Extinction is the learned inhibition of retrieval. Recently it was shown that a brief exposure to a novel environment enhances the extinction of contextual fear in rats, an effect explainable by a synaptic tagging-and-capture process. Here we examine whether this also happens with the extinction of another fear-motivated task, inhibitory avoidance (IA), and whether it depends on dopamine acting on D1 or D5 receptors. Rats were trained first in IA and then in extinction of this task. The retention of extinction was measured 24 h later. A 5-min exposure to a novel environment 30 min before extinction training enhanced its retention. Right after exposure to the novelty, animals were given bilateral intrahippocampal infusions of vehicle (VEH), of the protein synthesis inhibitor anisomycin, of the D1/D5 dopaminergic antagonist SCH23390, of the PKA inhibitor Rp-cAMP or of the PKC inhibitor Gö6976, and of the PKA stimulator Sp-cAMP or of the PKC stimulator PMA. The novelty increased hippocampal dopamine levels and facilitated the extinction, which was inhibited by intrahippocampal protein synthesis inhibitor anisomysin, D1/D5 dopaminerdic antagonist SCH23390, or PKA inhibitor Rp-cAMP and unaffected by PKC inhibitor Gö6976; additionally, the hippocampal infusion of PKA stimulator Sp-cAMP reverts the effect of D1/D5 dopaminergic antagonist SCH 23390, but the infusion of PKC stimulator PMA does not. The results attest to the generality of the novelty effect on fear extinction, suggest that it relies on synaptic tagging and capture, and show that it depends on hippocampal dopamine D1 but not D5 receptors.dopamine | inhibitory avoidance | modulation of extinction | novelty | behavioral tagging and capture F rey and Morris (1, 2) described the enhancing influence of neuronal plastic processes [long-term potentiation (LTP) or long-term depression (LTD)] generated at one set of hippocampal synapses on LTP and LTD generated at other synapses. This influence is explainable by interactions between new proteins, called plasticity-related proteins (PRPs), at the two sets of synapses; the PRPs that tag one of them can be captured by those of others and enhance their responsiveness (3-5). Many memories rely on hippocampal LTP and LTD (1, 2, 6-11), and the "synaptic tagging-and-capture" process has been applied to the explanation of interactions between concurrent memories (11-13), among which are novelty and fear acquisition (12,14) and novelty and fear extinction (15, 16). Exposure to novelty [an open field (OF) in which they had never been before] involves two consecutive processes: its detection, which is very brief (seconds), and the immediately ensuing habituation (17), which lasts much longer; both rely on hippocampal LTD (18). With a relatively restricted time window before and/or after an extinction trial, novelty can enhance the extinction of contextual fear conditioning (CFC) lastingly (15,16). This is obviously of potential importance for exposure therapy (18-21).In rodents, the exploration of a novel environment, object, ...
It is known from previous research that physical exercise prevents long-term memory deficits induced by maternal deprivation in rats. But we could not assume similar effects of physical exercise on short-term memory, as short- and long-term memories are known to result from some different memory consolidation processes. Here we demonstrated that, in addition to long-term memory deficit, the short-term memory deficit resultant from maternal deprivation in object recognition and aversive memory tasks is also prevented by physical exercise. Additionally, one of the mechanisms by which the physical exercise influences the memory processes involves its effects attenuating the oxidative damage in the maternal deprived rats' hippocampus and prefrontal cortex.
Maternal deprivation (MD) in early life affects the development of the brain, causing cognitive losses in adulthood. Oxidative imbalance may be one of the factors that trigger these deficits. Therapies with antioxidant components, like green tea from Camellia sinensis (GT) has been used to treat or prevent memory deficits in a variety of conditions related to oxidative stress. Here we demonstrate that memory deficits caused by MD can be prevented by GT antioxidant activity in hippocampus. Pregnant female rats were used. Her puppies were submitted to MD and intake of GT. Recognition and aversive memory were evaluated, as well as hippocampal oxidative status. Data showed that MD prejudice short and long-term recognition and aversive memory and that GT protected memory. Hippocampal reactive oxygen species levels were increased in MD rats; this increase was avoided by GT supplementation. GSH was decreased on hippocampus MD rats. GT did not avoid GSH decrease, but promote the increase of total antioxidant capacity in MD rats' hippocampus. In conclusion, GT protects against memory deficits related to MD, and one of the implicated mechanism seems to be the antioxidant effects of GT.
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