Altered hippocampal expression of calbindin-D-28k and calretinin in GABA(B(1))-deficient mice. Export

@article{citeulike:404779, abstract = {Balb/c GABA(B(1))(-/-) mice develop complex epileptiform activity, including spontaneous and audiogenic generalized seizures, 6-8 weeks after birth. The neuronal systems involved in these epilepsies have not been identified yet. Because the hippocampus is critically involved in epileptiform activity, we now investigated whether this brain region exhibits seizure-related alterations. Using semi-quantitative immunohistochemistry, we studied the temporal and cellular hippocampal expression pattern of two seizure-sensitive calcium-binding proteins, calbindin-D-28k and calretinin, in GABA(B(1))(-/-) mice. One month after birth, before the onset of overt epileptiform activity, wild-type (WT) and GABA(B(1))(-/-) mice exhibit comparable expression profiles for the two calcium-binding proteins. Three months after birth, once the epileptic phenotype is established, we observe clear alterations in the expression of calcium-binding proteins in the dentate gyrus area. GABA(B(1))(-/-) mice exhibit a 50\% decline in the staining intensity of calbindin-D-28k expressing neurons and a 70\% increase in the number of calretinin-positive neurons when compared to WT littermates. Six months after birth, the down-regulation of calbindin-D-28k protein is even more pronounced, while the calretinin expression in GABA(B(1))(-/-) mice reverts to the pattern seen in WT littermates. Our data demonstrate that the absence of functional GABA(B) receptors causes epileptiform activity through a mechanism that crucially involves dentate gyrus granule cells, and that this pathological activity is accompanied by adaptive changes.}, address = {Department of Clinical-Biological Sciences, Institute of Physiology, University of Basel, Klingelbergstrasse 50-70, CH-4056 Basel, Switzerland.}, author = {R\"{u}ttimann, E. and Vacher, C. M. and Gassmann, M. and Kaupmann, K. and Van der Putten, H. and Bettler, B.}, citeulike-article-id = {404779}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.bcp.2004.07.019}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15451404}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15451404}, day = {15}, doi = {10.1016/j.bcp.2004.07.019}, issn = {0006-2952}, journal = {Biochem Pharmacol}, keywords = {adult, calbindin, calretinin, dg, gaba, mouse, ng, sz}, month = {October}, number = {8}, pages = {1613--1620}, posted-at = {2005-11-22 17:43:01}, priority = {2}, title = {Altered hippocampal expression of calbindin-D-28k and calretinin in GABA(B(1))-deficient mice.}, url = {http://dx.doi.org/10.1016/j.bcp.2004.07.019}, volume = {68}, year = {2004} }

TY - JOUR ID - citeulike:404779 L3 - citeulike-article-id:404779 N2 - Balb/c GABA(B(1))(-/-) mice develop complex epileptiform activity, including spontaneous and audiogenic generalized seizures, 6-8 weeks after birth. The neuronal systems involved in these epilepsies have not been identified yet. Because the hippocampus is critically involved in epileptiform activity, we now investigated whether this brain region exhibits seizure-related alterations. Using semi-quantitative immunohistochemistry, we studied the temporal and cellular hippocampal expression pattern of two seizure-sensitive calcium-binding proteins, calbindin-D-28k and calretinin, in GABA(B(1))(-/-) mice. One month after birth, before the onset of overt epileptiform activity, wild-type (WT) and GABA(B(1))(-/-) mice exhibit comparable expression profiles for the two calcium-binding proteins. Three months after birth, once the epileptic phenotype is established, we observe clear alterations in the expression of calcium-binding proteins in the dentate gyrus area. GABA(B(1))(-/-) mice exhibit a 50% decline in the staining intensity of calbindin-D-28k expressing neurons and a 70% increase in the number of calretinin-positive neurons when compared to WT littermates. Six months after birth, the down-regulation of calbindin-D-28k protein is even more pronounced, while the calretinin expression in GABA(B(1))(-/-) mice reverts to the pattern seen in WT littermates. Our data demonstrate that the absence of functional GABA(B) receptors causes epileptiform activity through a mechanism that crucially involves dentate gyrus granule cells, and that this pathological activity is accompanied by adaptive changes. IS - 8 JF - Biochem Pharmacol SN - 0006-2952 AD - Department of Clinical-Biological Sciences, Institute of Physiology, University of Basel, Klingelbergstrasse 50-70, CH-4056 Basel, Switzerland. EP - 1620 TI - Altered hippocampal expression of calbindin-D-28k and calretinin in GABA(B(1))-deficient mice. VL - 68 SP - 1613 KW - adult KW - calbindin KW - calretinin KW - dg KW - gaba KW - mouse KW - ng KW - sz AU - Rüttimann, E AU - Vacher, CM AU - Gassmann, M AU - Kaupmann, K AU - Van der Putten, H AU - Bettler, B PY - 2004/10/15/ UR - http://dx.doi.org/10.1016/j.bcp.2004.07.019 ER -