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There is increasing evidence that oxytocin is involved in learning and memory process. This study investigated the effects of blockade of oxytocin receptors using the selective oxytocin receptor antagonist atosiban (ATO) on contextual fear memory consolidation and reconsolidation in male rats. Post-training injections of different doses of ATO (1, 10, 100 or 1000 µg/kg) impaired the 48 h retention performance in a dose-dependent manner. The same doses of ATO following memory reactivation did not impair subsequent expression of contextual fear memories which formed under low or high shock intensities and tested 24 h or one week following memory reactivation. Also, no effect was found when ATO was administrated in the absence of memory reactivation. Our finding is the first report that indicates endogenous oxytocin released during training play an important role in the consolidation, but not reconsolidation of contextual fear memory in rats. [ABSTRACT FROM AUTHOR]

Abstract: Granisetron, a serotonin 5-HT3 receptor antagonist, widely used as an antiemetic drug following chemotherapy, has been found to improve learning and memory. In this study, effects of granisetron on spatial recognition memory and fear memory and the involvement of nitric oxide (NO) have been determined in a Y-maze and passive avoidance test. Granisetron (3, 10mg/kg, intraperitoneally) was administered to scopolamine-induced memory-impaired mice prior to acquisition, consolidation and retrieval phases, either in the presence or in the absence of a non-specific NO synthase inhibitor, l-NAME (3, 10mg/kg, intraperitoneally); a specific inducible NO synthase (iNOS) inhibitor, aminoguanidine (100mg/kg); and a NO precursor, l-arginine (750mg/kg). It is demonstrated that granisetron improved memory acquisition in a dose-dependent manner, but it was ineffective on consolidation and retrieval phases of memory. The beneficial effect of granisetron (10mg/kg) on memory acquisition was significantly reversed by l-NAME (10mg/kg) and aminoguanidine (100mg/kg); however, l-arginine (750mg/kg) did not potentiate the effect of sub-effective dose of granisetron (3mg/kg) in memory acquisition phase. It is concluded that nitric oxide is probably involved in improvement of memory acquisition by granisetron in both spatial recognition memory and fear memory. This article is part of a Special Issue entitled The Cognitive Neuroscience. [Copyright &y& Elsevier]

Abstract: It was recently found that temporary inactivation of the dorsal hippocampus with lidocaine impaired fear memory, whereas temporary inactivation of the ventral hippocampus did not. These site-specific deficits, however, may have resulted from disruption of axonal signals arriving from structures outside of the hippocampus, or from disruption of axons that pass through the hippocampus entirely. This is problematic because the hippocampus receives extensive afferent input from both the amygdala and the septum, which also play very important roles in fear and fear memory. To mitigate this problem, rats were infused with the GABAA receptor agonist muscimol, into either the dorsal or the ventral hippocampus, just after an “acquisition” session in which the rats were shocked from an electrified probe. A “retention” test in the same apparatus was conducted 24h later, when the hippocampus was no longer inactivated, and the probe was no longer electrified. Dorsal hippocampal inactivation just after acquisition impaired conditioned fear behavior (probe avoidance) during the retention test, whereas ventral hippocampal inactivation after acquisition did not. However, muscimol inactivation of the ventral hippocampus during an “acquisition” session selectively impaired unconditioned fear behavior, replicating earlier findings with lidocaine, a sodium channel blocker. Because muscimol hyperpolarizes neurons through a post-synaptic, GABAA receptor-mediated increase of chloride conductance–whereas lidocaine produces indiscriminate disruption of all axonal signalling–its effects are more likely to be restricted to intrinsic neurons within the area of infusion. These results provide strong evidence that afferent input from brain structures located outside of the hippocampus is not responsible for the differential effects of dorsal and ventral hippocampal inactivation on fear memory. [Copyright &y& Elsevier]

Abstract: The roles of the dorsal and ventral hippocampus in fear and memory are unclear. This study examined the effects of temporary inactivation of the dorsal or ventral hippocampus on unconditioned and conditioned fear, using the shock-probe test. In , rats received either dorsal or ventral hippocampal infusions of lidocaine or saline, before exposure to an electrified shock-probe (). In , rats received lidocaine or saline infusions after exposure to the shock-probe (). In both experiments, a retention test in the same apparatus was given 24 h later, at which time the hippocampus was no longer inactivated, and the probe was disconnected from the shock-source. Because ventral hippocampal inactivation impaired fear behaviour during acquisition, and dorsal hippocampal inactivation impaired fear behaviour (probe avoidance) during retention, we concluded that 1) the ventral hippocampus plays a role in the expression of untrained fear reactions whereas 2) the dorsal hippocampus plays a role in encoding memory of the fearful experience. [Copyright &y& Elsevier]

Abstract: Mother–infant attachment is facilitated in altricial rodents through unique neural mechanisms that include impaired neonatal fear conditioning until the time that pups first begin to leave the nest (sensitive period). Here, we confirmed the developmental emergence of odor fear conditioning in neonatal rat pups, and examined synaptic plasticity of inputs to the basolateral amygdala in vitro. Coronal slices through the amygdala were obtained from sensitive (<10 days) and post-sensitive (>10, <19 days) period pups. Field potentials were recorded in the basolateral amygdala in response to stimulation of either the external capsule (neocortical inputs) or fibers from the cortical nucleus of the amygdala (olfactory inputs). The effects of tetanic stimulation were examined in each pathway. In both pathways, tetanic stimulation induce significant long-term synaptic plasticity in post-sensitive period pups, but no significant plasticity in sensitive period pups incapable of learning odor aversions. GABAA receptor blockade in post-sensitive period slices reverts synaptic plasticity to sensitive period characteristics. The results suggest that sensitive period deficits in fear conditioning may be related to impaired amygdala synaptic plasticity and the immature state of GABAergic inhibition and/or its modulation in the neonatal amygdala. [Copyright &y& Elsevier]

• Starting the KD on postnatal day (P) 21 in male mice reduced their body weight and lean mass. • KD-fed mice were hypoactive in the open field. • KD fed mice show deficits in spatial learning. • KD increases contextual and cued-based freezing behavior. The ketogenic diet (KD) is a non-pharmacological treatment for specific types of epilepsy. In addition, it has been shown to be effective in mitigating other neurologic disorders. The KD is also effective in reducing body mass, leading to an increase in use by the general population for weight loss. As the popularity of the clinical and general use of the KD has increased, it is important to develop adequate mouse models to better understand the effects of the KD in both normal and diseased states. Many times, the best outcome for disorders treatable with the KD would be achieved by commencing treatment in early life. Few studies have evaluated the cognitive effect of starting the KD in early life. To better understand these effects, male C57BL6/J mice were placed on a KD from postnatal day (P) 21 through young adulthood (~P90). KD-fed mice had increased blood ketone levels, reduced blood glucose, and reduced weight gain versus mice fed a control diet (CD). The weight loss in the KD-fed mice was not accompanied by a change in body fat percentage, suggesting that there was a loss of lean mass. Behavioral testing began on P60 while the mice were still on the diet. KD-fed mice were hypoactive with CD-fed mice. In the Morris water maze, KD-fed mice showed decreased path efficiency, suggesting a spatial learning deficits. No differences were observed in spatial memory or in novel object recognition memory. In a contextual and conditioned fear paradigm, the KD-fed mice had an increase in freezing behavior. These data suggest that early-life exposure to a KD leads to impaired body composition and long-term cognitive changes. [ABSTRACT FROM AUTHOR]