Search Results (2)

Emotionally charged distracters delay timing behavior. Increasing catecholamine levels within the prelimbic cortex has beneficial effects on timing by decreasing the delay after aversive distracters. Here we examined whether increasing catecholamine levels within the prelimbic cortex also protects against the deleterious timing delays caused by novel distracters or by familiar appetitive distracters. Rats were trained in a peak-interval procedure and tested in trials with either a novel (unreinforced) distracter, a familiar appetitive (food-reinforced) distracter, or no distracter after being locally infused with catecholamine reuptake blocker nomifensine within the prelimbic cortex. Prelimbic infusion of nomifensine did not alter timing accuracy and precision. However, it increased the delay caused by novel distracters in an inverted-U dose-dependent manner, while being ineffective for appetitive distracters. Together with previous data, these results suggest that catecholaminergic modulation of prelimbic top-down attentional control of interval timing varies with distracter’s valence: prelimbic catecholamines increase attentional control when presented with familiar aversive distracters, have no effect on familiar neutral or familiar appetitive distracters, and decrease it when presented with novel distracters. These findings detail complex interactions between catecholaminergic modulation of attention to timing and nontemporal properties of stimuli, which should be considered when developing therapeutic methods for attentional or affective disorders. Full article

Over 75% of depressed patients suffer from painful symptoms predicting a greater severity and a less favorable outcome of depression. Imaging, anatomical and functional studies have demonstrated the existence of common brain structures, neuronal pathways and neurotransmitters in depression and pain. In particular, the ascending serotonergic and noradrenergic pathways originating from the raphe nuclei and the locus coeruleus; respectively, send projections to the limbic system. Such pathways control many of the psychological functions that are disturbed in depression and in the perception of pain. On the other hand, the descending pathways, from monoaminergic nuclei to the spinal cord, are specifically implicated in the inhibition of nociception providing rationale for the use of serotonin (5-HT) and/or norepinephrine (NE) reuptake inhibitors (SSRIs, NRIs, SNRIs), in the relief of pain. Compelling evidence suggests that dopamine (DA) is also involved in the pathophysiology and treatment of depression. Indeed, recent insights have demonstrated a central role for DA in analgesia through an action at both the spinal and suprasinal levels including brain regions such as the periaqueductal grey (PAG), the thalamus, the basal ganglia and the limbic system. In this context, dopaminergic antidepressants (i.e., containing dopaminergic activity), such as bupropion, nomifensine and more recently triple reuptake inhibitors (TRIs), might represent new promising therapeutic tools in the treatment of painful symptoms with depression. Nevertheless, whether the addition of the dopaminergic component produces more robust effects than single- or dual-acting agents, has yet to be demonstrated. This article reviews the main pathways regulating pain transmission in relation with the monoaminergic systems. It then focuses on the current knowledge regarding the in vivo pharmacological properties and mechanism of action of monoaminergic antidepressants including SSRIs, NRIs, SNRIs and TRIs. Finally, a synthesis of the preclinical studies supporting the efficacy of these antidepressants in analgesia is also addressed in order to highlight the relative contribution of 5-HT, NE and DA to nociception. Full article