Data on the influences of stress on the function of long-term synaptic plasticity are analyzed. Using longterm potentiation (LTP) as an example, stress has been shown to have both stimulatory and inhibitory influences on the effectiveness of the induction of long-term modifications, the effect depending on the nature, duration, and intensity of the stress, the observation time point, the brain structure being studied, and, thus, the involvement in the stress response of the different mechanisms underlying LTP. Stress-induced increases in glucocorticoid levels did not obligately correlate with changes in long-term plasticity, while application of corticosterone in vivo and in vitro could lead to both activation and inhibition of LTP. Existing data provide evidence that changes in LTP are determined by the ratio of mineralocorticoid and glucocorticoid receptors, activation of the latter not so much impairing the mechanisms of generation as increasing the threshold of induction of LTP, regulating the metaplasticity of synapses. The unpredictability of the effects of stress is related in particular to the involvement of other transmitter systems regulating metaplasticity whose actions depend on the animal's individual experience in the stress reaction. The range of individual differences stimulates the ongoing search for significant factors determining the stress reactivity of longterm plasticity underlying stress resistance or susceptibility to its pathological consequences. Differences in the processing of signals arriving at neurons and their molecular mediation may constitute such a factor.
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