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===Theta Phase Separation===
In a framework first developed by Hasselmo and colleagues, theta phase separation implies that the theta rhythm of the hippocampus occurs in cycles and various phases of the rhythm entail encoding and retrieval as separate processes. An extra-hippocampal structure, the septum, initiates and regulates the theta rhythm and its associated memory processes. GABAergic activity within the septum inhibits certain classes of CA3 cells (a region of the hippocampus), the divide often drawn between basket cells, pyramidal cells, and interneurons, to distinguish encoding from retrieval mechanisms. The study emphasizes and models the CA3 subfield of the hippocampus as a primary inducement towards encoding and retrieval. Encoding as a procedure begins when septal GABAergic inhibition is at minimum, freeing basket cells to act within CA3[;], and during brief dis-inhibition periods, other cells receive input: a proximal entorhinal input toward pyramidal cells and a coincident dentate gyrus input toward interneurons.<ref name=c>{{cite journal | last1 = Kunec
CA3 is significant as it is amiable to auto-associative processes through a recurrent, collateral system.<ref name=c /> The theta phase separation model agrees generally with others on the significance of CA3 but is the first to attribute both the processes of encoding and retrieval to the subfield.<ref name=c />
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The reconsolidation hypothesis claims that objects encoded into long term memory experience a new period of consolidation, or the time and resource expended to stabilize a memory object, upon each recollection. This is in opposition to the classical consolidation hypothesis which regards consolidation as a one-time event, following the first encoding of a memory. A memory item in this hypothesis, upon reactivation, destabilizes for a brief period and thereafter invokes the neuronal processes requisite for stabilization.<ref name=d>{{cite journal | last1 = Morris | first1 = R. G. M. | last2 = Inglis | first2 = J. | last3 = Ainge | first3 = J. A. | last4 = Olverman | first4 = H. J. | last5 = Tulloch | first5 = J. | last6 = Dudai | first6 = Y. | last7 = Kelly | first7 = P. A. T. | year = 2006 | title = Memory reconsolidation: Sensitivity of spatial memory to inhibition of protein synthesis in dorsal hippocampus during encoding and retrieval | url = | journal = Neuron | volume = 50 | issue = 3| pages = 479–489 | doi = 10.1016/j.neuron.2006.04.012 }}</ref>
The reconsolidation hypothesis has lingered since the 1960s; however, a 2000 study, entitled “Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval”, examining fear conditioning in rats, has provided evidence in its favor.<ref name=e>{{cite journal | last1 = Nader
The reconsolidation hypothesis does not suppose that subsequent and precedent consolidation phases are necessarily identical in duration or in the neural mechanisms involved. Nevertheless, the commonality that exists in every consolidation phase is a short-lived destabilization of a memory object and a susceptibility for said object to react to amnesic agents—principally protein synthesis inhibitors.<ref name=d /> Morris and colleagues’ experiment indicates that the reconsolidation hypothesis could apply to particular memory types such as allocentric spatial memory, which is either acquired slowly or rapidly. As implied by the authors, however, such an application is feasible only in the case of rapidly acquired spatial memory, the degree to which is influenced by how thoroughly a spatial object is trained.<ref name=d />
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===Disease===
According to the Journal of Neurology, Neurosurgery, and Psychiatry, [[Alzheimer’s]] generally causes a reduction in tissue as well as neurodegeneration throughout the brain. Out of all areas in the brain, the hippocampus is among the first to be damaged by Alzheimer’s. One study located in the Journal of Neurology, Neurosurgery, and Psychiatry tested to see the volume changes of the hippocampus in Alzheimer’s disease patients. Results showed that there was 27% less volume in the hippocampus compared with the hippocampus found in normal cognition. Lastly, the difference between the hippocampus of an Alzheimer’s patient and that of a normal patient was shown through the notable loss seen in cortical grey matter in Alzheimer’s.<ref name=i>{{cite journal | last1 = Du
==Experiment==
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