Maturation of kainic acid seizure-brain damage syndrome in the rat. i. clinical, electrographic and metabolic observations

Tremblay, E.; Nitecka, L; Berger, Michael L.; Ben‐Ari, Yehezkel

doi:10.1016/0306-4522(84)90288-4

Cited by 201 publications

(116 citation statements)

References 55 publications

Supporting

Mentioning

107

Contrasting

Unclassified

Order By: Relevance

“…The behavioral effects induced by systemic administration of KA varied with the postnatal age, as previously described (Ben-Ari et al, 1981;Tremblay et al, 1984). Thus, in P10 animals scratchinglike movements appeared after 20 -25 min of KA injection, rapidly followed by tonicoclonic seizures.…”

Section: Seizures In Developing and Adult Ratssupporting

confidence: 55%

“…Nonetheless, evidence that neuronal activity per se may not be sufficient to trigger TIMP-1 expression is provided by the absence of TIMP-1 induction in 10-d-old animals, despite intense seizure activity manifested by tonicoclonic seizures. Full limbic seizures and emerging signs of pathology in response to KA are not present in rats until the third postnatal week Tremblay et al, 1984), at which time TIMP-1 mRNA first was seen abundantly induced in the hippocampus and areas of projection. By 35 d postnatal, when both seizures and pathology are indistinguishable from those of adult rats, TIMP-1 expression extended to all limbic and limbic-related structures.…”

Section: Timp-1 Mrna Expression Is Upregulated Differentially In Adulmentioning

confidence: 98%

See 1 more Smart Citation

Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) Is Differentially Induced in Neurons and Astrocytes after Seizures: Evidence for Developmental, Immediate Early Gene, and Lesion Response

et al. 1997

View full text Add to dashboard Cite

We investigated in vivo the expression of the tissue inhibitor of metalloproteinases-1 (TIMP-1) in the rat CNS after kainate (KA)-induced excitotoxic seizures. In situ hybridization revealed that TIMP-1 mRNA is induced rapidly and massively in most regions of the adult forebrain after KA treatment. Neuronal activity seems to be necessary but not sufficient to trigger TIMP-1 induction, because it is not observed in seizing 10-d-old pups, unlike what is observed in 21-and 35-d-old animals after seizures. The rapid induction of TIMP-1 is not prevented by the inhibitor of protein synthesis cycloheximide, suggesting that, after seizures, TIMP-1 is induced in neurons as an immediate early gene (IEG). The initial neuronal upregulation is followed by enhanced expression in astrocytes, as assessed by double-labeling experiments. In the hippocampus rapid increases in mRNA are followed by relatively delayed (8 hr after KA) increases in TIMP-1 immunoreactivity in the perisomatic and dendro-axonic areas, suggesting secretion of the protein. At 3 d after KA treatment, strong immunoreactivity is found in astrocytes and in the cell bodies and dendro-axonic projections of resistant neurons such as the dentate granule cells. Taken together, the results suggest that TIMP-1 may be instrumental for neurons and astrocytes in coupling early cellular events triggered by seizures with the regulation of long-lasting changes involved in tissue reorganization and/or neuroprotection.

show abstract

Section: Seizures In Developing and Adult Ratssupporting

confidence: 55%

Section: Timp-1 Mrna Expression Is Upregulated Differentially In Adulmentioning

confidence: 98%

Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) Is Differentially Induced in Neurons and Astrocytes after Seizures: Evidence for Developmental, Immediate Early Gene, and Lesion Response

et al. 1997

View full text Add to dashboard Cite

show abstract

“…PTZ injections were stopped when animals reached stage 5 and, because of the rapid turnover of the drug, animals recovered normal behavior by 1 h after the last PTZ injection. The validity of relying on behavioral monitoring to assess seizure activity in the brain has been demonstrated previously by studies correlating electrophysiological measures with observed seizure behaviors (Tremblay et al, 1984).…”

Section: Evaluation Of Seizure Threshold By Multiple Pentylenetetrazomentioning

confidence: 90%

proBDNF and p75NTR Control Excitability and Persistent Firing of Cortical Pyramidal Neurons

Gibon

Buckley

Unsain

et al. 2015

Journal of Neuroscience

View full text Add to dashboard Cite

Persistent firing of entorhinal cortex (EC) pyramidal neurons is a key component of working and spatial memory. We report here that a pro-brain-derived neurotrophic factor (proBDNF)-dependent p75NTR signaling pathway plays a major role in excitability and persistent activity of pyramidal neurons in layer V of the EC. Using electrophysiological recordings, we show that proBDNF suppresses persistent firing in entorhinal slices from wild-type mice but not from p75NTR-null mice. Conversely, function-blocking proBDNF antibodies enhance excitability of pyramidal neurons and facilitate their persistent firing, and acute exposure to function-blocking p75NTR antibodies results in enhanced firing activity of pyramidal neurons. Genetic deletion of p75NTR specifically in neurons or during adulthood also induces enhanced excitability and persistent activity, indicating that the proBDNF-p75NTR signaling cascade functions within adult neurons to inhibit pyramidal activity. Phosphatidylinositol 4,5-bisphosphate (PIP2)-sensitive transient receptor potential canonical channels play a critical role in mediating persistent firing in the EC and we hypothesized that proBDNF-dependent p75NTR activation regulates PIP2 levels. Accordingly, proBDNF decreases cholinergic calcium responses in cortical neurons and affects carbachol-induced depletion of PIP2. Further, we show that the modulation of persistent firing by proBDNF relies on a p75NTR-Rac1-PI4K pathway. The hypothesis that proBDNF and p75NTR maintain network homeostasis in the adult CNS was tested in vivo and we report that p75NTR-null mice show improvements in working memory but also display an increased propensity for severe seizures. We propose that the proBDNF-p75NTR axis controls pyramidal neuron excitability and persistent activity to balance EC performance with the risk of runaway activity.

show abstract

“…Fourteen of the 20 status epilepticus pups survived. Hallmarks of bilateral status epilepticus at this age are continuous hindlimb scratching, followed by swimming-like movements and prolonged tonic -clonic seizures (see Tremblay et al, 1984). The onset of tonic -clonic status epilepticus occurred within 30 min after kainic acid injection.…”

Section: Behavioral Manifestations Of Status Epilepticus Differ In P1mentioning

confidence: 93%

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

et al. 1997

View full text Add to dashboard Cite

In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces status epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizureinduced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in postnatal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene-and cell-specific manner, and that these changes vary with the developmental stage.

show abstract

Maturation of kainic acid seizure-brain damage syndrome in the rat. i. clinical, electrographic and metabolic observations

Cited by 201 publications

References 55 publications

Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) Is Differentially Induced in Neurons and Astrocytes after Seizures: Evidence for Developmental, Immediate Early Gene, and Lesion Response

Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) Is Differentially Induced in Neurons and Astrocytes after Seizures: Evidence for Developmental, Immediate Early Gene, and Lesion Response

proBDNF and p75NTR Control Excitability and Persistent Firing of Cortical Pyramidal Neurons

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

Contact Info

Product

Resources

About