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2 results

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

  • Mikkel Vestergaard Olesen, Casper René Gøtzsche, Søren Hofman Christiansen, David Paul Drucker Woldbye
  • Journal:
    Acta Neuropsychiatrica / Volume 30 / Issue 4 / August 2018
    Published online by Cambridge University Press:
    21 March 2018, pp. 192-202
  • 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.

  • Somatostatin inhibits calcium influx into rat rod bipolar cell axonal terminals

  • JULIETTE JOHNSON, MICHAEL L. CARAVELLI, NICHOLAS C. BRECHA
  • Journal:
    Visual Neuroscience / Volume 18 / Issue 1 / January 2001
    Published online by Cambridge University Press:
    10 April 2001, pp. 101-108

  • In the retina, somatostatin (SST), an inhibitory peptide that influences neuronal activity, is predominantly expressed by sparsely occurring amacrine cells. The SST subtype 2A receptor is expressed by rod bipolar cells, including their axonal terminals. We used Ca2+-imaging techniques and the ratiometric Ca2+ indicator dye fura-2 AM to investigate Ca2+ dynamics in rod bipolar cell terminals. Depolarization of rod bipolar cells by the addition of high K+ (50 or 100 mM) elicited a sustained increase in [Ca2+]i in rod bipolar terminals that returned to basal levels following K+ removal. The Ca2+ response was dependent on extracellular Ca2+, and was inhibited by the Ca2+ channel blocker Cd2+ and by the selective L-type Ca2+ channel blocker, nimodipine. SST inhibited a K+ depolarization-induced [Ca2+]i response in rod bipolar terminals. This inhibition was observed with 1 nM SST and was maximal with 1 μM SST. These findings indicate that SST may regulate transmitter release from rod bipolar terminals by activating the SST subtype 2A receptor through modulation of intracellular Ca2+.