Retarded kindling progression in mice deficient in the extracellular matrix glycoprotein tenascin-R.
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Retarded kindling progression in mice deficient in the extracellular matrix glycoprotein tenascin-R. / Hoffmann, Katrin; Sivukhina, Elena; Potschka, Heidrun; Schachner, Melitta; Löscher, Wolfgang; Dityatev, Alexander.
In: EPILEPSIA, Vol. 50, No. 4, 4, 2009, p. 859-869.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Retarded kindling progression in mice deficient in the extracellular matrix glycoprotein tenascin-R.
AU - Hoffmann, Katrin
AU - Sivukhina, Elena
AU - Potschka, Heidrun
AU - Schachner, Melitta
AU - Löscher, Wolfgang
AU - Dityatev, Alexander
PY - 2009
Y1 - 2009
N2 - PURPOSE: We investigated the role of the extracellular matrix glycoprotein tenascin-R (TNR) in formation of a hyperexcitable network in the kindling model of epilepsy. The idea that TNR may be important for this process was suggested by previous studies showing that deficiency in TNR leads to abnormalities in synaptic plasticity, perisomatic GABAergic inhibition and more astrocytes in the hippocampus of adult mice. METHODS: Constitutively TNR deficient (TNR-/-) mice and their wild-type littermates received repeated electrical stimulation in the amygdala over several days until they developed fully kindled generalized seizures at which time their brains were studied immunohistochemically. RESULTS: In TNR-/- mice, kindling progression was retarded compared with wild-type littermate controls. Morphological analysis of the mice used for the kindling studies revealed that, independently of genotype, numbers of parvalbumin-positive interneurons in the dentate gyrus correlated positively with afterdischarge threshold alterations in kindled mice. The kindling-induced increase in the number of S100 expressing astrocytes in the dentate gyrus was enhanced by TNR deficiency and correlated negatively with the kindling rate. DISCUSSION: Our data support the view that TNR promotes formation of a hyperexcitable network during kindling and suggest that an increase in S100-expressing astrocytes may contribute to retarded epileptogenesis in TNR-/- mice.
AB - PURPOSE: We investigated the role of the extracellular matrix glycoprotein tenascin-R (TNR) in formation of a hyperexcitable network in the kindling model of epilepsy. The idea that TNR may be important for this process was suggested by previous studies showing that deficiency in TNR leads to abnormalities in synaptic plasticity, perisomatic GABAergic inhibition and more astrocytes in the hippocampus of adult mice. METHODS: Constitutively TNR deficient (TNR-/-) mice and their wild-type littermates received repeated electrical stimulation in the amygdala over several days until they developed fully kindled generalized seizures at which time their brains were studied immunohistochemically. RESULTS: In TNR-/- mice, kindling progression was retarded compared with wild-type littermate controls. Morphological analysis of the mice used for the kindling studies revealed that, independently of genotype, numbers of parvalbumin-positive interneurons in the dentate gyrus correlated positively with afterdischarge threshold alterations in kindled mice. The kindling-induced increase in the number of S100 expressing astrocytes in the dentate gyrus was enhanced by TNR deficiency and correlated negatively with the kindling rate. DISCUSSION: Our data support the view that TNR promotes formation of a hyperexcitable network during kindling and suggest that an increase in S100-expressing astrocytes may contribute to retarded epileptogenesis in TNR-/- mice.
M3 - SCORING: Zeitschriftenaufsatz
VL - 50
SP - 859
EP - 869
JO - EPILEPSIA
JF - EPILEPSIA
SN - 0013-9580
IS - 4
M1 - 4
ER -
