Laboratory of Neurobiology and Genetics - Dr. Sidney Strickland
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Research Projects
Role of Laminin in Peripheral Nerve Development

Laminin, an extracellular matrix protein, is required for peripheral nerve myelination. Laminin is a hetero-trimeric glycoprotein composed of α-, β-, and γ-chains. Mutations in laminin α2, a subunit of laminin-2 (α2/β1/γ1; the major laminin isoform expressed in the PNS and muscle), not only cause muscular dystrophy but also peripheral nerve dysmyelination. Laminin γ1 is one of the most abundant chains and is present in all known laminin isoforms expressed in the PNS. Read more »

Genetic Network Interactions during Myelination

The development of myelinated axons in the PNS is mediated by complex Schwann cell-neuronal interactions. Key molecules in the pathways related to Schwann cell development, myelin biogenesis, and neuronal regulation have been studied extensively. These studies have generally employed single gene knock-out in mice to elucidate the role of the relevant protein in these pathways. While this research has yielded valuable information, the complexity of biological network interactions within and between Schwann cells and neuronal cells remains unclear. Read more »

Stem Cell Rescue of Peripheral Nerve Dysfunction

Members of the Strickland Laboratory are investigating the potential of stem cells to rescue peripheral nerve defects. Previous results show that murine Adipose Derived Stem Cells (mADSCs) can rescue sciatic nerve dysfunction in young adult laminin-deficient mice. Electrophysiology studies of laminin-deficient sciatic nerves reveals impaired nerve conduction velocity (NCV), maximum amplitude of compound motor action potential (CMAP), and the minimum current needed to induce muscle twitch (MCST) in comparison to control animals. Read more »

Laminin-Dependent Regulation of Kainate Receptor Expression in Excitotoxic Cell Death

Laminin plays important roles in the nervous system. Previous studies show that laminin is implicated in excitotoxic neuronal degeneration. To study the role of laminin in neuronal cell death, members of the Strickland Laboratory knocked out laminin gamma-1 expression specifically in the neurons of the hippocampal CA1 region. Read more »

Involvement of tPA in ethanol-induced apoptotic neurodegeneration in the developing mouse brain

In humans, ethanol (EtOH) exposure during the period of synaptogenesis can result in brain defects referred to as fetal alcohol syndrome (FAS). This disorder is characterized by hyperactivity, cognitive deficits, mental retardation, psychosis, depression, and schizophrenia. Read more »

Role of the tPA System in Behavioral and Biochemical Aspects of Anxiety and Depression

Anxiety is one of the most common mental illnesses in the United States, affecting nearly 20 million Americans each year. It is well documented that the amygdala and hippocampus are responsible for processing and interpreting stress signals as well as regulating the body's responses to stress. Read more »

Fibrin Deposition in Neurovascular Damage and Neuro-Inflammation in Mouse Models of Alzheimer's Disease

Cerebrovascular dysfunction contributes to the pathology and progression of Alzheimer's disease (AD) but the mechanisms are not completely understood. Using transgenic mouse models of Alzheimer's disease (TgCRND8, PDAPP, and Tg2576), members of the Strickland Laboratory evaluated blood-brain barrier damage and the role of fibrin and fibrinolysis in the progression of β-amyloid pathology. Read more »

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