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Porter, James

One or more keywords matched the following properties of Porter, James

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overview	Functional imaging studies in PTSD patients suggest that reduced activation of the medial prefrontal cortex (mPFC) contributes to the excessive fear response seen in these patients. To understand why the mPFC is less activated in PTSD patients, we need to understand the mechanisms by which fear conditioning and extinction alter mPFC excitability. Patch-clamp recordings of infralimbic (IL) neurons in the mPFC revealed that the intrinsic excitability of IL neurons was depressed by fear conditioning in rats. The depressed IL excitability could reduce IL activation and enhance conditioned fear responses. Consistent with this, reducing IL intrinsic excitability enhances conditioned fear response. These findings imply that intrinsic plasticity in IL contributes to the consolidation of the conditioned fear memory. Currently we are working to extend these results by examining the mechanisms and circuits involved in this fear conditioning-induced depression of IL intrinsic excitability. A better understanding of the mechanisms leading to intrinsic plasticity in this brain structure may provide direction for the development of novel treatments for PTSD. 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.

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overview

Functional imaging studies in PTSD patients suggest that reduced activation of the medial prefrontal cortex (mPFC) contributes to the excessive fear response seen in these patients. To understand why the mPFC is less activated in PTSD patients, we need to understand the mechanisms by which fear conditioning and extinction alter mPFC excitability. Patch-clamp recordings of infralimbic (IL) neurons in the mPFC revealed that the intrinsic excitability of IL neurons was depressed by fear conditioning in rats. The depressed IL excitability could reduce IL activation and enhance conditioned fear responses. Consistent with this, reducing IL intrinsic excitability enhances conditioned fear response. These findings imply that intrinsic plasticity in IL contributes to the consolidation of the conditioned fear memory. Currently we are working to extend these results by examining the mechanisms and circuits involved in this fear conditioning-induced depression of IL intrinsic excitability. A better understanding of the mechanisms leading to intrinsic plasticity in this brain structure may provide direction for the development of novel treatments for PTSD. 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.

One or more keywords matched the following items that are connected to Porter, James

Item Type	Name
Academic Article	Memory for fear extinction requires mGluR5-mediated activation of infralimbic neurons.
Academic Article	Learning-induced intrinsic and synaptic plasticity in the rodent medial prefrontal cortex.
Academic Article	Noradrenergic signaling in infralimbic cortex increases cell excitability and strengthens memory for fear extinction.
Academic Article	Fear conditioning and extinction differentially modify the intrinsic excitability of infralimbic neurons.
Concept	Fear
Academic Article	Fear extinction induces mGluR5-mediated synaptic and intrinsic plasticity in infralimbic neurons.
Academic Article	Modulating fear extinction memory by manipulating SK potassium channels in the infralimbic cortex.
Academic Article	Spontaneous recovery of fear reverses extinction-induced excitability of infralimbic neurons.
Grant	Fear Modulation of IL excitability
Grant	Fkbp5 modulation of prefrontal function.
Academic Article	M-type potassium channels modulate the intrinsic excitability of infralimbic neurons and regulate fear expression and extinction.
Academic Article	Muscarinic receptors modulate the intrinsic excitability of infralimbic neurons and consolidation of fear extinction.
Academic Article	Purinergic P2X7 receptor-mediated inflammation precedes PTSD-related behaviors in rats.
Academic Article	Contextual fear conditioning depresses infralimbic excitability.
Academic Article	Plasticity of NMDA Receptors at Ventral Hippocampal Synapses in the Infralimbic Cortex Regulates Cued Fear.
Academic Article	Candesartan ameliorates impaired fear extinction induced by innate immune activation.
Academic Article	Infralimbic EphB2 Modulates Fear Extinction in Adolescent Rats.
Academic Article	Sex-dependent effects of microglial reduction on impaired fear extinction induced by single prolonged stress.
Academic Article	Dynamic expression of FKBP5 in the medial prefrontal cortex regulates resiliency to conditioned fear.

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Fear