Acute stress, but not corticosterone injections, disrupts both short- and long-term forms of synaptic plasticity in rat dorsal subiculum via glucocorticoid receptor activation

Abstract

The subiculum serves as the major output structure of the hippocampus; therefore, exploring synaptic plasticity within this region is of great importance for understanding the dynamics of hippocampal circuitry and hippocampal-cortical interactions. Exposure to acute stress dramatically alters synaptic plasticity within the hippocampal formation. Using in vivo electrophysiological recordings in urethane-anesthetized adult male Sprague-Dawley rats, we tested the effects of either acute restraint stress (30 min) or corticosterone (CORT) injections (3 mg/kg; s.c.) on short- and long-term forms of synaptic plasticity in the CA1-subiculum pathway. Paired-pulse facilitation and two forms of long-term plasticity (long-term potentiation and late-developing potentiation) were significantly reduced after exposure to acute stress but not acute CORT treatment. Measurements of plasma CORT confirmed statistically similar levels of circulating hormone in animals exposed to either acute stress or acute CORT treatment. The disruptive effects of acute stress on both short- and long-term form of synaptic plasticity are mediated by glucocorticoid receptor (GR) activation as these disruptions were blocked by pre-treatment with the selective GR antagonist RU38486 (10 mg/kg; s.c.). The present results highlight the susceptibility of subicular plasticity to acute stress and provide evidence that GR activation is a necessary but not a sufficient physiological parameter for mediating these alterations.