RGD Reference Report - Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy. - Rat Genome Database

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Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy.

Authors: Akbarpour, B  Sayyah, M  Babapour, V  Mahdian, R  Beheshti, S  Kamyab, AR 
Citation: Akbarpour B, etal., Neurosci Bull. 2012 Dec;28(6):729-36. doi: 10.1007/s12264-012-1279-6. Epub 2012 Nov 12.
RGD ID: 7364770
Pubmed: PMID:23149765   (View Abstract at PubMed)
PMCID: PMC5561816   (View Article at PubMed Central)
DOI: DOI:10.1007/s12264-012-1279-6   (Journal Full-text)

OBJECTIVE: Understanding the molecular and cellular mechanisms underlying epileptogenesis yields new insights into potential therapies that may ultimately prevent epilepsy. Gap junctions (GJs) create direct intercellular conduits between adjacent cells and are formed by hexameric protein subunits called connexins (Cxs). Changes in the expression of Cxs affect GJ communication and thereby could modulate the dissemination of electrical discharges. The hippocampus is one of the main regions involved in epileptogenesis and has a wide network of GJs between different cell types where Cx30 is expressed in astrocytes and Cx32 exists in neurons and oligodendrocytes. In the present study, we evaluated the changes of Cx30 and Cx32 expression in rat hippocampus during kindling epileptogenesis. METHODS: Rats were stereotaxically implanted with stimulating and recording electrodes in the basolateral amygdala, which was electrically stimulated once daily at afterdischarge threshold. Expression of Cx30 and Cx32, at both the mRNA and protein levels, was measured in the hippocampus at the beginning, in the middle (after acquisition of focal seizures), and at the end (after establishment of generalized seizures) of the kindling process, by real-time PCR and Western blot. RESULTS: Cx30 mRNA expression was upregulated at the beginning of kindling and after acquisition of focal seizures. Then it was downregulated when the animals acquired generalized seizures. Overexpression of Cx30 mRNA at the start of kindling was consistent with the respective initial protein increase. Thereafter, no change was found in protein abundance during kindling. Regarding Cx32, mRNA expression decreased after acquisition of generalized seizures and no other significant change was detected in mRNA and protein abundance during kindling. CONCLUSION: We speculate that Cx32 GJ communication in the hippocampus does not contribute to kindling epileptogenesis. The Cx30 astrocytic network localized to perivascular regions in the hippocampus is, however, overexpressed at the initiation of kindling to clear excitotoxic molecules from the milieu.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
visual epilepsy  ISOGjb6 (Rattus norvegicus)7364770; 7364770 RGD 
visual epilepsy  IEP 7364770 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to electrical stimulus  IEP 7364770 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gjb6  (gap junction protein, beta 6)

Genes (Mus musculus)
Gjb6  (gap junction protein, beta 6)

Genes (Homo sapiens)
GJB6  (gap junction protein beta 6)


Additional Information