Alprazolam is a benzodiazepine drug first synthesized by Upjohn/Pfizer in 1969. It is sold under the trade name of Xanax for the treatment of anxiety. Alprazolam is also used to treat insomnia, panic and depression. According to the June 23, 2009, update in "Drug Bank," Xanax affects the central nervous system by causing several changes in the brain. These effects are achieved by inducing a general inhibition and by hitting specific targets. The brain changes induced by alprazolam also affect behavior.
Electrical Activity
Xanax reduces electrical flow in the brain. This change is evident in brain wave, also known as electroencephalogram or EEG, activity. A 1995 report in the "European Journal of Clinical Pharmacology" tested the effects of alprazolam on electrical responses to a series of stimuli. Results showed that Xanax reduced the amplitude of these "evoked potentials." This change indicates a drug-induced decrease in cognitive information processing capacity and an extension of stimulus evaluation time.
Blood Flow
A 1993 study in "Neuropsychopharmacology" shows that alprazolam reduced cerebral blood flow by at least 25 percent. A decrease in blood flow suggests a reduction in overall brain activity. These effects appeared within a week of treatment, but they dissipated on week two. The latter finding reveals the tolerance, or reduction in effectiveness, typically found with benzodiazepine drugs. The authors also noted that alprazolam caused sedation and amnesia. Such effects are commonly observed during Xanax use.
Receptor System
According to an online review published by McGill University, the main targets for alprazolam are benzodiazepine receptors. These receptors are present throughout the brain. They are located on the gamma-aminobutyric acid, or GABA, receptor complex. The chemical GABA is an inhibitory neurotransmitter which affects muscle tone. Xanax affects GABA by increasing the availability of its receptors. It does not, however, change the amount of GABA produced.
A 2008 review in "Pharmacology, Biochemistry, and Behavior" shows that panic can be induced by the inhalation of carbon dioxide. The authors suggest that this panic is mediated by GABA receptors. A 2009 report in the "Journal of Psychopharmacology" reveals that pretreatment with Xanax prevents the anxiety associated with carbon dioxide intake. The latter result demonstrates the role GABA plays in the behavioral effects of alprazolam.
Hormone System
E. Arvat and co-workers reviewed the effects of benzodiazepines on the hormone system. This paper, published in the September 2002 edition of the "Journal of Endocrinological Investigation," suggests that drugs like alprazolam target corticotropin-releasing hormone, or CRH, in the hypothalamus. This structure lies deep in the center of the brain, and it controls the timing of chemical release and behavioral state. The CRH is released in response to stress by the paraventricular nucleus. Xanax suppresses CRH, and thereby decreases the stress response.
Timing System
A 2007 experiment published in the "Journal of Neuroscience" indicates that alprazolam affects the output of the biological clock that controls the daily rhythms of mammals. This pacemaker is located in the suprachiasmatic nucleus of the hypothalamus. The authors intentionally bred mice which had poor rhythmicity. Daily application of Xanax restored brain rhythms and improved cognitive performance.
References
- Drug Bank: Showing drug card for Alprazolam (
- "European Journal of Clinical Pharmacology"; Acute effects of the anxiolytics suriclone and alprazolam on cognitive information processing utilizing topographic mapping of event-related brain potentials (P300) in healthy subjects; H. V. Semlitsch et al.; 1995
- "Neuropsychopharmacology"; Effects of acute and chronic alprazolam treatment on cerebral blood flow, memory, sedation, and plasma catecholamines; P. Roy-Byrne et al.; February 1993
- McGill University: The Brain from Top to Bottom



Member Comments