Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0036572 (
seizures
)
80,221
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The stargazer mouse mutation causes absence
seizures
that are more prolonged and frequent than any other petit mal mouse model. Stargazer mice also have an ataxic gait and vestibular problems, including a distinctive head-tossing motion. From the genotyping of a large intersubspecific cross, a panel of 53 recombinant DNAs between D15Mit29 and D15Mit2 has been assembled, and a fine genetic map of the stargazer region has been constructed on mouse Chromosome 15. The stargazer locus has been mapped between D15Mit30 and the parvalbumin gene, and six candidate genes have been excluded by genetic linkage analysis. A physical contig of YACs, BACs, and P1s stretching 1.1 Mb from D15Mit30 to the
somatostatin receptor 3
gene is reported, and the DNA interval including the stargazer locus has been narrowed to 150 kb.
...
PMID:Genetic and physical maps of the stargazer locus on mouse chromosome 15. 922 73
Neonatal or early-life
seizures
(ELS) are often associated with life-long neurophysiological, cognitive and behavioral deficits, but the underlying mechanisms contributing to these deficits remain poorly understood. Newborn, post-migratory cortical neurons sprout ciliary buds (procilia) that mature into primary cilia. Disruption of the growth or signaling capabilities of these cilia has been linked to atypical neurite outgrowth from neurons and abnormalities in neuronal circuitry. Here, we tested the hypothesis that generalized
seizures
induced by pentylenetetrazol (PTZ) or kainic acid (KA) during early postnatal development impair neuronal and/or glial ciliogenesis. Mice received PTZ (50 or 100mg/kg), KA (2mg/kg), or saline either once at birth (P0), or once daily from P0 to P4. Using immunohistochemistry and electron microscopy, the cilia of neurons and glia were examined at P7, P14, and P42. A total of 83 regions were analyzed, representing 13 unique neocortical and hippocampal regions. Neuronal cilia were identified by co-expression of NeuN and type 3 adenylyl cyclase (ACIII) or
somatostatin receptor 3
(
SSTR3
), while glial cilia were identified by co-expression of GFAP, Arl13b, and gamma-tubulin. We found that PTZ exposure at either P0 or from P0 to P4 induced convulsive behavior, followed by acute and lasting effects on neuronal cilia lengths that varied depending on the cortical region, PTZ dose, injection frequency, and time post-PTZ. Both increases and decreases in neuronal cilia length were observed. No changes in the length of glial cilia were observed under any of the test conditions. Lastly, we found that a single KA
seizure
at P0 led to similar abnormalities in neuronal cilia lengths. Our results suggest that
seizure
(s) occurring during early stages of cortical development induce persistent and widespread changes in neuronal cilia length. Given the impact neuronal cilia have on neuronal differentiation, ELS-induced changes in ciliogenesis may contribute to long-term pathology and abnormal cortical function.
...
PMID:Neonatal seizures induced by pentylenetetrazol or kainic acid disrupt primary cilia growth on developing mouse cortical neurons. 2718 11