Alprazolam: Difference between revisions

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==Pharmacology==
==Pharmacology==
Benzodiazepines produce a variety of effects by binding to the benzodiazepine receptor site and magnifying the efficiency and effects of the neurotransmitter [[GABA|gamma aminobutyric acid (GABA)]] by acting on its [[receptors]].<ref>{{cite journal | vauthors=((Haefely, W.)) | journal=Neuroscience Letters | title=Benzodiazepine interactions with GABA receptors | volume=47 | issue=3 | pages=201–206 | date=29 June 1984 | issn=0304-3940 | doi=10.1016/0304-3940(84)90514-7}}</ref> Alprazolam is a positive allosteric modulator of the gamma-aminobutyric acid (GABA) type A receptor. As this site is the most prolific inhibitory receptor set within the brain, its modulation results in the [[sedating]] (or [[anxiety suppression|calming effects]]) of alprazolam on the nervous system. The [[anticonvulsant]] properties of benzodiazepines may be, in part or entirely, due to binding to voltage-dependent sodium channels rather than benzodiazepine receptors.<ref>{{cite journal | vauthors=((McLean, M. J.)), ((Macdonald, R. L.)) | journal=The Journal of Pharmacology and Experimental Therapeutics | title=Benzodiazepines, but not beta carbolines, limit high frequency repetitive firing of action potentials of spinal cord neurons in cell culture | volume=244 | issue=2 | pages=789–795 | date= February 1988 | issn=0022-3565}}</ref>
Benzodiazepines produce a variety of effects by binding to the benzodiazepine receptor site and magnifying the efficiency and effects of the neurotransmitter [[GABA|gamma aminobutyric acid (GABA)]] by acting on its [[receptors]].<ref>{{cite journal | vauthors=((Haefely, W.)) | journal=Neuroscience Letters | title=Benzodiazepine interactions with GABA receptors | volume=47 | issue=3 | pages=201–206 | date=29 June 1984 | issn=0304-3940 | doi=10.1016/0304-3940(84)90514-7}}</ref> Alprazolam is a positive allosteric modulator of the gamma-aminobutyric acid (GABA) type A receptor. As this site is the most prolific inhibitory receptor set within the brain, its modulation results in the [[sedating]] (or [[anxiety suppression|calming effects]]) of alprazolam on the nervous system. <ref>{{cite journal | vauthors=((McLean, M. J.)), ((Macdonald, R. L.)) | journal=The Journal of Pharmacology and Experimental Therapeutics | title=Benzodiazepines, but not beta carbolines, limit high frequency repetitive firing of action potentials of spinal cord neurons in cell culture | volume=244 | issue=2 | pages=789–795 | date= February 1988 | issn=0022-3565}}</ref>


Alprazolam causes a marked suppression of the hypothalamic-pituitary-adrenal axis. Administration of alprazolam has been demonstrated to elicit an increase in striatal [[dopamine]] concentrations.<ref name="Bentue-Ferrer2001">{{cite journal | vauthors=((Bentué-Ferrer, D.)), ((Reymann, J. M.)), ((Tribut, O.)), ((Allain, H.)), ((Vasar, E.)), ((Bourin, M.)) | journal=European Neuropsychopharmacology: The Journal of the European College of Neuropsychopharmacology | title=Role of dopaminergic and serotonergic systems on behavioral stimulatory effects of low-dose alprazolam and lorazepam | volume=11 | issue=1 | pages=41–50 | date= February 2001 | issn=0924-977X | doi=10.1016/s0924-977x(00)00137-1}}</ref> This results in effects including reduced anxiety, muscle relaxant, antidepressant and anticonvulsant activity. The GABA chemical and receptor system mediates inhibitory or calming effects of alprazolam on the nervous system. Binding of alprazolam to the GABA<sub>A</sub> receptor, a chloride ion channel, enhances the effects of GABA, a neurotransmitter. When GABA binds the GABA<sub>A</sub> receptor the channel opens and chloride enters the cell which makes it more resistant to depolarization. Therefore, alprazolam has a depressant effect on synaptic transmission to reduce anxiety.<ref>{{cite book | vauthors=((Hitchings, A.)), ((Lonsdale, D.)), ((Burrage, D.)), ((Baker, E.)) | date= 2014 | title=Top 100 drugs: clinical pharmacology and practical prescribing | publisher=Churchill Livingstone | isbn=9780702055164}}</ref>
Alprazolam causes a marked suppression of the hypothalamic-pituitary-adrenal axis. Administration of alprazolam has been demonstrated to elicit an increase in striatal [[dopamine]] concentrations.<ref name="Bentue-Ferrer2001">{{cite journal | vauthors=((Bentué-Ferrer, D.)), ((Reymann, J. M.)), ((Tribut, O.)), ((Allain, H.)), ((Vasar, E.)), ((Bourin, M.)) | journal=European Neuropsychopharmacology: The Journal of the European College of Neuropsychopharmacology | title=Role of dopaminergic and serotonergic systems on behavioral stimulatory effects of low-dose alprazolam and lorazepam | volume=11 | issue=1 | pages=41–50 | date= February 2001 | issn=0924-977X | doi=10.1016/s0924-977x(00)00137-1}}</ref> This results in effects including reduced anxiety, muscle relaxant, antidepressant and anticonvulsant activity. The GABA chemical and receptor system mediates inhibitory or calming effects of alprazolam on the nervous system. Binding of alprazolam to the GABA<sub>A</sub> receptor, a chloride ion channel, enhances the effects of GABA, a neurotransmitter. When GABA binds the GABA<sub>A</sub> receptor the channel opens and chloride enters the cell which makes it more resistant to depolarization. Therefore, alprazolam has a depressant effect on synaptic transmission to reduce anxiety.<ref>{{cite book | vauthors=((Hitchings, A.)), ((Lonsdale, D.)), ((Burrage, D.)), ((Baker, E.)) | date= 2014 | title=Top 100 drugs: clinical pharmacology and practical prescribing | publisher=Churchill Livingstone | isbn=9780702055164}}</ref>