Entorhinal-hippocampal (EC-HIP) circuits are major synaptic organizations involved in episodic memory that is acquired, stored and retrieved through its auto-association network. Neurons in layer II of the entorhinal cortex send their direct projections to dentate gyrus, while the EC layer III neurons send their fibers directly to CA1, through perforant path. The EC-HIP synaptic connections have been believed to be responsible for object recognition memory (ORM) in animals. In this report, ORM test was first used to examine whether, if any, how pain can influence upon recollection of episodic memory? Then multi-electrode array recording technique and 2D-current source density imaging were used to check whether there are spatial and temporal changes in EC-HIP circuits in the hippocampal slices? Finally, the possible mechanisms underlying nociception-associated spatial and temporal changes in EC-HIP circuits were studied. Our major results are as follows: (1) rat’s OBM could be impaired by both acute inflammatory pain and chronic neuropathic pain although there was a time difference in onset. (2) peripheral blockade or morphine suppression of nociceptive afferent impulses could prevent OBM from impairing in inflammatory pain model, but not in neuropathic pain model, suggesting a difference in the underlying mechanisms. (3) when checking the induction of long-term potentiation (LTP) and long-term depression (LTD) between inflammatory and neuropathic pain states, it was surprisingly shown that higher LTP induction was accompanied by lower LTD induction in inflammatory pain model, whereas, lower LTP induction was accompanied by higher LTD induction in neuropathic pain model. Moreover, spatial enlargement of EC-HIP synaptic network was commonly observed in both types of pain models. In conclusions: (1) persistent or chronic pain impairs episodic memory recollection in rats regardless of etiology; (2) spatially and temporally functional alterations of EC-HIP circuits may contribute to pain-associated object recognition memory impairment; (3) nociceptive pain enhances LTP with blocking LTD, whereas, neuropathic pain, like stress, enhances LTD with blocking LTP. This pain etiology-specific temporal plasticity in the hippocampal formation may shed new light on the brain mechanisms of pain comorbidities such as amnesia, anxiety and depression.