Previously we have demonstrated that rapidly presented sensory stimulation (visual or auditory) can induce long-lasting increases in sensory evoked potentials recorded from the human cortex. Long-term potentiation was suggested as the underlying mechanism of these increases. In the present experiment, we applied the same visual paradigm to anesthetized rats to investigate the properties and mechanisms of this effect. Our results indicated that visual evoked responses were significantly enhanced for at least 1 h and, when followed, up to 5 h after the presentation of a 'photic tetanus.' Furthermore, the potentiation was N-methyl-D-aspartate receptor-dependent and cortically generated. This type of sensory long-term potentiation may underlie perceptual learning, and serves as a model system for investigating sensory-evoked plasticity.

Performance in hippocampus-dependent and other tasks can be improved by exposure to an enriched environment (EE), but the physiological changes in neural function that may mediate these effects are poorly understood. To date, there have been conflicting reports regarding potential mechanisms, such as an increase in basal synaptic transmission, an increase in cell excitability, or altered synaptic plasticity. Here, we reexamined in freely moving animals the conditions under which varying degrees of EE exposure might lead to increases in synaptic or neural function in the dentate gyrus of the hippocampus. Adult male Sprague-Dawley rats were chronically implanted with stimulating and recording electrodes in the perforant path and dentate gyrus, respectively, and housed singly in standard cages. After stable recordings were established for field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs), the effects of various degrees of periodic novel environment exposure for 19 days were assessed. Exposure to an EE increased fEPSPs, but only when animals were kept in nominally low-stress housing conditions. An increase in granule-cell excitability, as evidenced by PS increases, was induced by all environmental treatments with the greatest effect being induced by overnight EE exposure. EE exposure did not change the level of long-term potentiation (LTP) induced by a moderate high-frequency tetanus, but continued EE exposure post-tetanus produced a significantly faster decay of LTP relative to control animals. These results suggest that, in adult animals, EE exposure may augment hippocampal information processing, but may also speed turnover of information in the hippocampus during the maintenance period.

Exposure to an enriched environment (EE) is beneficial to the structure and function of the brain. The added sensory, social, and spatial complexity of the EE also improves cognitive functions such as memory in both healthy brains and damaged or diseased brains, yet the underlying neural mechanisms of these cognitive improvements are poorly understood. In particular, studies that have examined the effects of EE on cellular function in the hippocampus, a structure critical for memory storage, have produced somewhat confusing results. Experiments performed in ex vivo hippocampal slices have reported a variety of EE effects on synaptic transmission and plasticity in both CA1 and the dentate gyrus. However, together with data from in vivo recordings made during and after the EE treatment, the overall results suggest an evolution of changes in neuronal function in the hippocampus, whereby there is an early transient increase in cell activity and plasticity that gives rise to more subtle long-term enhancements in cellular and network function that may contribute to enhanced hippocampus-dependent cognition.

The mechanisms governing how the hippocampus selects neurons to exhibit place fields are not well understood. A default assumption in some previous studies was the uniform random draw with replacement (URDWR) model, which, theoretically, maximizes spatial "pattern separation", and predicts a Poisson distribution of the numbers of place fields expressed by a given cell per unit area. The actual distribution of mean firing rates exhibited by a population of hippocampal neurons, however, is approximately exponential or log-normal in a given environment and these rates are somewhat correlated across multiple places, at least under some conditions. The advantage of neural activity-dependent immediate-early gene (IEG) analysis, as a proxy for electrophysiological recording, is the ability to obtain much larger samples of cells, even those whose activity is so sparse that they are overlooked in recording studies. Thus, a more accurate representation of the activation statistics can potentially be achieved. Some previous IEG studies that examined behavior-driven IEG expression in CA1 appear to support URDWR. There was, however, in some of the same studies, an under-recruitment of dentate gyrus granule cells, indicating a highly skewed excitability distribution, which is inconsistent with URDWR. Although it was suggested that this skewness might be related to increased excitability of recently generated granule cells, we show here that CA1, CA3, and subiculum also exhibit cumulative under-recruitment of neurons. Thus, a highly skewed excitability distribution is a general principle common to all major hippocampal subfields. Finally, a more detailed analysis of the frequency distributions of IEG intranuclear transcription foci suggests that a large fraction of hippocampal neurons is virtually silent, even during sleep. Whether the skewing of the excitability distribution is cell-intrinsic or a network phenomenon, and the degree to which this excitability is fixed or possibly time-varying are open questions for future studies. © 2016 Wiley Periodicals, Inc.

Individuals with schizophrenia display a number of structural and cytoarchitectural alterations in the hippocampus, suggesting that other functions such as synaptic plasticity may also be modified. Altered hippocampal plasticity is likely to affect memory processing, and therefore any such pathology may contribute to the cognitive symptoms of schizophrenia, which includes prominent memory impairment. The current study tested whether prenatal exposure to infection, an environmental risk factor that has previously been associated with schizophrenia produced changes in hippocampal synaptic transmission or plasticity, using the maternal immune activation (MIA) animal model. We also assessed performance in hippocampus-dependent memory tasks to determine whether altered plasticity is associated with memory dysfunction. MIA did not alter basal synaptic transmission in either the dentate gyrus or CA1 of freely moving adult rats. It did, however, result in increased paired-pulse facilitation of the dentate gyrus population spike and an enhanced persistence of dentate long-term potentiation. MIA animals displayed slower learning of a reversed platform location in the water maze, and a similarly slowed learning during reversal in a spatial plus maze task. Together these findings are indicative of reduced behavioral flexibility in response to changes in task requirements. The results are consistent with the hypothesis that hippocampal plasticity is altered in schizophrenia, and that this change in plasticity mechanisms may underlie some aspects of cognitive dysfunction in this disorder.