# keywords[]
3214 Pharmacology And Pharmaceutical Sciences

# keywords[]
Interleukin 1 Receptor Antagonist Protein

# keywords[]
3214 Pharmacology And Pharmaceutical Sciences

# keywords[]
5204 Cognitive And Computational Psychology

# keywords[]
5201 Applied And Developmental Psychology

# keywords[]
5204 Cognitive And Computational Psychology

# keywords[]
5204 Cognitive And Computational Psychology

# keywords[]
5201 Applied And Developmental Psychology

# keywords[]
3214 Pharmacology And Pharmaceutical Sciences

# keywords[]
3403 Macromolecular And Materials Chemistry

# keywords[]
Physical Injury - Accidents And Adverse Effects

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
5204 Cognitive And Computational Psychology

# keywords[]
5201 Applied And Developmental Psychology

# keywords[]
Physical Injury - Accidents And Adverse Effects

# keywords[]
Sodium Potassium Chloride Symporter Inhibitors

# keywords[]
3214 Pharmacology And Pharmaceutical Sciences

# keywords[]
3214 Pharmacology And Pharmaceutical Sciences

# keywords[]
Physical Injury - Accidents And Adverse Effects

# keywords[]
1.1 Normal Biological Development And Functioning

# educationAndTraining[].organization.label
University of Colorado Boulder - (Boulder, Colorado, United States)

# educationAndTraining[].field
Psychology and Molecular, Cellular and Developmental Biology

# educationAndTraining[].organization.label
University of Pennsylvania - (Philadelphia, Pennsylvania, United States)

# educationAndTraining[].organization.label
University of Pennsylvania - (Philadelphia, Pennsylvania, United States)

# awardsAndHonors[].label
Mary Tucker Currie Professor of Liberal Arts

# publications[].label
Instrumental learning within the spinal cord: I. Behavioral properties.

# publications[].label
Exercise therapy and recovery after SCI: evidence that shows early intervention improves recovery of function.

# publications[].label
PAIN INDUCED HEMORRHAGE AFTER SPINAL CORD INJURY IS BLOCKED BY LIDOCAINE APPLIED ROSTRALLY TO INJURY

# publications[].label
Analysis of the unique cue in configural discriminations.

# publications[].label
A rodent model of functional electrical stimulation: Evidence spinal neurons modulate adaptive capacity

# publications[].label
Ionic Plasticity: Common Mechanistic Underpinnings of Pathology in Spinal Cord Injury and the Brain.

# publications[].label
Controllability, coping behavior, and stress-induced analgesia in the rat.

# publications[].label
Tail-flick test. I: Impact of a suprathreshold exposure to radiant heat on pain reactivity in rats.

# publications[].label
Brief exposure to a mild stressor enhances morphine-conditioned place preference in male rats.

# publications[].label
The impact of morphine after a spinal cord injury.

# publications[].label
Conditioned changes in pain reactivity: II. In search of the elusive phenomenon of conditioned hyperalgesia.

# publications[].label
Sparing of Descending Axons Rescues Interneuron Plasticity in the Lumbar Cord to Allow Adaptive Learning After Thoracic Spinal Cord Injury.

# publications[].label
AMPA receptor mediated behavioral plasticity in the isolated rat spinal cord.

# publications[].label
Activation of the Opioid and Nonopioid Hypoalgesic Systems at the Level of the Brainstem and Spinal Cord: Does a Coulometric Relation Predict the Emergence or Form of Environmentally Induced Hypoalgesia?

# publications[].label
Uncontrollable stimulation undermines recovery of function after spinal cord injury

# publications[].label
Shock-induced hyperalgesia: III. Role of the bed nucleus of the stria terminalis and amygdaloid nuclei.

# publications[].label
GABA(A) receptor activation is involved in noncontingent shock inhibition of instrumental conditioning in spinal rats.

# publications[].label
Activation of the opioid and nonopioid analgesic systems: evidence for a memory hypothesis and against the coulometric hypothesis.

# publications[].label
Cross tolerance between morphine and the long-term analgesic reaction to inescapable shock.

# publications[].label
Role of cholinergic systems in pain modulation: I. Impact of scopolamine on environmentally induced hypoalgesia and pain reactivity.

# publications[].label
Evidence that descending serotonergic systems protect spinal cord plasticity against the disruptive effect of uncontrollable stimulation.

# publications[].label
Intrathecal morphine attenuates recovery of function after a spinal cord injury.

# publications[].label
Analgesia or addiction?: implications for morphine use after spinal cord injury.

# publications[].label
Learning to promote recovery after spinal cord injury.

# publications[].label
Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.

# publications[].label
THE IMPACT OF NALTREXONE AND MORPHINE-TOLERANCE ON MILD SHOCK-INDUCED HYPOALGESIA

# publications[].label
Instrumental learning within the spinal cord: VI. The NMDA receptor antagonist, AP5, disrupts the acquisition and maintenance of an acquired flexion response.

# publications[].label
The central representation of an aversive event maintains the opioid and nonopioid forms of analgesia.

# publications[].label
Preserving and restoring behavioral potential within the spinal cord using an instrumental training paradigm.

# publications[].label
Central nociceptive sensitization vs. spinal cord training: opposing forms of plasticity that dictate function after complete spinal cord injury.

# publications[].label
BDNF and learning: Evidence that instrumental training promotes learning within the spinal cord by up-regulating BDNF expression.

# publications[].label
Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.

# publications[].label
Regulatory effects of intermittent noxious stimulation on spinal cord injury-sensitive microRNAs and their presumptive targets following spinal cord contusion.

# publications[].label
An IL-1 receptor antagonist blocks a morphine-induced attenuation of locomotor recovery after spinal cord injury.

# publications[].label
Ionic plasticity and pain: The loss of descending serotonergic fibers after spinal cord injury transforms how GABA affects pain.

# publications[].label
PERIPHERAL NOCICEPTIVE INPUT OVERDRIVES AMPA RECEPTOR ACTIVITY TO PRODUCE MALADAPTIVE PLASTICITY AFTER SPINAL CORD INJURY (SCI)

# publications[].label
Shock-induced hyperalgesia: II. Role of the dorsolateral periaqueductal gray.

# publications[].label
Long-term stress-induced analgesia and activation of the opiate system.

# publications[].publisher
American Association for the Advancement of Science (AAAS)

# publications[].label
Uncontrollable stimulation undermines recovery after spinal cord injury.

# publications[].label
Latent inhibition, overshadowing, and blocking of a conditioned antinociceptive response in spinalized rats.

# publications[].label
Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics.

# publications[].label
LONG-TERM EFFECTS OF FOOD-DEPRIVATION .1. IMPACT ON PAIN REACTIVITY AND SHOCK-INDUCED HYPOALGESIA

# publications[].label
CONDITIONED CHANGES IN PAIN REACTIVITY .1. A DISCRETE CS ELICITS HYPOALGESIA, NOT HYPERALGESIA, ON THE TAIL-FLICK TEST

# publications[].label
The time course of learned helplessness, inactivity, and nociceptive deficits in rats

# publications[].label
Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death.

# publications[].label
Peripheral inflammation undermines the plasticity of the isolated spinal cord.

# publications[].label
Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury.

# publications[].label
Spinal neurons exhibit a surprising capacity to learn and a hidden vulnerability when freed from the brain's control.

# publications[].label
Peripheral noxious stimulation reduces withdrawal threshold to mechanical stimuli after spinal cord injury: role of tumor necrosis factor alpha and apoptosis.

# publications[].label
The distinction between integral and separable dimensions: evidence for the integrality of pitch and loudness.

# publications[].label
Associative learning and memory for an antinociceptive response in the spinalized rat.

# publications[].label
Immunization of opioid analgesia: Effects of prior escapable shock on subsequent shock-induced and morphine-induced antinociception

# publications[].label
A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury.

# publications[].label
MicroRNA dysregulation following spinal cord contusion: implications for neural plasticity and repair.

# publications[].label
Engaging pain fibers after a spinal cord injury fosters hemorrhage and expands the area of secondary injury.

# publications[].label
PAIN-INDUCED HEMORRHAGE AFTER SCI DEPENDS ON LESION SEVERITY AND TIME SINCE INJURY

# publications[].label
Mechanisms of Pavlovian conditioning: role of protection from habituation in spinal conditioning.

# publications[].label
Timing in the absence of supraspinal input I: variable, but not fixed, spaced stimulation of the sciatic nerve undermines spinally-mediated instrumental learning.

# publications[].label
The behavioral deficit observed following noncontingent shock in spinalized rats is prevented by the protein synthesis inhibitor cycloheximide.

# publications[].label
Associative Learning and Memory for an Antinociceptive Response in the Spinalized Rat

# publications[].label
Localized and sustained release of brain-derived neurotrophic factor from injectable hydrogel/microparticle composites fosters spinal learning after spinal cord injury.

# publications[].label
Glial tumor necrosis factor alpha (TNF) generates metaplastic inhibition of spinal learning.

# publications[].label
AMPA Receptor Phosphorylation and Synaptic Colocalization on Motor Neurons Drive Maladaptive Plasticity below Complete Spinal Cord Injury.

# publications[].label
Instrumental learning within the spinal cord: IV. Induction and retention of the behavioral deficit observed after noncontingent shock.

# publications[].label
Exposure to intermittent nociceptive stimulation under pentobarbital anesthesia disrupts spinal cord function in rats.

# publications[].label
Role of Descending Serotonergic Fibers in the Development of Pathophysiology after Spinal Cord Injury (SCI): Contribution to Chronic Pain, Spasticity, and Autonomic Dysreflexia.

# publications[].label
Noxious Stimulation Induces Acute Hemorrhage and Impairs Long-Term Recovery after Spinal Cord Injury (SCI) in Female Rats: Evidence Estrous Cycle May Have a Modulatory Effect.

# publications[].label
Therapy and immunization of long-term analgesia in rats

# publications[].label
Evidence for spinal conditioning in intact rats.

# publications[].label
Instrumental learning within the spinal cord: V. Evidence the behavioral deficit observed after noncontingent nociceptive stimulation reflects an intraspinal modification.

# publications[].label
Pain Input Impairs Recovery after Spinal Cord Injury: Treatment with Lidocaine.

# publications[].label
Pavlovian and instrumental conditioning within the spinal cord: Methodological issues

# publications[].label
Influence of naloxone on shock-induced freezing and analgesia.

# publications[].label
Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?

# publications[].label
Spinal glia modulate both adaptive and pathological processes.

# publications[].label
Instrumental learning within the rat spinal cord: localization of the essential neural circuit.

# publications[].label
NOXIOUS STIMULATION AFTER SPINAL CORD INJURY (SCI) INDUCES A BRAIN-DEPENDENT INCREASE IN HEMORRHAGE

# publications[].label
Fixed spaced stimulation restores adaptive plasticity within the spinal cord: Identifying the eliciting conditions.

# publications[].label
THE IMPACT OF SHOCK ON REACTIVITY TO A TACTILE STIMULUS

# publications[].label
The Lower Bounds of Cognition: What Do Spinal Cords Reveal?

# publications[].label
Impact of shock on pain reactivity: II. Evidence for enhanced pain.

# publications[].label
Impact of behavioral control on the processing of nociceptive stimulation.

# publications[].label
Neurofunctionalism Revisited: Learning is More Than You Think It Is

# publications[].label
Evidence That the Central Nervous System Can Induce a Modification at the Neuromuscular Junction That Contributes to the Maintenance of a Behavioral Response.

# publications[].label
An animal model of functional electrical stimulation: evidence that the central nervous system modulates the consequences of training.

# publications[].label
Instrumental learning within the spinal cord. II. Evidence for central mediation.

# publications[].label
BUMETANIDE PROMOTES FUNCTIONAL RECOVERY OF HINDLIMB FUNCTION AND REDUCES HEMORRHAGE AFTER SPINAL CORD INJURY

# publications[].label
Complete spinal cord injury (SCI) transforms how brain derived neurotrophic factor (BDNF) affects nociceptive sensitization.

# publications[].label
Tail-flick test: II. The role of supraspinal systems and avoidance learning.

# publications[].label
Timing in the absence of supraspinal input III: regularly spaced cutaneous stimulation prevents and reverses the spinal learning deficit produced by peripheral inflammation.

# publications[].label
The relationship between shock severity and the form of the antinociception observed in pentobarbital-anesthetized rats

# publications[].label
A Simple Post Hoc Transformation that Improves the Metric Properties of the BBB Scale for Rats with Moderate to Severe Spinal Cord Injury

# publications[].label
Learning from the spinal cord: how the study of spinal cord plasticity informs our view of learning.

# publications[].label
Learning about Time within the Spinal Cord II: Evidence that Temporal Regularity Is Encoded by a Spinal Oscillator.

# publications[].label
Frontal cortex lesions block the opioid and nonopioid hypoalgesia elicited by brief shocks but not the nonopioid hypoalgesia elicited by long shocks.

# publications[].label
Spinal Cord Plasticity Alterations in Reflex Function

# publications[].label
Frontal Cortex Lesions Block the Opioid and Nonopioid Hypoalgesia Elicited by Brief Shocks but Not the Nonopioid Hypoalgesia Elicited by Long Shocks

# publications[].label
Metaplasticity within the spinal cord: Evidence brain-derived neurotrophic factor (BDNF), tumor necrosis factor (TNF), and alterations in GABA function (ionic plasticity) modulate pain and the capacity to learn.

# publications[].label
Brain dependent processes contribute to the adverse consequences of uncontrollable stimulation on the recovery of function

# publications[].label
Instrumental learning within the spinal cord: underlying mechanisms and implications for recovery after injury.

# publications[].label
Opiate antagonists and long-term analgesic reaction induced by inescapable shock in rats.

# publications[].label
Activation of the opioid and nonopioid hypoalgesic systems at the level of the brainstem and spinal cord: does a coulometric relation predict the emergence or form of environmentally induced hypoalgesia?

# publications[].label
Behavioral studies of spinal conditioning: The spinal cord is smarter than you think it is.

# publications[].label
Intermittent noxious stimulation following spinal cord contusion injury impairs locomotor recovery and reduces spinal brain-derived neurotrophic factor-tropomyosin-receptor kinase signaling in adult rats.

# publications[].label
Impact of shock on pain reactivity: III. The magnitude of hypoalgesia observed depends on test location.

# publications[].label
Monitoring recovery after injury: procedures for deriving the optimal test window.

# publications[].label
Group I metabotropic glutamate receptors control metaplasticity of spinal cord learning through a protein kinase C-dependent mechanism.

# publications[].label
Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization.

# publications[].label
The association between spinal cord trauma-sensitive miRNAs and pain sensitivity, and their regulation by morphine.

# publications[].label
Impact of shock on pain reactivity: I. Whether hypo- or hyperalgesia is observed depends on how pain reactivity is tested.

# publications[].label
When Pain Hurts: Nociceptive Stimulation Induces a State of Maladaptive Plasticity and Impairs Recovery after Spinal Cord Injury.

# publications[].label
A Neural-Functionalist Approach to Learning

# publications[].label
Role of supraspinal systems in environmentally induced antinociception: effect of spinalization and decerebration on brief shock-induced and long shock-induced antinociception.

# publications[].label
Loss of learning in the spinal cord: Role of glutamate systems

# publications[].label
Two chronic motor training paradigms differentially influence acute instrumental learning in spinally transected rats.

# publications[].label
Brain-derived neurotrophic factor promotes adaptive plasticity within the spinal cord and mediates the beneficial effects of controllable stimulation.

# publications[].label
Instrumental learning within the spinal cord: III. Prior exposure to noncontingent shock induces a behavioral deficit that is blocked by an opioid antagonist.

# publications[].label
Timing in the absence of supraspinal input II: regularly spaced stimulation induces a lasting alteration in spinal function that depends on the NMDA receptor, BDNF release, and protein synthesis.

# publications[].label
Shock-induced hyperalgesia: evidence forebrain systems play an essential role.

# publications[].label
Extent and control of shock affects naltrexone sensitivity of stress-induced analgesia and reactivity to morphine.

# publications[].label
Presentation of a distractor speeds the decay of a pentobarbital-insensitive nonopioid hypoalgesia in rats

# publications[].label
Pain in a balance: noxious events engage opposing processes that concurrently modulate nociceptive reactivity.

# publications[].label
Role of Cholinergic Systems in Pain Modulation: I. Impact of Scopolamine on Environmentally Induced Hypoalgesia and Pain Reactivity

# publications[].label
Temporal regularity determines the impact of electrical stimulation on tactile reactivity and response to capsaicin in spinally transected rats.

# publications[].label
Learning about time within the spinal cord: evidence that spinal neurons can abstract and store an index of regularity.

# publications[].label
LONG-TERM EFFECTS OF FOOD-DEPRIVATION .2. IMPACT ON MORPHINE REACTIVITY

# publications[].label
Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury.

# publications[].label
A simple post hoc transformation that improves the metric properties of the BBB scale for rats with moderate to severe spinal cord injury.

# publications[].label
Opioid regulation of spinal cord plasticity: evidence the kappa-2 opioid receptor agonist GR89696 inhibits learning within the rat spinal cord.

# publications[].label
Pain and negative affect: evidence the inverse benzodiazepine agonist DMCM inhibits pain and learning in rats.

# publications[].label
Nociceptive plasticity inhibits adaptive learning in the spinal cord.

# publications[].label
PAIN INPUT AFTER SPINAL CORD INJURY INCREASES TISSUE LOSS AND IMPAIRS LONG-TERM RECOVERY IN FEMALE RATS

# researcherOn[].label
Effect of Inflammation on Recovery and Pain After Spinal Cord Injury

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# researcherOn[].label
Nociceptive Input After Spinal Cord Injury (SCI) Expands the Region of Secondary Injury and Undermines Long-Term Recovery

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# researcherOn[].label
Neural Progenitor Cells for Mitigating Pain after Spinal Cord Injury

# researcherOn[].awardedBy.label
Craig H Neilsen Foundation - (Los Angeles, California, United States)

# researcherOn[].label
How and when does peripheral input affect recovery after SCI

# researcherOn[].awardedBy.label
Craig H Neilsen Foundation - (Los Angeles, California, United States)

# researcherOn[].label
Nociceptive (Pain) Input After Spinal Cord Injury (SCI) Enhances Secondary Injury: Identifying Treatments That Can Be Translated to Clinical Practice

# researcherOn[].awardedBy.label
United States Army - (Washington D.C., District of Columbia, United States)

# streetAddress
Texas A&M University; Psychology; 4235 TAMU

# etdChairOf[].label
Lee, Kuan Hsien (2013-08). Timing in the Absence of Supraspinal Input: Effects of Temporally Regular Stimulation on Spinal Plasticity. Doctoral Dissertation.

# etdChairOf[].label
Huang, Yung-Jen (2015-05). Spinal Cord Injury (SCI) Switches How GABA Affects Nociceptive Plasticity. Doctoral Dissertation.