Hippocampus function

This test exploits a natural tendency of rodents to explore novel objects and to show an exploratory preference for replaced or displaced objects. The dependence of object recognition memory on the hippocampus is related to the protocol of a test. Short delays between initial exploration phase and a memory test make ORtest independent from the hippocampus (136), however, when longer delays (hours) are implemented, OR memory depends on hippocampus function (158, 159). Object memory impairment is demonstrated when an animal shows no preference in exploration (close proximity, nose contact) of a new or displaced object. 

Neuronal excitotoxicity AEA levels are elevated in the hippocampus of mice treated with kainic acid. 2-AG levels are elevated in rats treated with pilocarpine These are two animal models of epileptic seizures, where the endocannabinoids play an anti-convulsant and protective function Inhibitors of cellular re-uptake... 

Collection of interconnected subcortical and cortical brain structures (including hypothalamus, amygdala, and hippocampus) integrating multimodal intero- and exteroceptive information to produce coherent neuroendocrine and behavioral output, and to support memory functions. 

Extrahypothalamic OX-B-like immunoreactivity, reminiscent to that of CRF, has been described in clustered GABAergic neuronal populations, in the lateral division of central nucleus ofthe amygdala, the bednucleus of the stria terminalis, and in the hippocampus. Moreover, ectopic expression of preproorexin mRNA in the gut, ependymal cells, neuroblastomas, and of orexin receptors in adrenal gland, cancer and hematopietic stem cells suggests yet unexplored roles of orexins as paracrine factors controlling blood-brain barrier, and tumor or stem cell function. 

Jung H, Toth PT, White PA, Miller RJ (2008) Monocyte chemoattractant protein-1 functions as a neuromodulator in dorsal root ganglia neurons. J Neurochem 104 254-263 Kahn L, Alonso G, Normand E, Manzoni OJ (2005) Repeated morphine treatment alters polysia-lylated neural cell adhesion molecule, glutamate decarboxylase-67 expression and ceU proliferation in the adult rat hippocampus. Em J Nemosci 21 493-500 Kaul M, Ma Q, Medders KE, Desai MK, Lipton SA (2007) HIV-1 coreceptors CCR5 and CXCR4 both mediate neuronal cell death but CCR5 paradoxically can also contribute to protection. Cell Death Differ (2) 296-305... 

The role of the kainate receptor system in the brain is at an early stage since there are as yet few pharmacological tools to study its function. However, mutations in the kainate receptor genes have been made in mice and there is a GluR6 kainate receptor knock-out mouse. Kainate binding is absent in areas of the brain which normally have high levels such as the hippocampus. Here, in normal animals kainate receptors mediate a postsynaptic current which is absent in the GluR6 knock-out mouse. The mice have... 

Few antagonists exist at present but the distribution of the peptide with high levels in cortex, hippocampus, amyglada and spinal cord may give some clues to potential functions of the peptide. 

Even if there is a link between the presence of tangles and plaques and the emergence of AzD, it is by no means certain how those markers could be responsible for all the symptoms. They do not seem to be sufficiently numerous or widely spread to disrupt brain function to the extent that eventually occurs in AzD, although their preferential location in the hippocampus and the known association of that area with memory processing could explain the loss of that faculty. 

Low concentrations of solubilised jS-albumin inhibit ACh release in slices from rat hippocampus and cortex areas which show degeneration in AzD, but not in slices from the striatum which is unaffected. While not totally specific to ACh, since some inhibition of NA and DA and potentiation of glutamate release have been reported, this effect is achieved at concentrations of A/i below those generally neurotoxic. Since jS-amyloid can inhibit choline uptake it is also possible (see Auld, Kar and Quiron 1998) that in order to obtain sufficient choline for ACh synthesis and the continued function of cholinergic neurons, a breakdown of membrane phosphatidyl choline is required leading to cell death (so-called autocannibalism), /i-amyloid can also reduce the secondary effects of Mi receptor activation such as GTPase activity... 

So if ACh is involved in memory function, what does it do Any attempt to answer that question has to follow some consideration of how memory is thought to be processed. Many neuroscientists believe that memory is achieved by changes in the strength of synaptic connections (activation) between neurons and that increases in such synaptic activity somehow reinforce the pattern of neuronal activity during the memorising of an event so that it can be more easily restored later. One form of such plasticity is longterm potentiation (LTP), which has been mostly studied in the hippocampus where, as in other areas associated with memory, there is the appropriate complex synaptic morphology. 

In that and subsequent studies (Kosofsky 1985 Blue et al. 1988a), a distinct laminar pattern of innervation was found in somatosensory cortex, and a quite different pattern in the cingulate cortex, hippocampus, and dentate gyrus, where there are distinct bands of highly varicose axons. In the primate, the 5-HT innervation of cerebral cortex is denser and more highly differentiated among different architectonic and functional areas (Kosofsky et al. 1984 Morrison et al. 1982 Morrison and Foote 1986 Wilson and Molliver 1986 Wilson et al. 1989). For example, marked differences in the density and distribution of 5-HT axons are found in the macaque on either side of the central sulcus, in primary motor and somatosensory cortex while... 

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