Different effects of ionotropic and metabotropic glutamate receptor antagonists on attention and the attentional properties of nicotine

The duration of nicotine-induced attentional enhancement in the five-choice serial reaction time task: lack of long-lasting cognitive improvement

“…The combined effect of these changes in different aspects of performance was a substantial 11.2% increase in reinforcers earned. The increase in anticipatory responding is considered to be a less robust finding because it has been observed in some, but not all, similar previous investigations Bizarro et al, 2004;Quarta et al, 2007). A drug-induced increase in general motor activity may have contributed to the improvements in response speed and reduction of omission errors, but it cannot account for the improved accuracy of stimulus detection.…”

“…Nicotine-facilitated DA release would then continue after direct effects of nicotine on its receptors ends. The finding that the N-methyl-D-aspartate receptor antagonist CPPene blocked the ability of nicotine to enhance accuracy in the 5-CSRTT supports this explanation (Quarta et al, 2007). However, mesolimbic DA seems to have little involvement in nicotine-induced attentional enhancement, which originates, at least in part, in the prefrontal cortex (Hahn et al, 2003).…”

“…Bizarro et al, 2004;Quarta et al, 2007). Initial doses of nicotine often disrupt performance by producing a general suppression and slowing of responding; just one or two doses of nicotine seem sufficient to induce tolerance to these disruptive effects and then robust improvements in accuracy, omission errors and response latencies may be seen .…”

Glutamatergic Contributions to Nicotinic Acetylcholine Receptor Agonist-Evoked Cholinergic Transients in the Prefrontal Cortex

“…Specifically, Quarta et al (2007) reported that blockade of NMDA receptor attenuated the beneficial effects of nicotine on the performance of rats tested in the fivechoice serial reaction time task. The present result that NMDA receptor stimulation is necessary for nAChR agonist-evoked cholinergic activity, combined with evidence that cholinergic inputs to the mPFC are necessary for the performance of such a task (Dalley et al, 2004), are consistent with the findings reported by Quarta et al Evidence indicating the necessity of combined activity at nAChR and ionotropic glutamate receptors for learning (Gould and Lewis, 2005) suggests that such glutamatergic-cholinergic interactions generally contribute to fundamental cognitive processes.…”

The potential of nicotinic enhancement of cognitive remediation training in schizophrenia

“…Nicotine, for example, interacts with every major neurotransmitter system in the brain (Wonnacott et al, 2006). There is indication that noradrenergic (Hahn and Stolerman, 2005) and glutamatergic (Quarta et al, 2007), but not dopaminergic (Hahn et al, 2002a(Hahn et al, , 2003 neurotransmission is involved in its attention-enhancing effects; muscarinic cholinergic and serotonergic neurotransmission in the effects on working memory (Levin et al, 2006); and GABAergic interneurons in the effects on sensory gating (Martin et al, 2004). However, more work remains to be done before there is a rationale for attempting to target specific systems with subtype-selective agonists.…”