Vascular endothelial growth factor is up-regulated after status epilepticus and protects against seizure-induced neuronal loss in hippocampus

Nicoletti, Jamee N.; Shah, Sachin K.; McCloskey, Daniel P.; Goodman, Jeffrey H.; Elkady, Ahmed; Atassi, Hadi; Hylton, Donna; Rudge, John S.; Scharfman, Helen E.; Croll, Susan D.

doi:10.1016/j.neuroscience.2007.09.083

Cited by 118 publications

(115 citation statements)

References 37 publications

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“…VEGF upregulation could be analogous to heat shock protein expression, which occurs in neurons that are exposed to insults but do not die. Given that VEGF protects neurons from insults such as experimental ischemia or seizure-induced damage [6,11,29], and motorneurons [10,25,31], it is possible that the upregulation of VEGF is an endogenous protective mechanism.…”

Section: Vegf Upregulation After Seizures: a Response To Insult Or Inmentioning

confidence: 99%

“…In addition, the primary pattern of expression of VEGF in hippocampus appears to be punctate immunoreactivity outlining glia [6]. Glia are known to express VEGF receptors, and glia are known to modulate neurotransmission [11,29].…”

Section: Vegf Suppression Of Evoked Responsesmentioning

confidence: 99%

“…Also, impairing VEGF production through genetic manipulation results in degeneration of lower motor neurons in adulthood [14,23]. VEGF has also been shown to be neuroprotective in animal models of ischemia or other types of insult or injury [6,25].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, descending and peripheral inputs would be likely to activate motor neurons more than would occur under normal conditions. Animals were evaluated for changes in VEGF expression 24 hrs after the onset of status, because this time appeared to be associated with increased VEGF expression in forebrain [6]. It also appears to be the time when activity-dependent changes in other growth factors are maximal [20] To predict any clinical potential for VEGF therapy, it would be useful to clarify its effects on motor neuron function.…”

Section: Introductionmentioning

confidence: 99%

“…

AbstractPrevious studies have shown that VEGF expression in forebrain increases after experimental manipulations that increase neuronal activity [6,12]. One question is whether this also occurs in motor neurons.

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mentioning

confidence: 99%

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Modulation of vascular endothelial growth factor (VEGF) expression in motor neurons and its electrophysiological effects

McCloskey¹,

Hintz²,

Scharfman³

2008

Brain Research Bulletin

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Previous studies have shown that VEGF expression in forebrain increases after experimental manipulations that increase neuronal activity [6,12]. One question is whether this also occurs in motor neurons. If so, it could be potentially advantageous from a therapeutic perspective, because VEGF prevents motor neuron degeneration [2,10,24]. Therefore, we asked whether endogenous VEGF expression in motor neurons could be modulated. We also asked what VEGF exposure would do to motor neurons using electrophysiology.Immunocytochemistry showed that motor neuron VEGF expression increased after a stimulus that increases neuronal and motor activity, i.e., convulsions. The increase in VEGF immunoreactivity occured in all motor neuron populations that were examined 24 hrs later. This effect was unlikely to be due to seizure-induced toxicity, because silver degeneration stain did not show the typical appearance of a dying or dead neuron.

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Section: Vegf Upregulation After Seizures: a Response To Insult Or Inmentioning

confidence: 99%

Section: Vegf Suppression Of Evoked Responsesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…

…”

mentioning

confidence: 99%

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Modulation of vascular endothelial growth factor (VEGF) expression in motor neurons and its electrophysiological effects

McCloskey¹,

Hintz²,

Scharfman³

2008

Brain Research Bulletin

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Aquaporin‐4 and epilepsy

Binder

Nagelhus

Ottersen

2012

Glia

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120

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Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4 2/2 mice) or a-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets. V

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Water maze experience and prenatal choline supplementation differentially promote long‐term hippocampal recovery from seizures in adulthood

et al. 2011

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Status epilepticus (SE) in adulthood dramatically alters the hippocampus and produces spatial learning and memory deficits. Some factors, like environmental enrichment and exercise, may promote functional recovery from SE. Prenatal choline supplementation (SUP) also protects against spatial memory deficits observed shortly after SE in adulthood, and we have previously reported that SUP attenuates the neuropathological response to SE in the adult hippocampus just 16 days after SE. It is unknown whether SUP can ameliorate longer-term cognitive and neuropathological consequences of SE, whether repeatedly engaging the injured hippocampus in a cognitive task might facilitate recovery from SE, and whether our prophylactic prenatal dietary treatment would enable the injured hippocampus to more effectively benefit from cognitive rehabilitation. To address these issues, adult offspring from rat dams that received either a control (CON) or SUP diet on embryonic days 12-17 first received training on a place learning water maze task (WM) and were then administered saline or kainic acid (KA) to induce SE. Rats then either remained in their home cage, or received three additional WM sessions at 3, 6.5, and 10 weeks after SE to test spatial learning and memory retention. Eleven weeks after SE, the brains were analyzed for several hippocampal markers known to be altered by SE. SUP attenuated SEinduced spatial learning deficits and completely rescued spatial memory retention by 10 weeks post-SE. Repeated WM experience prevented SE-induced declines in glutamic acid decarboxylase (GAD) and dentate gyrus neurogenesis, and attenuated increased glial fibrilary acidic protein (GFAP) levels. Remarkably, SUP alone was similarly protective to an even greater extent, and SUP rats that were water maze trained after SE showed reduced hilar migration of newborn neurons. These findings suggest that prophylactic SUP is protective against the long-term cognitive and neuropathological effects of KA-induced SE, and that rehabilitative cognitive enrichment may be partially beneficial.

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Vascular endothelial growth factor is up-regulated after status epilepticus and protects against seizure-induced neuronal loss in hippocampus

Cited by 118 publications

References 37 publications

Modulation of vascular endothelial growth factor (VEGF) expression in motor neurons and its electrophysiological effects

Modulation of vascular endothelial growth factor (VEGF) expression in motor neurons and its electrophysiological effects

Aquaporin‐4 and epilepsy

Water maze experience and prenatal choline supplementation differentially promote long‐term hippocampal recovery from seizures in adulthood

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