It is generally believed that consolidation of long-term memory requires activation protein kinases, transcription genes, and new synthesis. However, little known about the signal cascades involved in extinction memory, which occurs when conditioned stimulus no longer followed by unconditioned stimulus. Here, we show for first time an intra-amygdala injection inhibitor actinomycin D at dose blocked acquisition failed to affect a learned response. Conversely, synthesis anisomycin both...

Memory consolidation is mediated by new protein synthesis. However, the transcriptional pathways induced in neurons behavioral training that activate gene responses have yet to be fully delineated. We previously shown nuclear factor κB (NF-κB) activated amygdala after fear conditioning. Here we report conditioning resulted an increase histone acetyl-transferase activity, association between NF-κB p65 and CBP, acetylated p65. Pretreating animals with deacetylase (HDAC) inhibitors prolonged...

It has been recognized that the risk of cognitive decline during aging can be reduced if one maintains strong social connections, yet neural events underlying this beneficial effect have not rigorously studied. Here, we show amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice demonstrate improvement in memory after they are cohoused with wild-type mice. The was associated increased mRNA levels BDNF hippocampus. Concomitantly, number BrdU(+)/NeuN(+) cells...

Memory extinction refers to a gradual decrease of the previously acquired response when exposed conditional stimulus without pairing with unconditional stimulus. Here we show for first time that fear training-induced phosphorylation specific substrates in rat amygdala is reduced after trials and accompanied by an increase protein level enzymatic activity calcineurin. In parallel, calcineurin inhibitors prevented extinction-induced dephosphorylation as well memory. Thus, training increased...

If fear memory is expressed by a long-term potentiation (LTP) of synaptic transmission in the amygdala, then reversal LTP (depotentiation) this area brain may provide an important mechanism for amelioration anxiety and post-traumatic stress disorder. Herein, we show that low-frequency stimulation (LFS) external capsule elicits depotentiation lateral nucleus amygdala. The induction requires activation of<i>N</i>-methyl-d-aspartate receptors voltage-dependent calcium channels but independent...

Understanding the mechanism of how fear memory can be extinguished could provide potential therapeutic strategies for treatment posttraumatic stress disorders. Here we show that infusion CB1 receptor antagonist into infralimbic (IL) subregion medial prefrontal cortex (mPFC) retarded cue-alone-induced reduction fear-potentiated startle. Conversely, cannabinoid agonist WIN55212-2 (WIN) facilitated extinction. Unexpectedly, administration WIN without cue-alone trials reduced startle...

Much evidence indicates that extinction training does not erase memory traces but instead forms inhibitory learning prevents the expression of original memory. Fear conditioning induces long-term potentiation and drives synaptic insertion AMPA receptors into amygdala. Here we show applied 1 h after reversed conditioning-induced increase in surface glutamate receptor subunit (GluR1) parallel with inhibition startle potentiation. However, if 24 training, reduced without influencing GluR1...

We have demonstrated previously that brain-derived neurotrophic factor (BDNF) signaling in the amygdala is required for consolidation of fear memory. This study designed to characterize signal cascades by which conditioning modulates transcriptional and translational expression BDNF. Real-time reverse transcription-coupled polymerase chain reaction showed a significant increase BDNF exon I- III-containing mRNA fear-conditioned rats, indicating was capable up-regulating mRNA. Bilateral...

The expression of hypoxia-inducible factor-1-alpha (HIF-1α) is upregulated in ischemic stroke, but its function still unclear. In the present study, biphasic HIF-1α was observed during 1-12 h and after 48 neurons exposed to stress vitro vivo. Treating with 2-methoxyestradiol (2ME2) 0.5 or pre-silencing small interfering RNA (siRNA) decreased brain injury, edema number apoptotic cell, downregulates Nip-like protein X (Nix) expression. Conversely, applying 2ME2 8 silencing siRNA 12...

ABSTRACT Epidemiological studies have shown that early life adverse events long‐term effects on the susceptibility to subsequent stress exposure in adolescence, but precise mechanism is unclear. In present study, mice postnatal day 21–28 were randomly assigned either a group or isolated cages for 8 weeks. The socially (SI) exhibited higher level of spontaneous locomotor activity, longer duration immobility forced swimming test (FST), significantly less prepulse inhibition (PPI) and an...

Minocycline has been shown to alleviate several neurological disorders. Unexpectedly, we found that minocycline had opposite effects on glioma cells: induced nonapoptotic cell death in cells. The was associated with the presence of autophagic vacuoles cytoplasm. autophagy confirmed by acridine orange, monodansylcadaverine (MDC) stainings vesicle formation and conversion microtubule-associated proteins light chain 3 (LC3-I) LC3-II. Pretreatment inhibitor 3-methyladenine (3-MA) suppressed...

LAMOTRIGINE (LAG) is a new anticonvulsant drug for the treatment of partial and secondarily generalized seizures. The present study was aimed at elucidating possible involvement Ca2+ channels in action LAG using whole-cell patch clamp recordings acutely dissociated amygdalar neurones. Whole-cell currents (ICa) were elicited by 200 ms step commands from −70 mV to −10 mV. Application reduced ICa an average 40.3 ± 3.2%. inhibition markedly or eliminated presence N-type channel blocker...

The actions of serotonin on rat basolateral amygdala neurons were studied with conventional intracellular recording techniques and fura-2 fluorimetric recordings. Bath application 5-hydroxytryptamine (5-HT or serotonin) reversibly suppressed the excitatory postsynaptic potential in a concentration-dependent manner without affecting resting membrane neuronal input resistance. Extracellular Ba2+ pertussis toxin pretreatment did not affect depressing effect 5-HT suggesting that it is mediated...

The cannabinoid CB1 receptor has been shown to be critically involved in the extinction of fear memory. Systemic injection a antagonist prior training blocked extinction. Conversely, administration uptake inhibitor AM404 facilitated dose-dependent manner. Here we show that bilateral infusion agonists into amygdala after memory reactivation reconsolidation measured with fear-potentiated startle. effect was and could by AM251, specific antagonist. In contrast, on no longer seen if omitted....

Docosahexaenoic acid (DHA) has been suggested to be required for neuronal development and synaptic plasticity. However, in view of the fact that DHA facilitates NMDA responses blocks K+ channels, it might predispose neurons epileptiform bursting. By using extracellular recording population spikes CA1 region rat hippocampal slices, we tested this possibility by examining effect on activity induced bicuculline or Mg2+-free medium. When stimuli were delivered Schaffer collateral/commissural...

Fear conditioning has been ascribed to presynaptic mechanisms, particularly facilitation of transmission at thalamo- and cortico-amygdala synapses. Here, by labeling surface receptors with biotin or using membrane fractionation approaches, we report that fear resulted in an increase expression GluR1 subunit α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid the amygdala, whereas total mRNA protein levels were unchanged. The control group received conditioned stimulus (CS) unconditioned...