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L-Lactate is a positive modulator of NMDAR-mediated signaling resulting in plasticity gene induction and memory consolidation.
During the three testing days, the participants went through (1) fear acquisition, (2) stress induction and memory reactivation (or the corresponding control conditions), (3) fear extinction, reinstatement and reinstatement test.
Aβ is critical for LTP induction and memory acquisition [30].
Late-midliverstage antigens (unexposed at skinstage) however, should initially escape significant Treg induction and memory inhibition in the skinstage, and do show protectivity [17], [26], [27], [68], [346], [347] into adolescence [347].
However, it is plausible that the essential elements of these models – synaptic tagging, gene induction, and reinforcement of strengthened synapses by ongoing neuronal activity –qualitatively describe L-LTP induction and memory maintenance at cortical as well as hippocampal synapses.
GluA1 phosphorylation correlates with lowered thresholds for LTP induction and memory formation.
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Induction, specificity and memory of the immune system seem to occur following pro- and eukaryotic infections in invertebrates and vertebrates [1], [2], [3], although the proximate mechanisms might differ substantially.
Dendritic cells (DCs) play a key role in the induction of adaptive and memory immune responses.
Dendritic cells (DCs) are professional antigen-presenting cells playing a key role in the induction of adaptive and memory immune responses as well as in tolerance to self-antigens [1], [2].
Thus, we consider multiple pathways of PCB action to be involved in the induction of learning and memory disorders.
Understanding learning and the formation of complex memory requires not only the identification of mechanisms necessary for the induction and formation of memory but also the identification of mechanisms involved in the maintenance of LTM.
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