In contrast, pre-training or pre-test NPS injections were ineffective, suggesting that NPS had no Daporinad solubility dmso effect on IA
memory acquisition or recall. Peripheral administration of a synthetic NPSR antagonist attenuated NPS-induced IA memory enhancement, showing pharmacological specificity. NPS also enhanced hippocampal-dependent non-aversive memory in the novel object recognition task. In contrast, NPSR knockout mice displayed deficits in IA memory, novel object recognition, and novel place or context recognition, suggesting that activity of the endogenous NPS system is required for memory formation. Blockade of adrenergic signaling by propranolol attenuated NPS-induced memory enhancement in the IA task, indicating involvement of central MK1775 noradrenergic systems. These results provide evidence for a facilitatory role of NPS in long-term memory, independent of memory content, possibly by acting as a salience signal or as an arousal-promoting factor. Neuropsychopharmacology
(2011) 36, 744-752; doi:10.1038/npp.2010.207; published online 8 December 2010″
“Although chemosensory signals generated by mouse pups may trigger maternal behavior of females, the mechanism for detection of these signals has not been fully defined. As some odorant receptors are coupled to the type 3 adenylyl cyclase (AC3), we evaluated the role of AC3 for maternal behavior using AC3(-/-) female mice. Here, we report that maternal behavior is impaired in virgin and postpartum AC3(-/-) mice. Female AC3(-/-) mice failed the pup retrieval Sinomenine assay, did not construct well-defined nests, and did not exhibit maternal aggression.
Furthermore, AC3(-/-) females could not detect odorants or pup urine in the odorant habituation test and were unable to detect pups by chemoreception. In contrast to wild-type mice, AC activity in main olfactory epithelium (MOE) preparations from AC3(-/-) female mice was not stimulated by odorants or pheromones. Moreover, odorants and pheromones did not evoke electro-olfactogram (EOG) responses in the MOE of AC3(-)/(-) female mice. We hypothesize that the detection of chemical signals that trigger maternal behavior in female mice depends upon AC3 in the MOE. Neuropsychopharmacology (2011) 36, 772-781; doi:10.1038/npp.2010.211; published online 8 December 2010″
“Chronic methamphetamine (meth) abuse can lead to persisting cognitive deficits. Here, we utilized a long-access meth self-administration (SA) protocol to assess recognition memory and metabotropic glutamate receptor (mGluR) expression, and the possible reversal of cognitive impairments with the mGluR5 allosteric modulator, 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB). Male, Long-Evans rats self-administered i.v. meth (0.02 mg/infusion) on an schedule of reinforcement or received yoked-saline infusions.