author_facet Gardoni, F.
Kamal, A.
Bellone, C.
Biessels, G. J.
Ramakers, G. M. J.
Cattabeni, F.
Gispen, W. H.
Di Luca, M.
Gardoni, F.
Kamal, A.
Bellone, C.
Biessels, G. J.
Ramakers, G. M. J.
Cattabeni, F.
Gispen, W. H.
Di Luca, M.
author Gardoni, F.
Kamal, A.
Bellone, C.
Biessels, G. J.
Ramakers, G. M. J.
Cattabeni, F.
Gispen, W. H.
Di Luca, M.
spellingShingle Gardoni, F.
Kamal, A.
Bellone, C.
Biessels, G. J.
Ramakers, G. M. J.
Cattabeni, F.
Gispen, W. H.
Di Luca, M.
Journal of Neurochemistry
Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
Cellular and Molecular Neuroscience
Biochemistry
author_sort gardoni, f.
spelling Gardoni, F. Kamal, A. Bellone, C. Biessels, G. J. Ramakers, G. M. J. Cattabeni, F. Gispen, W. H. Di Luca, M. 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1046/j.0022-3042.2001.00713.x <jats:title>Abstract</jats:title><jats:p>In animal models of diabetes mellitus, such as the streptozotocin‐diabetic rat (STZ‐rat), spatial learning impairments develop in parallel with a reduced expression of long‐term potentiation (LTP) and enhanced expression of long‐term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ‐diabetes and insulin treatment on the hippocampal post‐synaptic glutamate <jats:italic>N</jats:italic>‐methyl‐<jats:sc>d</jats:sc>‐aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post‐synaptic density (PSD) fraction. In addition, the functional properties of the NMDA‐receptor complex were examined. One month of STZ‐diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr‐dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and αCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ‐rats compared with age‐matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ‐rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII–NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post‐synaptic glutamatergic transmission is␣related to deficits in learning and plasticity in this animal model.</jats:p> Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats Journal of Neurochemistry
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series Journal of Neurochemistry
source_id 49
title Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_unstemmed Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_full Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_fullStr Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_full_unstemmed Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_short Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_sort effects of streptozotocin‐diabetes on the hippocampal nmda receptor complex in rats
topic Cellular and Molecular Neuroscience
Biochemistry
url http://dx.doi.org/10.1046/j.0022-3042.2001.00713.x
publishDate 2002
physical 438-447
description <jats:title>Abstract</jats:title><jats:p>In animal models of diabetes mellitus, such as the streptozotocin‐diabetic rat (STZ‐rat), spatial learning impairments develop in parallel with a reduced expression of long‐term potentiation (LTP) and enhanced expression of long‐term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ‐diabetes and insulin treatment on the hippocampal post‐synaptic glutamate <jats:italic>N</jats:italic>‐methyl‐<jats:sc>d</jats:sc>‐aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post‐synaptic density (PSD) fraction. In addition, the functional properties of the NMDA‐receptor complex were examined. One month of STZ‐diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr‐dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and αCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ‐rats compared with age‐matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ‐rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII–NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post‐synaptic glutamatergic transmission is␣related to deficits in learning and plasticity in this animal model.</jats:p>
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author Gardoni, F., Kamal, A., Bellone, C., Biessels, G. J., Ramakers, G. M. J., Cattabeni, F., Gispen, W. H., Di Luca, M.
author_facet Gardoni, F., Kamal, A., Bellone, C., Biessels, G. J., Ramakers, G. M. J., Cattabeni, F., Gispen, W. H., Di Luca, M., Gardoni, F., Kamal, A., Bellone, C., Biessels, G. J., Ramakers, G. M. J., Cattabeni, F., Gispen, W. H., Di Luca, M.
author_sort gardoni, f.
container_issue 3
container_start_page 438
container_title Journal of Neurochemistry
container_volume 80
description <jats:title>Abstract</jats:title><jats:p>In animal models of diabetes mellitus, such as the streptozotocin‐diabetic rat (STZ‐rat), spatial learning impairments develop in parallel with a reduced expression of long‐term potentiation (LTP) and enhanced expression of long‐term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ‐diabetes and insulin treatment on the hippocampal post‐synaptic glutamate <jats:italic>N</jats:italic>‐methyl‐<jats:sc>d</jats:sc>‐aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post‐synaptic density (PSD) fraction. In addition, the functional properties of the NMDA‐receptor complex were examined. One month of STZ‐diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr‐dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and αCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ‐rats compared with age‐matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ‐rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII–NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post‐synaptic glutamatergic transmission is␣related to deficits in learning and plasticity in this animal model.</jats:p>
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spelling Gardoni, F. Kamal, A. Bellone, C. Biessels, G. J. Ramakers, G. M. J. Cattabeni, F. Gispen, W. H. Di Luca, M. 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1046/j.0022-3042.2001.00713.x <jats:title>Abstract</jats:title><jats:p>In animal models of diabetes mellitus, such as the streptozotocin‐diabetic rat (STZ‐rat), spatial learning impairments develop in parallel with a reduced expression of long‐term potentiation (LTP) and enhanced expression of long‐term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ‐diabetes and insulin treatment on the hippocampal post‐synaptic glutamate <jats:italic>N</jats:italic>‐methyl‐<jats:sc>d</jats:sc>‐aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post‐synaptic density (PSD) fraction. In addition, the functional properties of the NMDA‐receptor complex were examined. One month of STZ‐diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr‐dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and αCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ‐rats compared with age‐matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ‐rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII–NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post‐synaptic glutamatergic transmission is␣related to deficits in learning and plasticity in this animal model.</jats:p> Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats Journal of Neurochemistry
spellingShingle Gardoni, F., Kamal, A., Bellone, C., Biessels, G. J., Ramakers, G. M. J., Cattabeni, F., Gispen, W. H., Di Luca, M., Journal of Neurochemistry, Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats, Cellular and Molecular Neuroscience, Biochemistry
title Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_full Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_fullStr Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_full_unstemmed Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_short Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
title_sort effects of streptozotocin‐diabetes on the hippocampal nmda receptor complex in rats
title_unstemmed Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
topic Cellular and Molecular Neuroscience, Biochemistry
url http://dx.doi.org/10.1046/j.0022-3042.2001.00713.x