Intrahippocampal injection of kainic acid produces significant pyramidal cell loss in neonatal rats

Cook, T. M.; Cruicher, K.A.

doi:10.1016/0306-4522(86)90180-6

Cited by 50 publications

(20 citation statements)

References 48 publications

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“…Studies mapping brain metabolic changes with 2-deoxyglucose utilization during seizures have shown that the hippocampus is highly active at all ages tested in both KA status epilepticus (as early as 3 days old; Tremblay et al, 1984) and kindled seizures (16 days old; Ackermann et al, 1989). Nor is the resistance of P16 rats to KA-induced neuronal damage due to an absence of hippocampal KA receptors , since direct hippocampal infusion of KA produces local excitotoxic lesions as early as P5-7 (Cook and Crutcher, 1986;Leite et al, 1996). Furthermore, the lack of supragranular Timm staining in immature rats following KA or kindling is not due to an inability of the immature dentate to support mossy-fiber sprouting.…”

Section: Discussionmentioning

confidence: 98%

Resistance of immature hippocampus to morphologic and physiologic alterations following status epilepticus or kindling

et al. 2001

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Seizures in adult rats result in long-term deficits in learning and memory, as well as an enhanced susceptibility to further seizures. In contrast, fewer lasting changes have been found following seizures in rats younger than 20 days old. This age-dependency could be due to differing amounts of hippocampal neuronal damage produced by seizures at different ages. To determine if there is an early developmental resistance to seizure-induced hippocampal damage, we compared the effects of kainic acid (KA)-induced status epilepticus and amygdala kindling on hippocampal dentate gyrus anatomy and electrophysiology, in immature (16 day old) and adult rats. In adult rats, KA status epilepticus resulted in numerous silver-stained degenerating dentate hilar neurons, pyramidal cells in fields CA1 and CA3, and marked numerical reductions in CA3c pyramidal neuron counts (-57%) in separate rats. Two weeks following the last kindled seizure, some, but significantly less, CA3c pyramidal cell loss was observed (-26%). Both KA status epilepticus and kindling in duced mossy-fiber sprouting, as evidenced by ectopic Timm staining in supragranular layers of the dentate gyrus. In hippocampal slices from adult rats, paired-pulse stimulation of perforant path axons revealed a persistent enhancement of dentate granule-cell inhibition following KA status epilepticus or kindling. While seizures induced by KA or kindling in 16-day-old rats were typically more severe than in adults, the immature hippocampus exhibited markedly less KA-induced cell loss (-22%), no kindling-induced loss, no detectable synaptic rearrangement, and no change in dentate inhibition. These results demonstrate that, in immature rats, neither severe KA-induced seizures nor repeated kindled seizures produce the kind of hippocampal damage and changes associated with even less severe seizures in adults. The lesser magnitude of seizure-induced hippocampal alterations in immature rats may explain their greater resistance to long-term effects of seizures on neuronal function, as well as future seizure susceptibility. Conversely, hippocampal neuron loss and altered synaptic physiology in adults may contribute to increased sensitivity to epileptogenic stimuli, spontaneous seizures, and behavioral deficits.

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Section: Discussionmentioning

confidence: 98%

Resistance of immature hippocampus to morphologic and physiologic alterations following status epilepticus or kindling

et al. 2001

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“…Exogenous administration of glutamatergic agonists that activate KA or NMDA receptors in cultured primary neurons has proven to be a useful model system for studying the mechanisms of excitotoxic brain injury in mature neurons [27, 28] [29]. …”

Section: Discussionmentioning

confidence: 99%

Low‐level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro

Huang

Nagata

Tedford³

et al. 2013

Journal of Biophotonics

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Excitotoxicity describes a pathogenic process whereby death of neurons releases large amounts of the excitatory neurotransmitter glutamate, which then proceeds to activate a set of glutamatergic receptors on neighboring neurons (glutamate, N-methyl-D-aspartate (NMDA), and kainate), opening ion channels leading to an influx of calcium ions producing mitochondrial dysfunction and cell death. Excitotoxicity contributes to brain damage after stroke, traumatic brain injury, and neurodegenerative diseases, and is also involved in spinal cord injury. We tested whether low level laser (light) therapy (LLLT) at 810-nm could protect primary murine cultured cortical neurons against excitotoxicity in vitro produced by addition of glutamate, NMDA or kainate. Although the prevention of cell death was modest but significant, LLLT (3 J/cm2 delivered at 25 mW/cm2 over 2 min) gave highly significant benefits in increasing ATP, raising mitochondrial membrane potential, reducing intracellular calcium concentrations, reducing oxidative stress and reducing nitric oxide. The action of LLLT in abrogating excitotoxicity may play a role in explaining its beneficial effects in diverse central nervous system pathologies. ((Figure: 5a)) Effect of 810-nm laser on intracellular reactive oxygen species (ROS) in cortical neurons with excitotoxicity

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“…An exogenous administration of excitatory amino acids that activate NMDA receptors in living animals or in cultured primary neurons has proven a useful model system to prove the mechanisms of excitotoxic brain injury in mature neurons (Cook and Crutcher, 1986;Hilton et al, 2006). Some clinical evidence shows that apoptosis is likely to be the major cause of death of neurons in neurodegenerative disorders, i.e., Parkinson's disease and Alzheimer's disease (Bredesen et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of the pyrolyzates derived from bamboo against neuronal damage and hematoaggregation

Hong

Jung

Lee

et al. 2010

Journal of Ethnopharmacology

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Intrahippocampal injection of kainic acid produces significant pyramidal cell loss in neonatal rats

Cited by 50 publications

References 48 publications

Resistance of immature hippocampus to morphologic and physiologic alterations following status epilepticus or kindling

Resistance of immature hippocampus to morphologic and physiologic alterations following status epilepticus or kindling

Low‐level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro

Protective effects of the pyrolyzates derived from bamboo against neuronal damage and hematoaggregation

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