Biomedical subjects

Sujatha Narayan

Publications and source records attributed to Sujatha Narayan.

4 recordsLinked to original sources

PubMed2025

A suite of enhancer AAVs and transgenic mouse lines for genetic access to cortical cell types.

The mammalian cortex is comprised of cells classified into types according to shared properties. Defining the contribution of each cell type to the processes guided by the cortex is essential for understanding its function in health and disease. We use transcriptomic and epigenomic cortical cell-type taxonomies from mouse and human to define marker genes and putative enhancers and create a large toolkit of transgenic lines and enhancer adeno-associated viruses (AAVs) for selective targeting of cortical cell populations. We report creation and evaluation of fifteen transgenic driver lines, two reporter lines, and >1,000 different enhancer AAV vectors covering most subclasses of cortical cells. The tools reported here have been made publicly available, and along with the scaled process of tool creation, evaluation, and modification, they will enable diverse experimental strategies toward understanding mammalian cortex and brain function.

Animals↗

PubMed2007

Chronic haloperidol treatment results in a decrease in the expression of myelin/oligodendrocyte-related genes in the mouse brain.

Schizophrenia is a complex psychiatric illness that manifests as a combination of positive symptoms, negative symptoms, and cognitive deficits. Antipsychotic drugs, such as haloperidol, attenuate dopamine receptor signaling in neurons and constitute the frontline treatment for the positive symptoms of schizophrenia. However, haloperidol treatment has also been reported to exacerbate preexisting negative symptoms/cognitive deficits and the severity of these deficits has been correlated with white matter pathology in schizophrenia. Indeed, several studies implicate oligodendrocyte function in the pathophysiology of schizophrenia, but it is unknown whether these effects are related to drug treatment. It is well established that haloperidol alters gene expression in neurons. However, its effect on oligodendrocytes is unknown. In this study, we investigate the effects of chronic haloperidol treatment on the expression of eight genes known to play critical roles in myelin/oligodendrocyte function. We treated male mice with haloperidol (2 mg/kg/day) for 30 days and measured gene expression changes by using in situ hybridization analysis and quantitative densitometry. Haloperidol caused a decrease in the expression of these genes in several white matter regions of the mouse CNS. In contrast, clozapine (10 mg/kg/day) had no effect on the expression of a subset of these genes. This has important implications for both disease pathology and the consideration of treatment options for patients.

Analysis of Variance↗

PubMed2004

Transport of a synaptotagmin-YFP fusion protein in sympathetic neurons during early neurite outgrowth in vitro after transfection in vivo.

Developing neurons are engaged in neurite outgrowth as well as the synthesis and transport of proteins involved in synaptic transmission. Very little is known about when transport is established in these rudimentary neurites. We used a novel technique to visualize protein transport during the early hours of neurite outgrowth in culture. Recombinant adenoviruses were used to express a synaptotagmin-YFP fusion protein in the superior cervical ganglia of neonatal rats in vivo and protein transport was examined in neuronal cultures established from the superior cervical ganglions (SCGs). We find that, as early as 4h in culture, synaptotagmin-YFP was present in the cytoplasm, lamellipodia, filopodia and growth cones. Protein expression appeared punctate in neurites at 8h in vitro and is consistent with a vesicular localization. These results indicate that the machinery to transport synapse-specific proteins is functional in rudimentary neurites at this time and indicates that this technique can be used to study early neuronal development.

Adenoviridae↗

PubMed2002

The formation of sensorimotor circuits.

Recent studies have identified some of the key molecular pathways that control the genesis of spinal sensorimotor circuits. Transcription factors play a central role in these events, regulating both the specification of neurons that constitute these sensorimotor pathways and the expression of downstream molecules that control the wiring up of these neurons into topologically interconnected neuronal networks.

Animals↗