Sandeep Sundara Rajan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Sandeep Sundara Rajan has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Christophe. D. Proulx
CERVO Brain Research Center, Department of Psychiatry and Neuroscience, Faculty of medicine, Université Laval
1 shared publication - Emmanouil Metzakopian
UK Dementia Research Institute, University of Cambridge, Clifford Albutt Building, Cambridge Biomedical Campus, Cambridge CB2 0AH, UK
1 shared publication - Lydia Saïdi
CERVO Brain Research Centre, Quebec City, QC, Canada, G1J 2G3
1 shared publication Marie-Josée Wallman
Universite Laval, Quebec City, QC, Canada, G1V 0A6
1 shared publication- Martin Lévesque
Department of Psychiatry and Neurosciences, Faculty of Medicine, Université Laval, Québec, QC, Canada
1 shared publication - Martin Parent
CERVO Brain Research Center, Department of Psychiatry and Neuroscience, Faculty of Medicine, Université Laval, Quebec City, Canada
1 shared publication
Latest Publications
- Open Access
CRISPR/CAS9-MEDIATED LOSS OF VESICULAR GLUTAMATE TRANSPORTER IN SEROTONIN NEURONS OF THE DORSAL RAPHE NUCLEUS LEADS TO SYNAPTIC CHANGES AND ANXIETY-LIKE BEHAVIORS
Vesicular glutamate transporter 3 (VGluT3) is expressed in a large subset of serotonin (5-HT) neurons of the dorsal raphe nucleus (DRN), suggesting a potential for glutamate co-transmission. Although VGluT3 has been implicated in the physiology of several non-glutamatergic neuronal populations, its specific role in the organization and function of 5-HT axons remains unclear. Here, we used CRISPR-Cas9 mediated knockdown and viral overexpression of VGluT3 in DRN 5-HT neurons of adult mice to assess its contribution to synaptic architecture in the lateral hypothalamus (LHA) and to 5-HT-related behaviors. VGluT3 depletion did not significantly alter synaptic incidence or organization of 5-HT DRN terminals in the LHA. In contrast, VGluT3 overexpression increased the proportion of asymmetric synapses without changing the overall synaptic incidence. In behavioral assays, VGluT3 depletion impaired motor coordination and increased anxiety-like, repetitive, and social behavior, whereas VGluT3 overexpression selectively reduced repetitive behavior. Basal locomotion and depressive-like behaviors were unchanged by either manipulation. Together, these findings indicate that VGluT3 modulates both the structural organization and behavioral output of DRN 5-HT neurons, supporting a modulatory role for VGluT3-dependent signaling within 5-HT circuits.
Open AccessCRISPR/CAS9-MEDIATED LOSS OF VESICULAR GLUTAMATE TRANSPORTER IN SEROTONIN NEURONS OF THE DORSAL RAPHE NUCLEUS LEADS TO SYNAPTIC CHANGES AND ANXIETY-LIKE BEHAVIORS
Vesicular glutamate transporter 3 (VGluT3) is expressed in a large subset of serotonin (5-HT) neurons of the dorsal raphe nucleus (DRN), suggesting a potential for glutamate co-transmission. Although VGluT3 has been implicated in the physiology of several non-glutamatergic neuronal populations, its specific role in the organization and function of 5-HT axons remains unclear. Here, we used CRISPR-Cas9 mediated knockdown and viral overexpression of VGluT3 in DRN 5-HT neurons of adult mice to assess its contribution to synaptic architecture in the lateral hypothalamus (LHA) and to 5-HT-related behaviors. VGluT3 depletion did not significantly alter synaptic incidence or organization of 5-HT DRN terminals in the LHA. In contrast, VGluT3 overexpression increased the proportion of asymmetric synapses without changing the overall synaptic incidence. In behavioral assays, VGluT3 depletion impaired motor coordination and increased anxiety-like, repetitive, and social behavior, whereas VGluT3 overexpression selectively reduced repetitive behavior. Basal locomotion and depressive-like behaviors were unchanged by either manipulation. Together, these findings indicate that VGluT3 modulates both the structural organization and behavioral output of DRN 5-HT neurons, supporting a modulatory role for VGluT3-dependent signaling within 5-HT circuits.