The subiculum (SUB) 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. Previous research has shown exposure to acute stress dramatically alters synaptic plasticity within the hippocampus proper. 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 Cornu Ammonis 1-SUB 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 CORT treatment. Measurements of plasma CORT confirmed similar levels of circulating hormone in animals exposed to either acute stress or CORT treatment. The disruptive effects of acute stress on both short- and long-term forms 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 necessary but not sufficient for mediating these alterations.

Long-term potentiation (LTP) of excitatory synaptic transmission in the hippocampus has been investigated in great detail over the past 40 years. Where and how LTP is actually expressed, however, remain controversial issues. Considerable evidence has been offered to support both pre- and postsynaptic contributions to LTP expression. Though it is widely held that postsynaptic expression mechanisms are the primary contributors to LTP expression, evidence for that conclusion is amenable to alternative explanations. Here, we briefly review some key contributions to the ‘locus’ debate and describe data that support a dominant role for presynaptic mechanisms. Recognition of the state-dependency of expression mechanisms, and consideration of the consequences of the spatial relationship between postsynaptic glutamate receptors and presynaptic vesicular release sites, lead to a model that may reconcile views from both sides of the synapse.

The Cornu Ammonis-1 (CA1) subfield and subiculum (SUB) serve as major output structures of the hippocampal formation. Exploring forms of synaptic plasticity simultaneously within these two output regions may improve understanding of the dynamics of hippocampal circuitry and information transfer between hippocampal and cortical brain regions. Using a novel dual-channel electrophysiological preparation in urethane-anesthetized adult male Sprague-Dawley rats in vivo, we examined the effects of acute restraint stress (30 min) on short- and long-term forms of synaptic plasticity in both CA1 and SUB by stimulating the CA3 region. Paired-pulse facilitation was disrupted in SUB but not CA1 in the dual-channel experiments following exposure to acute stress. Disruptions in CA1 PPF were evident in subsequent single-channel experiments with a more anterior recording site. Acute stress disrupted long-term potentiation induced by high-frequency stimulation (10 bursts of 20 pulses at 200 Hz) in both CA1 and SUB. Low-frequency stimulation (900 pulses at 1 Hz) did not alter CA1 plasticity while a late-developing potentiation was evident in SUB that was disrupted following exposure to acute stress. These findings highlight differences in the sensitivity to acute stress for distinct forms of synaptic plasticity within synapses in hippocampal output regions. The findings are discussed in relation to normal and aberrant forms of hippocampal-cortical information processing.

Understanding the mechanisms by which long-term synaptic plasticity is expressed remains an important objective in neuroscience. From a physiological perspective, the strength of a synapse can be considered a consequence of several parameters including the probability that a presynaptic action potential (AP) evokes the release of neurotransmitter, the mean number of quanta of transmitter released when release is evoked, and the mean amplitude of a postsynaptic response to a single quantum. Various methods have been employed to estimate these quantal parameters from electrophysiological recordings; such “quantal analysis” has been used to support competing accounts of mechanisms of expression of long-term plasticity. Because electrophysiological recordings, even with minimal presynaptic stimulation, can reflect responses arising at multiple synaptic sites, these methods are open to alternative interpretations. By combining intracellular electrical recording with optical detection of transmission at individual synapses, however, it is possible to eliminate such ambiguity. Here, we describe methods for such combined optical and electrical monitoring of synaptic transmission in brain slice preparations and illustrate how quantal analyses thereby obtained permit more definitive conclusions about the physiological changes that underlie long-term synaptic plasticity.

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