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dc.contributor.advisorMichael Francis, PhD
dc.contributor.authorBanerjee, Navonil
dc.date2022-08-11T08:08:46.000
dc.date.accessioned2022-08-23T16:07:33Z
dc.date.available2022-08-23T16:07:33Z
dc.date.issued2016-12-14
dc.date.submitted2017-04-26
dc.identifier.doi10.13028/M2B609
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32270
dc.description<p>This dissertation includes 3 movies.</p>
dc.description.abstractNeuropeptide signaling play critical roles in maintaining distinct behavioral states and orchestrating transitions between them. However, elucidating the mechanisms underlying neuropeptide modulation of neural circuits in vivo remains a major challenge. The nematode Caenorhabditis elegans serves as an excellent model organism to study neuropeptide signaling mechanisms encoded in relatively simple neural circuits. We have used the C. elegans egg-laying circuit as a model to understand how neuropeptide signaling modifies circuit activity to generate opposing behavioral outcomes. C. elegans egg-laying behavior is composed of alternating cycles of two states – short bursts of egg deposition (active phases) and prolonged periods of quiescence (inactive phases). We have identified two neuropeptides (NLP-7 and FLP-11) that are locally released from a group of neurosecretory cells (uv1) and coordinate the temporal organization of egglaying by prolonging the duration of inactive phases. These neuropeptides regulate activity within the core circuit by inhibiting serotonergic transmission between its individual components (HSN motorneurons and Vm2 vulval muscles). This inhibition is achieved at least in part, by reducing synaptic vesicle abundance in the HSN synaptic regions. To identify potential downstream signaling components that mediate the actions of these neuropeptides, we have performed a forward genetic screen and have identified a strong candidate. In addition, we are trying to identify the receptor(s) of these neuropeptides by using a candidate gene approach. Together, we demonstrate that local neuropeptide signaling maintains the periodicity of distinct behavioral states by regulating serotonergic transmission in the core neural circuit.
dc.language.isoen_US
dc.rightsLicensed under a Creative Commons license
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectC. elegans
dc.subjectNeuromodulation
dc.subjectNeuropeptide signaling
dc.subjectBehavioral Neurobiology
dc.titleTemporal Organization of Behavioral States through Local Neuromodulation in C. elegans
dc.typeDoctoral Dissertation
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1895&amp;context=gsbs_diss&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_diss/892
dc.legacy.embargo2017-04-26T00:00:00-07:00
dc.identifier.contextkey10081362
dc.file.descriptionMovie II-1. uv1 photostimulation in control animals
dc.file.descriptionMovie II-2. uv1 photostimulation in nlp-7(lf);flp-11(lf) double mutants
dc.file.descriptionMovie II-3. HSN photostimulation
refterms.dateFOA2022-08-23T17:02:26Z
html.description.abstract<p>Neuropeptide signaling play critical roles in maintaining distinct behavioral states and orchestrating transitions between them. However, elucidating the mechanisms underlying neuropeptide modulation of neural circuits <em>in vivo</em> remains a major challenge. The nematode <em>Caenorhabditis elegans</em> serves as an excellent model organism to study neuropeptide signaling mechanisms encoded in relatively simple neural circuits. We have used the <em>C. elegans</em> egg-laying circuit as a model to understand how neuropeptide signaling modifies circuit activity to generate opposing behavioral outcomes. <em>C. elegans</em> egg-laying behavior is composed of alternating cycles of two states – short bursts of egg deposition (active phases) and prolonged periods of quiescence (inactive phases). We have identified two neuropeptides (NLP-7 and FLP-11) that are locally released from a group of neurosecretory cells (uv1) and coordinate the temporal organization of egglaying by prolonging the duration of inactive phases. These neuropeptides regulate activity within the core circuit by inhibiting serotonergic transmission between its individual components (HSN motorneurons and Vm2 vulval muscles). This inhibition is achieved at least in part, by reducing synaptic vesicle abundance in the HSN synaptic regions. To identify potential downstream signaling components that mediate the actions of these neuropeptides, we have performed a forward genetic screen and have identified a strong candidate. In addition, we are trying to identify the receptor(s) of these neuropeptides by using a candidate gene approach. Together, we demonstrate that local neuropeptide signaling maintains the periodicity of distinct behavioral states by regulating serotonergic transmission in the core neural circuit.</p>
dc.identifier.submissionpathgsbs_diss/892
dc.contributor.departmentFrancis Lab
dc.contributor.departmentNeurobiology
dc.description.thesisprogramNeuroscience
dc.identifier.orcid0000-0001-9613-5652


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