John Shallcross

PhD Student / Behavioral and Cognitive Neuroscience

Marek Schwendt Lab

Areas of interest/Research

My work focuses mainly on identifying underpinning neural mechanisms of post traumatic stress disorder (PTSD). Our lab utilizes a predator odor model of trauma in rats coupled with a post trauma  battery of anxiety tests which allows us to reliably generate both PTSD susceptible and resilient phenotypes out of heterogeneous populations of sprague-dawley rats. My main focus has been using fluorescent in situ hybridization (FISH) molecular techniques to localize and quantify mRNA of target proteins involved in plasticity mechanisms in brain areas associated with fear learning, and comparing expression of these target mRNAs among our phenotyped groups of animals – some of these targets include Group I metabotropic glutamate receptors (specifically mGluR5), and cannabinoid receptors (CB1); regions of interest include basal lateral amygdala, infralimbic prefrontal cortex, dorsal hippocampus, and nucleus accumbens.  We are also focused on testing novel drugs including mGluR allosteric modulators and CB1 agonists on our PTSD susceptible pheynotype in an attempt to pharmacologically reproduce some of the specific neurobiologies we have seen in our resilient animals

 

    

Brain atlas showing target regions of the amygdala vs. boundaries identified in a slice of tissue stained with glutamate marker vGlut1 (green) and nuclear counterstain DAPI (blue).

 

      

Left:  FISH image of excitatory BLA neurons in a resilient animal showing co-expression of glutamate marker vGlut1 mRNA (green) and mGluR5 mRNA (red) along with DAPI nuclear counterstain (blue); Right:  Inhibitory BLA neurons in a resilient animal showing co-expression of GABAergic marker GAD65 (green) and mGluR5 (red) with DAPI (blue).

 

              

Left:  Group I mGluRs can initiate activity dependent biphasic neuroplasticity by either activating an inositol triphosphate initiated Ca++ mediated potentiation of synapses (LTP), or by activation of diacylglycerol initiated weakening of synapses (LTD) in the BLA; Right:  Proposed mechanism for mGluR5 initiated activation of PLCb and DAG resulting in endocannabinoid synthesis and subsequent retrograde signalling via presynaptic cannabinoid receptors (CB1).  Resilient rats show much higher expression of mGluR5 than both control or PTSD suseptible animals.

 

Background

MS – Georgia Regents University, Augusta, GA.

BS – Emory University, Atlanta, GA.

Contact Information

Email: jshallcross@ufl.edu
Phone: (352) 273-5555
Office: 311N Psychology

Office Hours: By appointment

Mailing address:

114 Psychology Building
945 Center Drive
Gainesville, FL 32611-2250