Many observations in humans and experimental animals support the view that the hippocampus is critical immediately after learning in order for long-term memory formation to take place. However, exactly when the medial temporal cortices adjacent to the hippocampus are necessary for this process to occur normally is not yet well known. Using a spatial task, we studied whether the perirhinal cortex of rats is necessary to establish representations in long-term memory. Results showed that, in a spatial task sensitive to hippocampal lesions, control and perirhinal lesioned rats can both learn at the same rate (Experiment 1). Interestingly, a differential involvement of the perirhinal cortex in memory retention was observed as time passes after learning. Thus, 24 days following the end of learning, lesioned and control rats remembered the task perfectly as measured by a retraining test. In contrast, 74 days after the learning the perirhinal animals showed a profound impairment in the retention of the spatial information (Experiment 2). Taken together, these results suggest that the perirhinal region is critical for the formation of long-term spatial memory. However, its contribution to memory formation and retention is time-dependent, it being necessary only long after learning takes place and not during the phase immediately following acquisition.
"Although abundant studies shows the hippocampus is crucial for memory acquisition and recalling, it is still in controversy whether the hippocampus is critical for familiarity recognition or not . By contrast, the perirhinal cortex mediates spatial memory retention  and is also crucial for the discrimination and memorization of novel and familiar individual objects . In addition, the parietal cortex is essential for long-term spatial memory  and object recognition  in rats. "
[Show abstract][Hide abstract] ABSTRACT: We previously hypothesized that achievement of recovery of brain function after the injury requires the reconstruction of neuronal networks, including neurite regeneration and synapse reformation. Kihi-to is composed of twelve crude drugs, some of which have already been shown to possess neurite extension properties in our previous studies. The effect of Kihi-to on memory deficit has not been examined. Thus, the goal of the present study is to determine the in vivo and in vitro effects of Kihi-to on memory, neurite growth and synapse reconstruction.
Effects of Kihi-to, a traditional Japanese-Chinese traditional medicine, on memory deficits and losses of neurites and synapses were examined using Alzheimer's disease model mice. Improvements of Abeta(25-35)-induced neuritic atrophy by Kihi-to and the mechanism were investigated in cultured cortical neurons.
Administration of Kihi-to for consecutive 3 days resulted in marked improvements of Abeta(25-35)-induced impairments in memory acquisition, memory retention, and object recognition memory in mice. Immunohistochemical comparisons suggested that Kihi-to attenuated neuritic, synaptic and myelin losses in the cerebral cortex, hippocampus and striatum. Kihi-to also attenuated the calpain increase in the cerebral cortex and hippocampus. When Kihi-to was added to cells 4 days after Abeta(25-35) treatment, axonal and dendritic outgrowths in cultured cortical neurons were restored as demonstrated by extended lengths of phosphorylated neurofilament-H (P-NF-H) and microtubule-associated protein (MAP)2-positive neurites. Abeta(25-35)-induced cell death in cortical culture was also markedly inhibited by Kihi-to. Since NF-H, MAP2 and myelin basic protein (MBP) are substrates of calpain, and calpain is known to be involved in Abeta-induced axonal atrophy, expression levels of calpain and calpastatin were measured. Treatment with Kihi-to inhibited the Abeta(25-35)-evoked increase in the calpain level and decrease in the calpastatin level. In addition, Kihi-to inhibited Abeta(25-35)-induced calcium entry.
In conclusion Kihi-to clearly improved the memory impairment and losses of neurites and synapses.
BMC Complementary and Alternative Medicine 02/2008; 8(1):49. DOI:10.1186/1472-6882-8-49 · 2.02 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The hippocampus has a critical role in certain kinds of spatial memory processes. Hippocampal "place" cells, fire selectively when an animal is in a particular location within the environment. It is thought that this activity underlies a representation of the environment that can be used for memory-based spatial navigation. But how is this representation constructed and how is it "read"? A simple mechanism, based on place field density across an environment, is described that could allow hippocampal representations to be "read" by other brain regions for the purpose of navigation. The possible influence of activity in neighboring brain regions such as the perirhinal cortex, and pre- and para-subiculum on the construction of the hippocampal spatial representation is then discussed.
[Show abstract][Hide abstract] ABSTRACT: The CA1 to perirhinal cortex projection is one of multiple hippocampal-neocortical projections considered to be involved in memory consolidation. This projection has been shown to sustain long-term potentiation (LTP) following stimulation of CA1. Here we examined the pharmacological properties underpinning the plasticity observed in this projection. A stimulating electrode was inserted into the area CA1 and a recording electrode was inserted into the perirhinal cortex of urethane-anaesthetised Wistar rats. Rats (n=6 in each drug group) were administered with either saline (0.09%), MK-801 (NMDA antagonist; 0.1 mg/kg) or CNQX (AMPA/kainate antagonist; 1.5 mg/kg). Baseline recordings were made for 10 min by stimulating area CA1 (0.05 Hz stimulation protocol). High-frequency stimulation (HFS; 250 Hz) was performed and post-HFS fEPSP recordings were made for 1 h (0.05 Hz, as above). Baseline and post-HFS paired-pulse facilitation (PPF) recordings were performed across six different interpulse intervals. CA1 and perirhinal cortex tissue samples were taken from the stimulated and unstimulated hemispheres of each rat brain and analysed using a brain-derived neurotrophic factor (BDNF) ELISA. Results indicate that LTP was induced in the saline and MK-801 groups but not in the CNQX group; fEPSPs in the latter group rapidly returned to baseline levels following a short period of post-tetanic potentiation. Drug treatment and HFS had no effect on PPF levels. Drug treatment significantly reduced concentrations of both CA1 and perirhinal BDNF and prevented stimulation-induced increases in BDNF in CA1. This molecular and electrophysiological data suggests that LTP in the CA1-perirhinal cortex projection may require activation of postsynaptic AMPA/kainate receptors in order to sustain LTP.
Brain research 03/2009; 1265:53-64. DOI:10.1016/j.brainres.2009.01.067 · 2.84 Impact Factor
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