Psychopharmacology
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Neuropathic pain is associated with a number of disease states of diverse aetiology that can share common pathophysiological mechanisms. Antiepileptic drugs modulate ion channel function and antidepressants increase extracellular monoamine levels, and both drug classes variously attenuate signs and symptoms of neuropathic pain. Thus, coadministration of the antiepileptic gabapentin and the antidepressant venlafaxine may provide superior pain relief to administration of either drug alone. ⋯ Venlafaxine compromises the antiallodynic effects of coadministered gabapentin most probably as consequence-increased diuresis.
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Increases in depressive symptoms during smoking cessation have been associated with risk for relapse. Several studies have linked plasma levels of cortisol and dehydroepiandrosterone (DHEA) or DHEA-sulfate (DHEAS) to depressive symptoms. ⋯ A decrease in the plasma DHEA/cortisol ratio during 8 days of smoking abstinence was associated with relapse over the following week. Further research is needed to fully characterize sex-specific relationships between abstinence-induced changes in neuroactive steroid levels, depressive or withdrawal symptoms, and relapse. Such research may lead to new interventions for refractory smoking dependence.
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Randomized Controlled Trial
Dose-dependent retrograde facilitation of verbal memory in healthy elderly after acute oral lorazepam administration.
Retrograde facilitation (RF) refers to a paradoxical phenomenon in which recall of information presented before acute administration of agents generally associated with anterograde amnestic and sedative effects, such as benzodiazepines, is enhanced relative to a placebo condition. However, it is unclear whether this effect occurs in elderly individuals and if it is influenced by plasma drug levels, baseline cognitive function, or genetic factors such as the APOE e-4 allele, that may modulate drug-induced cognitive toxicity. ⋯ In healthy elderly, acute oral lorazepam administration resulted in dose-dependent RF, which was associated with greater anterograde amnestic and sedative effects.
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Platelet monoamine oxidase (MAO) activity reflects serotonergic functioning associated with impulsive behaviour, but the significance of these associations to real-life impulsive behaviour in healthy subjects is not clear. ⋯ This study demonstrates different expressions of functional and dysfunctional impulsivity in behaviour. While platelet MAO activity is lower in alcohol-related risky behaviour, non-alcohol-related self-acknowledged risky behaviour is related to higher platelet MAO activity. Thus, deviance towards lower as well as higher end of central serotonergic functioning may lead to impulsive behaviour. While self-reported impulsivity did not correlate with MAO activity, both MAO activity and impulsivity were related to risky behaviour.
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Although convergent evidence exists for a role of glutamate in the regulation of anxiety, the involvement of specific glutamate receptor subtypes has yet to be defined. ⋯ These data along with those in the literature suggest that AMPA and/or kainate receptor blockade may be an important component to producing anxiolytic-like effects and may therefore be a target for compounds with efficacy in the therapeutic treatment of anxiety disorders.