Home | School Profile | Administration | Library | Student Affairs | Academic Affairs | Academic Programs |
Research Training
| Alumni | Outpatient Clinics | Contact Us

     

 


 

 

James Porter, PhD

Associate Professor

Department of Physiology, Pharmacology and Toxicology

 

 





 

 

Research Info



























 














 

  1. Cellular Mechanisms that encode extinction of learned fear

    Cellular Mechanisms that encode extinction of learned fear. Rather than erase fear memory, extinction is thought to form a new memory that signals safety. The goal of this project is to understand how extinction memory is encoded at the level of single neurons. Since a growing body of literature implicates enhanced activity in the infralimbic region (IL) of the medial prefrontal cortex in the retention of fear extinction, we are examining the intrinsic and synaptic mechanisms that mediate the enhanced activity of the IL neurons after extinction training. We are applying a multidisciplinary approach combining patch-clamp electrophysiology in brain slices, histology, behavioral training, molecular techniques, optogenetics and in vitro and in vivo neuropharmacology.

            
     

  2. Modulation of extinction memory by manipulating the excitability of IL neurons

    Modulation of extinction memory by manipulating the excitability of IL neurons. To determine whether the retention of extinction memory can be modulated by manipulating the excitability of IL neurons, we are identifying receptors that control intrinsic excitability in IL neurons. We are examining the effects of agonists of muscarinic receptors and metabotropic glutamate receptors subtype 5 (mGluR5) on the intrinsic excitability of IL neurons in brain slices. We are also determining whether antagonists of these receptors disrupt extinction memory. In addition, we are examining whether the stimulation of muscarinic or mGluR5 receptors in vivo can augment the recall of extinction training and increase the synaptic or intrinsic excitation of IL neurons. .
     
  3. Cellular Mechanisms that Modulate Thalamocortical Circuits

    We are studying how thalamic excitation of the cortex is inhibited by presynaptic adenosine, GABAB, and group II metabotropic glutamate receptors in brain slices with intact thalamocortical circuitry. Understanding how the activation of these cortical circuits is regulated will provide important insights into how sensory processing can be altered pharmacologically. Perhaps in the future one would have the ability to alter sensory processing via receptor agonists or antagonists in order to assist in new skill learning, relearning after an accident or stroke, or prevent aberrant cortical reorganization such as occurs in phantom limb pain.



     
  4. BDNF-modulation of Mossy fiber synaptic plasticity and Fear Extinction

    In collaboration with Dr. Kenira Thompson at PSM, we are initially planning to determine whether brain derived neurotrophic factor (BDNF) enhances mossy fiber long-term plasticity in hippocampal brain slices. In future experiments, we will attempt to enhance extinction memory by infusing BDNF directly into the hippocampus.


        


     
  5. Effects of HIV proteins on Neuronal Circuitry

    In collaboration with Dr. Richard Noel at PSM, we are planning on examining the effects of HIV-encoded proteins on neuronal circuitry in cultured hippocampal slices. Our hypothesis is that HIV proteins will decrease synaptic connections between neurons and inhibit the induction of synaptic plasticity.

 




















































































 

 

 
     
  Ongoing Research Support
 
 
 
  • Active
    R15 MH101700 James T. Porter (PI)
    National Institute of Mental Health
    Title: Fear Modulation of IL excitability
    Reduced activation of the medial prefrontal cortex contributes to excessive fear responses in patients with PTSD and phobias. Our research aims to examine the receptors, ion channels, signaling cascades, and circuits which modulate medial prefrontal cortex excitability in animals during fear conditioning and fear extinction. A better understanding of the mechanisms that control the activation of this brain structure may lead to better treatments for PTSD and other anxiety disorders.

     
  • Completed
    IOS 0842159 James T. Porter (Co-PI); Dr. Gregory Quirk (Co-PI)
    National Science Foundation
    Title: Applying in vitro recording techniques to extinction of conditioned fear
    The goal of this project is to combine behavioral analyses with intracellular slice recordings and in vivo single neuron recordings to characterize extinction-induced changes in the intrinsic excitability of IL neurons.

     
  • Active
    R36 MH102080- Emmanuel A. Cruz Torres (PI)
     Title: Role of Infralimbic EphB2 in Fear Extinction