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===HIPER (hippocampal encoding/retrieval) model===
Meta-[[positron emission tomography]] (PET) analysis has lent support toward a division of the hippocampus between caudal and rostral regions.<ref name=b>{{cite journal | last1 = Lepage | first1 = M. | last2 = Habib | first2 = R. | last3 = Tulving | first3 = E. | year = 1998 | title = Lepage, M., Habib, R. & Tulving, E. Hippocampal PET Activations of memory encoding and retrieval: the HIPER model" ''Hippocampus'' 8, 313-322
HIPER is a model resulting from and therefore a reflection of certain experimental phenomena, but cannot completely explain hippocampal encoding and retrieval on its own.<ref name=b /> Nevertheless, the model suggests a broad division of labor in encoding and retrieval, whether they involve separate regions of the hippocampus or act simultaneously or independently within a single, more inclusive process.
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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.<ref name=c>{{cite journal | last1 = Hasselmo | first1 = ME | last2 = Bodelon | first2 = C | last3 = Wyble | first3 = BP | year = 2002 | title = A proposed function for hippocampal theta rhythm: separate phases of encoding and retrieval enhance reversal of prior learning
CA3 is significant as it is allows 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 /><ref name=m />
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===Reconsolidation hypothesis===
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
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 | first1 = Karim | last2 = Schafe | first2 = Glenn E. | last3 = Le Doux | first3 = Joseph E. | year = 2000 | title = Fear Memories Require Protein Synthesis In The Amygdala For Reconsolidation After Retrieval
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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===Psychiatric disorders===
Individuals who develop hippocampal lesions often fare poorly on measures of verbal declarative memory. Tests involving the recall of paragraphs or strings of words, as cited by Bremner and colleagues, illustrate a degree of dysfunction among lesion patients proportionate to the percentage of hippocampal volume and the amount of cells lost.<ref name=f>{{cite journal | last1 = Bremner | first1 = J. | last2 = Vythilingam | first2 = M. | last3 = Vermetten | first3 = E. | last4 = Southwick | first4 = S. | last5 = MaGlashan | first5 = T. | last6 = Nazeer | first6 = A. | last7 = Khan | first7 = S. | last8 = Vaccarino | first8 = V. | last9 = Soufer | first9 = R. | last10 = Garg | first10 = P. | last11 = Chin | first11 = K. | last12 = Staib | first12 = L. | last13 = Duncan | first13 = J. | last14 = Charney | first14 = D. | year = 2003 | title = MRI and PET study of deficits in hippocampal structure and function in women with childhood sexual abuse and posttraumatic stress disorder
As precursors toward later studies that would showcase the effect of [[post-traumatic stress disorder]] (PTSD) on the human hippocampus, animal studies have broadly demonstrated a susceptibility of the mammalian hippocampus to stressors. In particular, stressed animals develop functional deficits in memory, changes in hippocampal form, and an impairment in neurogenesis, or the ability to produce new neurons.<ref name=f />
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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 | first1 = A. | last2 = Schuff | first2 = N. | last3 = Amend | first3 = D. | last4 = Laakso | first4 = M. | last5 = Hsu | first5 = Y. | last6 = Jagust | first6 = W. | last7 = Yaffe | first7 = K. | last8 = Kramer | first8 = J. | last9 = Reed | first9 = B. | last10 = Norman | first10 = D. | last11 = Chui | first11 = H. | last12 = Weiner | first12 = M. | year = 2001 | title = Magnetic resonance imaging of the entorhinal cortex and hippocampus in mild cognitive impairment and alzheimer's disease
==Experiment==
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===Methods===
In an experiment performed by Zeineh and colleagues, ten subjects were scanned by fMRI while engaged in a face-name associative task that linked a sequence of faces unknown to the participants with the names of the individuals to whom they belonged.<ref name=j>{{cite journal | last1 = Zeineh | first1 = M | year = 2003 | title = Dynamics of the Hippocampus During Encoding and Retrieval of Face-Name Pairs
===Results===
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