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“Recent studies suggest that intracellular signaling pathways involving cyclic adenosine monophosphate (cAMP) may be related to fear processing and long-term memory formation. The type IV phosphodiesterase (PDE4) inhibitor rolipram prevents breakdown of cAMP, enhances long-term memory and may reduce anxiety. In the present study we investigated

the role of rolipram in the expression (0, 0.2, or 1 mg/kg), acquisition (0, 0.03, 0.2 or 1 mg/kg), and extinction (0, 0.03, 0.2, 1 mg/kg) of fear using a fear-potentiated startle paradigm in mice. It was shown that rolipram reduced the expression (Experiment 1), did not influence acquisition (Experiment 2) and disturbed U0126 chemical structure between-session extinction (Experiments 3 and 4) of fear responses to conditioned tones. Because BMS-754807 molecular weight within-session extinction was not impaired by rolipram and because low (i.e. 0.03 and 0.2 mg/kg) doses strongly affected extinction but not expression of fear, these findings suggest that the effect of rolipram on extinction is not directly dependent on its effect on fear expression. Taken together, these experiments indicate that preventing breakdown of cAMP interferes with the expression and extinction consolidation of conditioned fear. (C) 2010 Elsevier Ltd. All rights reserved.”
“Modafinil is a psychostimulant drug used widely for the treatment of narcolepsy, which also has additional

positive effects on cognition. Here, we investigate the effects of modafinil on behavioural performance and synaptic plasticity in rats. Improved acquisition in the water maze task was observed in animals that underwent chronic treatment with modafinil. We found that the distance traveled and escape latency were reduced after the first day in chronically-treated

rats, compared to controls. Importantly, swim velocity was similar for both groups, excluding pharmacological effects on motor skills. We also found that modafinil increases synaptic plasticity in the dentate gyrus of urethane-anaesthetized rats; modafinil induced a robust augmentation of the population spike, evident after application of 2 bursts of 200 Hz high-frequency stimulation. Furthermore, the modafinil-dependent enhancement of postsynaptic potentials correlated BIBW2992 in vitro selectively with theta rhythm augmentation. We propose that modafinil may facilitate hippocampal-associated spatial representation via increased theta-related hippocampal plasticity. (C) 2010 Elsevier Ltd. All rights reserved.”
“Excitotoxin induces neurodegeneration via glutamatergic activation or oxidative stress, which means that the blockade of glutamate receptors and the scavenging of free radicals are potential therapeutic targets in neurodegenerative diseases. Sinapic acid (SA) has a GABA(A) receptor agonistic property and free radical scavenging activity. We investigated the neuroprotective effects of SA on kainic acid (KA)-induced hippocampal brain damage in mice.