Recognition memory provides the ability to distinguish familiar from novel objects and places, and is important for recording and updating events to guide appropriate behavior. The hippocampus (HPC) and medial prefrontal cortex (mPFC) have both been implicated in recognition memory, but the nature of HPC-mPFC interactions, and its impact on local circuits in mediating this process is not known. Here we show that novelty discrimination is accompanied with higher theta activity (4-10 Hz) and increased c-Fos expression in both these regions. Moreover, theta oscillations were highly coupled between the HPC and mPFC during recognition memory retrieval for novelty discrimination, with the HPC leading the mPFC, but not during initial learning. Principal neurons and interneurons in the mPFC responded more strongly during recognition memory retrieval compared with learning. Optogenetic silencing of HPC input to the mPFC disrupted coupled theta activity between these two structures, as well as the animals' (male Sprague Dawley rats) ability to differentiate novel from familiar objects. These results reveal a key role of monosynaptic connections between the HPC and mPFC in novelty discrimination via theta coupling and identify neural populations that underlie this recognition memory-guided behavior.

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Stroke is one of the leading causes of death and adult disability globally, representing one of the highest burdens of disease worldwide. Recent advancements of neuromodulation techniques emerge as promising tools for enhancing stroke recovery, such as transcranial electric stimulation and transcranial magnetic stimulation, which can induce short- and long-term changes of synaptic excitability to restore the impaired functions in stroke patients. The review focuses on discussing the neuroplastic mechanisms of those brain stimulation techniques in stroke rehabilitation, also including some new options for neuromodulation which have great potential in stroke rehabilitation, such as optogenetic stimulation and environmental stimulation. In general, these techniques allow the excitation and synchronization of the neural activity after stroke, which could potentially induce long-term potentiation. As a result, the neuroplastic effect can lead to better functional connection in the brain network in assisting stroke recovery. Future directions include the clarification of the pathways of synaptic plasticity in the whole brain network following neuromodulation after stroke, and investigation of the different roles of distinctive cell populations in neural plasticity enhancement. Additional studies are essential for developing standard protocols in neuromodulation based on a better understanding of the molecular and cellular processes for the ultimate optimization of clinical efficacy.