Articles by Cynthia K. McClard in JoVE
An Objective and Reproducible Test of Olfactory Learning and Discrimination in Mice Gary Liu*1,2, Jay M. Patel*2,3, Burak Tepe1, Cynthia K. McClard2,4, Jessica Swanson4, Kathleen B. Quast4, Benjamin R. Arenkiel1,3,4,5 1Program in Developmental Biology, Baylor College of Medicine, 2Medical Scientist Training Program, Baylor College of Medicine, 3Department of Neuroscience, Baylor College of Medicine, 4Department of Molecular and Human Genetics, Baylor College of Medicine, 5 Here, we train mice on an associative learning task to test odor discrimination. This protocol also allows for studies on learning-induced structural changes in the brain.
Other articles by Cynthia K. McClard on PubMed
Olfactory Cued Learning Paradigm Bio-protocol. May, 2017 | Pubmed ID: 28752111 Sensory stimulation leads to structural changes within the CNS (Central Nervous System), thus providing the fundamental mechanism for learning and memory. The olfactory circuit offers a unique model for studying experience-dependent plasticity, partly due to a continuous supply of integrating adult born neurons. Our lab has recently implemented an olfactory cued learning paradigm in which specific odor pairs are coupled to either a reward or punishment to study downstream circuit changes. The following protocol outlines the basic set up for our learning paradigm. Here, we describe the equipment setup, programming of software, and method of behavioral training.
POU6f1 Mediates Neuropeptide-Dependent Plasticity in the Adult Brain The Journal of Neuroscience : the Official Journal of the Society for Neuroscience. Feb, 2018 | Pubmed ID: 29305536 The mouse olfactory bulb (OB) features continued, activity-dependent integration of adult-born neurons, providing a robust model with which to examine mechanisms of plasticity in the adult brain. We previously reported that local OB interneurons secrete the neuropeptide corticotropin-releasing hormone (CRH) in an activity-dependent manner onto adult-born granule neurons and that local CRH signaling promotes expression of synaptic machinery in the bulb. This effect is mediated via activation of the CRH receptor 1 (), which is developmentally regulated during adult-born neuron maturation. CRHR1 is a G-protein-coupled receptor that activates CREB-dependent transcription in the presence of CRH. Therefore, we hypothesized that locally secreted CRH activates CRHR1 to initiate circuit plasticity programs. To identify such programs, we profiled gene expression changes associated with CRHR1 activity in adult-born neurons of the OB. Here, we show that CRHR1 activity influences expression of the brain-specific Homeobox-containing transcription factor POU Class 6 Homeobox 1 (). To elucidate the contributions oftoward activity-dependent circuit remodeling, we targeted CRHR1neurons in male and female mice for cell-type-specific manipulation ofexpression. Whereas loss ofin CRHR1neurons resulted in reduced dendritic complexity and decreased synaptic connectivity, overexpression ofin CRHR1neurons promoted dendritic outgrowth and branching and influenced synaptic function. Together, these findings suggest that the transcriptional program directed bydownstream of local CRH signaling in adult-born neurons influences circuit dynamics in response to activity-dependent peptide signaling in the adult brain.Elucidating mechanisms of plasticity in the adult brain is helpful for devising strategies to understand and treat neurodegeneration. Circuit plasticity in the adult mouse olfactory bulb is exemplified by both continued cell integration and synaptogenesis. We previously reported that these processes are influenced by local neuropeptide signaling in an activity-dependent manner. Here, we show that local corticotropin-releasing hormone (CRH) signaling induces dynamic gene expression changes in CRH receptor expressing adult-born neurons, including altered expression of the transcription factorWe further show thatis necessary for proper dendrite specification and patterning, as well as synapse development and function in adult-born neurons. Together, these findings reveal a novel mechanism by which peptide signaling modulates adult brain circuit plasticity.