Data di Pubblicazione:
2002
Citazione:
Effects of streptozotocin-diabetes on the hippocampal NMDA receptor complex in rats / F. Gardoni, A. Kamal, C. Bellone, G.J. Biessels, G.M.J. Ramakers, F. Cattabeni, W.H. Gispen, M.M.G. Di Luca. - In: JOURNAL OF NEUROCHEMISTRY. - ISSN 0022-3042. - 80:3(2002), pp. 438-447.
Abstract:
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 N-methyl-D-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 αCaMKIl 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.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
CaMKII; Diabetes; Hippocampus; NMDA; Streptozotocin; Synaptic plasticity
Elenco autori:
F. Gardoni, A. Kamal, C. Bellone, G.J. Biessels, G.M.J. Ramakers, F. Cattabeni, W.H. Gispen, M.M.G. Di Luca
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