Dataset Information

Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation.

ABSTRACT: The defensive withdrawal reflexes of Aplysia are important behaviors for protecting the animal from predation. Habituation and dishabituation allow for experience-dependent tuning of these reflexes and the mechanisms underlying these forms of behavioral plasticity involve changes in transmitter release from the sensory to motor neuron synapses through homosynaptic depression and the serotonin-mediated recovery from depression, respectively. Interestingly, dishabituation is reduced in older animals with no corresponding change in habituation. Here we show that the cultured sensory neurons of heavier animals (greater than 120 g) that form synaptic connections with motor neurons have both reduced recovery from depression and reduced novel PKC Apl II activation with 5HT. The decrease in the recovery from depression correlated better with the size of the animal than the age of the animal. Much of this change in PKC activation and synaptic facilitation following depression can be rescued by direct activation of PKC Apl II with phorbol dibutyrate, suggesting a change in the signal transduction pathway upstream of PKC Apl II activation in the sensory neurons of larger animals.

SUBMITTER: Dunn TW

PROVIDER: S-EPMC4552628 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation.

Dunn Tyler William TW Sossin Wayne S WS

PloS one 20150828 8

The defensive withdrawal reflexes of Aplysia are important behaviors for protecting the animal from predation. Habituation and dishabituation allow for experience-dependent tuning of these reflexes and the mechanisms underlying these forms of behavioral plasticity involve changes in transmitter release from the sensory to motor neuron synapses through homosynaptic depression and the serotonin-mediated recovery from depression, respectively. Interestingly, dishabituation is reduced in older anima ...[more]

PMID: 26317974

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Project description:Major depressive disorder (MDD) is a debilitating condition that affects over 14 million Americans. Remission occurs only in a minority of individuals after first-line antidepressant treatment (∼35%); predictors of treatment outcome are therefore needed. Using PET imaging with a radiotracer specific for the serotonin transporter (5-HTT), 11C-McN5652, we found that patients with MDD who did not achieve remission after 12 mo of naturalistic treatment had lower pretreatment midbrain and amygdala binding than healthy volunteers. Here, using a superior 5-HTT tracer, 11C-DASB, we repeated this study with a prospective design with 8 wk of standardized treatment with escitalopram. As this same cohort also underwent 11C-WAY100635 scans (serotonin-1A receptor [5-HT1A]), we examined whether using both pretreatment 5-HTT and 5-HT1A binding could improve prediction of posttreatment remission status. Methods: Thirty-one healthy controls (Hamilton Depression Rating Scale-24 item [HDRS-24] = 1.7) and 26 medication-free patients with MDD (HDRS-24 = 24.8) underwent PET scanning using 11C-DASB. MDD subjects then received 8 wk of standardized pharmacotherapy with escitalopram. The relationship between pretreatment binding and posttreatment clinical status was examined. Arterial blood samples were collected to calculate the metabolite-corrected arterial input function. The outcome measure was VT/fP (VT is volume of distribution in region of interest, fP is free fraction in plasma). Remission was defined as a posttreatment depression score of less than 10 as well as 50% or more reduction in the score from baseline, resulting in 14 nonremitters (HDRS-24 = 17.6) and 12 remitters (HDRS-24 = 5.3). Results: A linear mixed-effects model comparing group differences in the a priori regions of interest (amygdala and midbrain) revealed a significant difference in amygdala binding between controls and remitters (P = 0.03, unadjusted), where remitters had an 11% lower amygdala binding than controls. Differences in amygdala binding between remitters and nonremitters approached significance (P = 0.06). No additional differences were found between any groups (all P > 0.05). Additionally, we found no relationship between pretreatment amygdala binding and posttreatment depression score, and were unable to predict posttreatment depression severity using both pretreatment 5-HTT (in the amygdala) and 5-HT1A binding (in the raphe). Conclusion: These results suggest 5-HTT amygdala binding should be examined further, in conjunction with other measures, as a potential biomarker for remission after standardized escitalopram treatment.

Dataset Information

Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation.

Publications

Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation.

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