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dc.contributor.authorHolland, Carl Seileren_US
dc.date.accessioned2016-07-12T19:04:08Z
dc.date.available2016-07-12T19:04:08Z
dc.date.issued2016
dc.identifier.urihttps://hdl.handle.net/2144/17017
dc.description.abstractBoth neuroinflammation, and an increase in microglial cells, have been associated with Autism Spectrum Disorder (ASD) through observation in human subjects as well as in mouse models. A mother having an infection early in pregnancy increases the chances for autism in her child. (Atladottir et al., 2012). This process is known as Maternal Immune Activation (MIA), and the proposed mechanism is that inflammatory signals cross from the mother to child; then in response to increased pro-inflammatory cytokines, microglia within the brain are activated to combat the infection. Microglia are essential to healthy synaptogenesis and neuronal growth, and a change in their signaling early in development has been shown to alter behavior in mouse models that replicate MIA. We use microglial depletion as a therapy to counteract the potentially harmful pro-inflammatory response in the developing mouse brain. Four experimental groups - control, MIA, microglial depleted, and a therapy group (MIA plus microglial depletion)- were run through a comprehensive series of behavioral and electrophysiological assessments. Layer 5 pyramidal cells (L5PNs) were targeted for recording in medial frontal cortex – a mouse cortical area important for cognition and social behavior. L5PNs are a heterogeneous population with cortical and subcortical targeting. Subcortical targeting neurons are thick tufted morphologically, and have an intrinsically bursting spike pattern. Analysis of the intrinsically bursting neurons revealed significant differences between the maternal inflammation and the microglial depletion groups across multiple physiological properties. Therefore, the therapy group had electrophysiological characteristics more consistent with the microglial depleted model than the autism model.en_US
dc.language.isoen_US
dc.subjectNeurosciencesen_US
dc.subjectASDen_US
dc.subjectAutismen_US
dc.subjectElectrophysiologyen_US
dc.subjectLayer 5en_US
dc.subjectPyramidal neuronsen_US
dc.titleElectrophysiological properties of layer 5 pyramidal neurons in a mouse model of autism spectrum disorderen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-06-18T22:28:54Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineAnatomy & Neurobiologyen_US
etd.degree.grantorBoston Universityen_US


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