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Differential plastic changes in synthesis and binding in the mouse somatostatin system after electroconvulsive stimulation

Published online by Cambridge University Press:  21 March 2018

Mikkel Vestergaard Olesen
Affiliation:
Laboratory of Neural Plasticity, Center for Neuroscience, University of Copenhagen, Copenhagen, Denmark Research Laboratory for Stereology and Neuroscience, Bispebjerg-Frederiksberg Hospital, Copenhagen University Hospital, Denmark
Casper René Gøtzsche
Affiliation:
Laboratory of Neural Plasticity, Center for Neuroscience, University of Copenhagen, Copenhagen, Denmark
Søren Hofman Christiansen
Affiliation:
Laboratory of Neural Plasticity, Center for Neuroscience, University of Copenhagen, Copenhagen, Denmark
David Paul Drucker Woldbye*
Affiliation:
Laboratory of Neural Plasticity, Center for Neuroscience, University of Copenhagen, Copenhagen, Denmark
*
Assoc. Prof. David P.D. Woldbye, MD, PhD, Laboratory of Neural Plasticity, Center for Neuroscience, University of Copenhagen, 3 Blegdamsvej, Panum Institute, Maersk Tower 5th floor, DK-2200 N Copenhagen, Denmark. Tel: +45 40156389 Fax: +45 35360116 E-mail: [email protected]

Abstract

Objective

Electroconvulsive therapy (ECT) is regularly used to treat patients with severe major depression, but the mechanisms underlying the beneficial effects remain uncertain. Electroconvulsive stimulation (ECS) regulates diverse neurotransmitter systems and induces anticonvulsant effects, properties implicated in mediating therapeutic effects of ECT. Somatostatin (SST) is a candidate for mediating these effects because it is upregulated by ECS and exerts seizure-suppressant effects. However, little is known about how ECS might affect the SST receptor system. The present study examined effects of single and repeated ECS on the synthesis of SST receptors (SSTR1–4) and SST, and SST receptor binding ([125I]LTT-SST28) in mouse hippocampal regions and piriform/parietal cortices.

Results

A complex pattern of plastic changes was observed. In the dentate gyrus, SST and SSTR1 expression and the number of hilar SST immunoreactive cells were significantly increased at 1 week after repeated ECS while SSTR2 expression was downregulated by single ECS, and SSTR3 mRNA and SST binding were elevated 24 h after repeated ECS. In hippocampal CA1 and parietal/piriform cortices, we found elevated SST mRNA levels 1 week after repeated ECS and elevated SST binding after single ECS and 24 h after repeated ECS. In hippocampal CA3, repeated ECS increased SST expression 1 week after and SST binding 24 h after. In the parietal cortex, SSTR2 mRNA expression was downregulated after single ECS while SSTR4 mRNA expression was upregulated 24 h after repeated ECS.

Conclusion

Considering the known anticonvulsant effects of SST, it is likely that these ECS-induced neuroplastic changes in the SST system could participate in modulating neuronal excitability and potentially contribute to therapeutic effects of ECT.

Type
Original Article
Copyright
© Scandinavian College of Neuropsychopharmacology 2018 

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