called neurons.
- These neurotransmitters are secreted by neurons into spaces called neurons, where they can bind to special proteins called receptors, which are designed to bind to specific neurotransmitters.
Zolpidem
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Ambien's active ingredient is a chemical called zolpidem. Zolpidem is similar in structure to another class of medication called benzodiazepines. Benzodiazepines have a variety of effects on the brain. They have the ability to reduce anxiety, prevent seizures, and they also work as sedatives. The different effects of benzodiazepines are mediated by different types of receptors. Zolpidem is not a benzodiazepine, but it binds to some of the same receptors to which benzodiazepine drugs bind. As the Merck Manual explains, zolpidem binds to the receptors in the brain that are responsible for benzodiazepine's sedative properties 1. As a result, zolpidem can cause sedation without generating any of the other effects of benzodiazepines.
- Ambien's active ingredient is a chemical called zolpidem.
- As a result, zolpidem can cause sedation without generating any of the other effects of benzodiazepines.
GABA Receptors
As a 1998 article in CNS Drug Reviews explains, zolpidem binds to a subtype of GABA receptor. GABA is a neurotransmitter that primarily works to inhibit the activity of neurons. When zolpidem binds to this receptor, it slows and stops activity in certain parts of the brain. For this reason, zolpidem is often classified as a hypnotic. It diminishes activity in parts of the brain that are responsible for processing thoughts. By slowing cognition, zolpidem makes it easier for patients to fall asleep. Some formulations of Ambien release a constant amount of zolpidem over a period of time, which makes it easier for patients to both fall asleep and stay asleep.
- As a 1998 article in CNS Drug Reviews explains, zolpidem binds to a subtype of GABA receptor.
- When zolpidem binds to this receptor, it slows and stops activity in certain parts of the brain.
Related Articles
References
- Merck Manual: Insomnia Treatments
- Bomalaski, MN et al. “Zolpidem for the Treatment of Neurologic Disorders: A Systematic Review.” JAMA Neurol. Published online June 26, 2017. doi:10.1001/jamaneurol.2017.1133.
- Kilduff, TS and Mendelson, WB. “Hypnotic Medications: Mechanisms of Action and Pharmacologic Effects,” in Principles and Practices of Sleep Medicine. Edited by Kryger MH, Roth T, Dement WC. St. Louis, Missouri, Elsevier Saunders, 2017, p. 429.
- Miyazaki, Y et al. “Efficacy of Zolpidem for Dystonia: a Study Among Different Subtypes.” Front Neurol. 2012 Apr 17;3:58.
- Sateia, MJ et al. “Clinical Practice Guideline for the Pharmacologic Treatment of Chronic Insomnia in Adults: An American Academy of Sleep Medicine Clinical Practice Guideline.” Journal of Clinical Sleep Medicine. 2017;13(2)307-349.
- Sutton, JA and Clauss, RP. “A review of the Evidence of Zolpidem Efficacy in Neurological Disability After Brain Damage Due to Stroke, Trauma and Hypoxia: A Justification of Further Clinical Trials.” Brain Inj. 2017;31(8):1019-1027.
Writer Bio
Adam Cloe has been published in various scientific journals, including the "Journal of Biochemistry." He is currently a pathology resident at the University of Chicago. Cloe holds a Bachelor of Arts in biochemistry from Boston University, a M.D. from the University of Chicago and a Ph.D. in pathology from the University of Chicago.