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  • Publicado : 27 de noviembre de 2009
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“Serotonin has effects throughout the brain and acts to decrease
impulsivity and aggression. Norepinephrine commonly acts to stimulate
neuronal systems and is involved in alerting responses. Dopamine helps regulate pleasure and assists in reward mechanisms. All of these neurochemicals are distributed widely throughout the brain and have many, sometimes differing, impactsupon behavior and emotion.”


“The SSRI’s primary mechanism of action is believed to be blockade of
the serotonin transporter that brings released serotonin back into the neuron. This results in elevated synaptic serotonin levels almost immediately.”


“Fluoxetine, sertraline, and fluvoxamine all have FDA approval in some anxiety disorders. Benzodiazepinesare used frequently in adults with anxiety disorders. These agents act on chloride channels in similar ways to that of ethanol. Unfortunately, many youth experience a disinhibition on benzodiazepines. Therefore, the use of benzodiazepines in youth is infrequent. Buspirone acts predominantly upon presynaptic serotonin receptors. This mechanism has been exploited to treat anxiety disorders and toaugment the actions of antidepressants.”


“The older antipsychotics frequently are referred to as typical antipsychotics.The major effect of these agents is in the blockade of dopaminergic neurotransmission. This is primarily at the dopamine 2 receptor. The atypical antipsychotics block dopamine in different ways. Some agents (eg, risperidone, olanzapine, and ziprasidone) blockdopamine receptors tightly, with low dissociation constants. Quetiapine binds loosely for short periods of time. Aripiprazole is considered a partial dopamine agonist”


“Among the most widely studied augmentation agents is lithium augmentation (>600 mg/d) of tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and selectiveserotonin reuptake inhibitors (SSRIs)”


“Evidence from preclinical studies suggests that bipolar
disorder may share some biologic mechanisms with epilepsy. It has been
hypothesized that an imbalance between the excitatory (primarily glutamate) and inhibitory (mainly c-aminobutyric acid [GABA]) amino acids and dysfunctional cation pumps (sodium and calcium channels) may be involvedin the pathogenesis of both epilepsy and bipolar disorder [1].”


“Atypical antipsychotic agents have higher affinity to 5-HT2A receptors than to dopamine D2 receptors, and it has been argued that this unique property gives these medications a lower propensity toward EPS and increased efficacy against negative symptoms [2,3].”


“Persistent enhancement ofstress reactivity could explain the findings of
heightened HPA-axis activity, including elevated peripheral cortisol [1,19,20] and central corticotrophin-releasing hormone [21,22], in some depressed patients. The interplay of genetic predisposition and early adversity then would lead to a vulnerable phenotype. Moreover, this interplay is likely to result in heightened stress reactivity by atleast two mechanisms. The first would be the biologic diathesis. The second would be a pattern of maladaptive responses to stressors. For example, withdrawal from a stressor would be highly adaptive in the case of early abuse. That same behavior manifested in adult life would be equally maladaptive. These factors, then, would combine to elevate risk for


Fig. 2.Cell surface receptors, such as norepinephrine ß receptors, are coupled to stimulatory G (Gs) proteins. (1) On transmitter binding, Gs activates adenylate cyclase (AC), catalyzing the formation of cyclic AMP from ATP. (2) Cyclic AMP is degraded to AMP by phosphodiesterases (PDE), which inactivate the cyclic AMP signal. (3) Cyclic AMP binds to the regulator subunits (R) of protein kinase A (PKA),...
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