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Diabetes onset influences hippocampal synaptic plasticity in streptozotocin-treated rats

S Sasaki-Hamada1, H Sacai, J-I Oka

  • 1Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan.

Neuroscience
|October 17, 2012
PubMed

Insights

Type 1 diabetes impacts children's cognition. This study reveals that the age of diabetes onset affects synaptic plasticity in rat models, influencing cognitive difficulties differently based on when diabetes begins.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Diabetology

Background:

  • Type 1 diabetes mellitus (DM) is linked to cognitive difficulties in children.
  • The specific synaptic mechanisms underlying cognitive changes related to the age of diabetes onset are not well understood.

Purpose of the Study:

  • To investigate how the age of diabetes onset affects synaptic plasticity and excitatory synaptic transmission in a rat model.
  • To determine if early-onset diabetes has different impacts on synaptic function compared to young adult-onset diabetes.

Main Methods:

  • Used streptozotocin-induced diabetes (STZ) in rats with varying onset ages.
  • Examined synaptic plasticity (LTP/LTD) and excitatory synaptic transmission at hippocampal Schaffer collateral-CA1 (SC-CA1) synapses.
  • Analyzed AMPA and NMDA receptor-mediated currents and the AMPA/NMDA ratio.

Main Results:

  • Young adult-onset STZ-rats showed impaired long-term potentiation (LTP) and a decreased AMPA/NMDA ratio.
  • Juvenile-onset STZ-rats exhibited impaired long-term depression (LTD) with increased AMPA and NMDA receptor-mediated EPSCs.
  • NMDA receptor antagonist treatment restored LTD in juvenile-onset STZ-rats.

Conclusions:

  • The age of diabetes onset significantly influences the pathophysiology of diabetes-induced cognitive difficulties.
  • Different synaptic mechanisms underlie cognitive impairments depending on whether diabetes onset is juvenile or young adult.

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