Hippocampus cell death

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... 

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... 

Both PAF [57] and COX-2 are potent mediators of the injury/inflammatory response (Fig. 33-5). PAF and COX-2 are also interrelated in neuronal plasticity. The PAF transcriptional activation of COX-2 may provide clues about novel neuronal cell-death pathways. In fact, the delayed induction of COX-2 by kainic acid precedes selective neuronal apoptosis by this agonist in the hippocampus [42,58]. 

Brain cannabinoid receptor. In humans, psychoactive cannabinoids produce euphoria, enhancement of sensory perception, tachycardia, antinociception, difficulties in concentration, and impairment of memory. The cognitive deficiencies persist after withdrawal. The toxicity of cannabis has been underestimated for a long time, since recent findings revealed that A-9-THG-induced cell death with shrinkage of neurons and DNA fragmentation in the hippocampus. The acute effects of cannabinoids, as well as the development of tolerance, are mediated by G protein-coupled cannabinoid receptors. The CBl receptor and its splice variant, CBl A, are found predominantly in the brain with highest densities in the hippocampus, cerebellum, and striatum. The CB2 receptor is found predominantly in the spleen and in hemopoi-... 

We reported the effects of ethanol extract of C. sativus and its purified components on the central nervous system in terms of learning behaviors in mice and the LTP in the dentate gyrus of hippocampus in anesthetized rats and in the CA1 region of rat hippocampal slices [11-13], This review also discusses the values of folk medicines in modulating apoptotic cell death, together with our recent data of crocin s effect on neuronal cell death. 

Post-mitotic cell death of newly-generated neuronal cells in the adult hippocampus (Cameron and McKay, 2001)... 

Thus, this excess excitation leads to cell death by either apoptosis or necrosis in the neurons affected, which was found to be mostly in the hippocampus and amygdale, although some occurred in the cerebral cortex also. 

Danial NN, Korsmeyer SJ (2004) Cell death critical control points. Cell 116(2) 205-219 Decking UK, Schlieper G, Kroll K, Schrader J (1997) Hypoxia-induced inhibition of adenosine kinase potentiates cardiac adenosine release. Circ Res 81(2) 154—164 Dunwiddie TV, Diao L, Proctor WR (1997) Adenine nucleotides undergo apid, quantitative conversion to adenosine in the extracellular space in rat hippocampus. J Neurosci 17(2) 7673-7682... 

Ong W. Y., Lu X. R., Hu C. Y., and Halliwell B. (2000b). Distribution of hydroxynonenal-modified proteins in the kainate-lesioned rat hippocampus evidence that hydroxynonenal formation precedes neuronal cell death. Free Radio. Biol. Med. 28 1214-1221. 

Neuritic plaques regulate neuronal cell death during development, aiding neural recovery from injury and ageing. Found in high density throughout the hippocampus and neocortex of patients with Alzheimer s disease. Density of plaques correlated with degree of... 

Heinemarm, U., Buchheim, K., Gabriel, S. (2002). Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus. Prog. Brain Res. 135 197-210. 

The protein kinase C (PKC) signaling pathway has been associated with modulation of A-methyl-D-aspartate (NMDA) receptor activity, motor behavior, learning, and memory, all of which are severely impaired in intoxication with sarin and similar OPs. There was a reduction in the immunoreactivity levels of betall-PKC and Zeta-PKC in the frontal cortex (up to 24 h), and in the striatum (up to 5 days) post-sarin exposure, in contrast to the increase in the immunoreactivity of both enzymes in the hippocampus or thalamus, following a IxLDso exposure to sarin. These observations suggest a role for both conventional and atypical PKC isozymes in OP-induced neuropathy in the rat and further support their role in cell death (Bloch-Shilderman et al., 2005). 

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