Hypoxia, excitotoxicity, and neuroprotection in the hippocampal slice preparation

Schurr, Avital; Payne, Ralphiel S.; Heine, Michael F.; Rigor, Benjamin M.

doi:10.1016/0165-0270(94)00203-s

Cited by 54 publications

(29 citation statements)

References 52 publications

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“…The procedure was based on Schurr et al (1995) as modified by us (Ferchmin et al, 2000). Unless otherwise stated, the excitotoxic stimulus used was the application of 0.5 mM NMDA for 10 min in the presence of 95% O 2 , 5% CO 2 and 10 mM glucose.…”

Section: Methodsmentioning

confidence: 99%

“…The measurement of the area of population spikes (PSs) to determine the physiological status of acute hippocampal slices was successfully used to study the effect of anoxia, oxygen, and glucose deprivation, and excitotoxic amino acids on hippocampal neurons (Schurr et al, 1995;Small et al, 1997;Wang et al, 1999;Ferchmin et al, 2000). As a model of excitotoxic damage, this preparation has the advantages of an in vitro preparation with most of the circuitry of the original hippocampus intact as shown by its capability to express complex functions such as long-term potentiation.…”

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confidence: 99%

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Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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Although in neuronal cultures nicotine was reported to prevent early and delayed excitotoxic death, no studies with nicotinic drugs have been done with acute hippocampal slices. We investigated the effect of nicotine and methyllycaconitine (MLA) on the toxicity of N-methyl-D-aspartate (NMDA) in the CA1 area of hippocampal slices. The excitotoxic effect of NMDA was assessed as decreased recovery of the capability to produce synaptically evoked population spikes (PSs). Application of nicotine or MLA before NMDA application increased the recovery of PSs. This electrophysiological recovery was used as a measure of the early neuroprotective events. The neuroprotection conferred by both nicotine and MLA was inhibited by dihydro-␤-erythroidine, showing mediation of neuroprotection by ␣4␤2 neuronal nicotinic receptors (nAChRs). Because nicotine activates ␣4␤2 and other nAChR subtypes, whereas 10 nM MLA inhibits the ␣7 subtype, we propose the involvement of a neuronal circuitry-dependent mechanism for nicotinic neuroprotection. The effect of nicotine downstream from the receptors was investigated using inhibitors of cell signaling. The results suggest that the effect of nicotine is mediated by tyrosine receptor kinases, 1,2-phosphatidylinositol-3 kinase, and the mitogen-activated extracellular signal-regulated kinases. Although nicotine neuroprotection is Ca 2ϩ -dependent, neither L-type Ca 2ϩ channels nor calmodulin-dependent protein kinase is involved in the effect of nicotine. In summary, these results suggest that in acute slices nicotinic protection is initiated either by direct activation of ␣4␤2 or indirectly by inhibition of ␣7 followed by signal transduction involving tyrosine kinases, phospholipid-dependent kinases, and mitogen-activated kinases.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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“…The availability of simple in vitro systems for the study of ischemic injury in the central nervous system has greatly helped our understanding of this process over the past two decades (Schurr et al, 1995). Moreover, the development of imaging techniques using¯uor-escent probes for Ca 2 has enabled us to determine the temporal changes in the two-dimensional distribution of intracellular Ca 2 concentration {[Ca 2 ] i } in cultured cells or tissues.…”

Section: Introductionmentioning

confidence: 99%

“…Biochemical and morphological studies have been conducted under ischemic conditions in the isolated retina of rat, rabbit or chick (Ames, 1983;Winkler, 1983;Doberstein et al, 1994;Neal et al, 1994;Romano et al, 1998). However, to date, intracellular Ca 2 responses to an in vitro ischemia have not been determined in retinal slice preparations, as has been performed using brain slices (Kass and Lipton, 1986;Mitani et al, 1990;Schurr et al, 1995;Laake et al, 1999). Studies using in vivo ischemic models of the retina have demonstrated that inner retinal neurons are more vulnerable to ischemia than outer retinal neurons (Hughes, 1991;Szabo et al, 1991;Peachey, Green and Ripps, 1993;Osborne, Larsen and Barnett, 1995;Larsen and Osborne, 1996;Rosenbaum et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Intracellular Ca2+Changes Induced by in vitro Ischemia in Rat Retinal Slices

Kuriyama

Nakagawa²,

Tsuda³

2001

Experimental Eye Research

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“…Calcium was omitted and the magnesium concentration was elevated (to 10mM) in the buffer during the preparation and equilibration period in order to limit calcium-mediated damage (Feig and Lipton, 1990;Garthwaite and Garthwaite, 1986;Johnson and Bywood, 1998a). Similarly, we included ascorbic acid and desferrioxamine mesylate in the buffer to limit damage produced by the formation of free radicals (Rice et al, 1994;Schurr et al, 1995).…”

Section: Brain Slice Preparation and Equilibrationmentioning

confidence: 99%

Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

Bywood

Johnson

2001

neurotox res

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We investigated whether specific types of catecholamine neurons were differentially vulnerable to damage induced by excitatory amino acids (EAAs) in vitro in a rat brain slice preparation. Brain slices, 300 micro m thick, were cut horizontally, exposed to either N-methyl-D-aspartate (NMDA) or kainic acid (KA) for 2h, fixed and then cut into thin (30 micro m) sections in the same (horizontal) plane as the slice. The sections were immunolabelled for tyrosine hydroxylase to identify different groups of catecholamine neurons (substantia nigra (SN), paranigral (PN), interfascicular (IF) and hypothalamic A11, A13 and A14) which exhibited prominent dendritic projections in the horizontal plane. Loss of dendrites was used as a sensitive index of damage that precedes the loss of the cell body. Catecholamine neurons differed strikingly in their vulnerability of EAA-induced dendrite degeneration. The most vulnerable were those in the dorsal tier of the SN, whereas the most resistant were those in the hypothalamic A11 group. For example, in the dorsal tier of SN, NMDA (50 micro M) reduced the proportion of neurons with dendrites from 64% (+/- 8% SEM) in controls to 13% (+/- 7%) whereas the majority of A11 neurons (69 +/- 10%) retained their dendrites compared to controls (89% +/- 8%). The other groups of catecholamine neurons exhibited intermediate vulnerability. An essentially similar pattern of differential vulnerability was observed with KA. An understanding of the cellular mechanisms that underlie the particular vulnerability of SN neurons in the slice will aid the discovery of pharmacological therapies to prevent or slow the pathological process in neurodegenerative diseases which involve these neurons.

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Hypoxia, excitotoxicity, and neuroprotection in the hippocampal slice preparation

Cited by 54 publications

References 52 publications

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Intracellular Ca2+Changes Induced by in vitro Ischemia in Rat Retinal Slices

Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

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