The initial stage of reversal learning is impaired in mice hemizygous for the vesicular glutamate transporter (VGluT1)

B. Granseth, F. K. Andersson, S. H. Lindström
  • Genes Brain & Behavior, July 2015, Wiley
  • DOI: 10.1111/gbb.12230

Glutamate circuits contribute to behavioral flexibility

What is it about?

Behavioral flexibility is an essential cognitive skill for survival in our constantly changing world. Patients with schizophrenia, Parkinson's disease, or damage to the prefrontal cortex often have deficits in behavioral flexibility. There are reasons to believe that glutamate neurotransmission may play a role in this behavioral deficit. In this study, we find that mice with a mild deficit in glutamate release (from primarily modulatory synapses) have similar deficits in behavioral flexibility.

Why is it important?

This study provides further evidence for the hypothesis that glutamate neurotransmission plays an important role in schizophrenia. Thus new treatments that target glutamate pathways may help address symptoms of schizophrenia that are not helped by existing treatments. This study also suggests that glutamate signalling from the prefrontal cortex to the striatum (mediated by VGluT1) is important for complex behaviors such as reversal learning. In contrast, initial discrimination learning was not impaired by the reduction in VGluT1 expression.

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The following have contributed to this page: Dr Sarah H Lindstrom and Dr Björn Granseth