Vishnu Suppiramaniam
Kennesaw State University, GA·Neuroscience
Cannabis is one of the most commonly used illicit drugs during pregnancy, and its use is expected to rise as legalization spreads. Clinical studies show that children exposed to cannabinoids before birth can have lasting problems with thinking and memory.
- Fields
Neuroscience
Pharmacology
Physiology
- Topics
prenatal cannabinoid exposure
cannabis
marijuana
- Grants
- 1 known grant, through Feb 2027
What they work on
- Investigate the molecular mechanisms behind memory and synaptic plasticity deficits after prenatal cannabinoid exposure, using behavioral tests and hippocampal measurements of long-term potentiation and long-term depression in exposed animals.
- Determine how loss of PSA-NCAM, a cell-surface molecule needed for neuron wiring and memory, alters signaling through GluN2A- and GluN2B-containing NMDA receptors and the GluN2B-Ras-GRF1-p38 MAPK pathway in exposed offspring.
- Test whether a PSA mimetic and drugs that modulate GluN2A- and GluN2B-containing NMDA receptors can reverse the synaptic plasticity and memory deficits caused by prenatal cannabinoid exposure.
More about the research
Cannabinoids are the active compounds in cannabis. Little is known about which molecular steps in the developing brain cause these deficits, and no treatments exist. This project aims to find those steps and to test a possible therapy.
Why it matters
No treatments currently exist for the learning and memory problems seen in children exposed to cannabinoids before birth. Pinpointing the PSA-NCAM and NMDA receptor pathway behind these deficits could reveal treatment targets. A PSA mimetic, already shown to correct memory deficits in another rodent model, may offer a possible therapy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Andre Antonio Fenton
New York University, NY·Neuroscience
Test whether erasing aPKC-dependent synaptic strengthening, via genetic manipulation of PKMζ and PKCι/λ targeted to memory-encoding hippocampal neurons, permanently erases a long-term active place avoidance memory.
Jason D Shepherd
University of Utah, UT·Neuroscience
Test whether LTP increases Arc protein in dendrites and its assembly into virus-like capsids, using live imaging of neurons.
Johannes W Hell
University of California-Davis, CA·Neuroscience
Test whether norepinephrine taken into neurons by the transporters OCT3 and PMAT activates internal β2ARs to drive GluA1 phosphorylation, AMPAR surface delivery and LTP, using inhibitors, knockout mice, immunoblotting and immunofluorescence.
The school
Kennesaw State University: 6 labs on PI Pages, $52M a year on research, 82 research doctorates a year.
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