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Papers by Eric Crown
Gut and Liver, Nov 15, 2021
Brain Research Reviews, Apr 1, 2009
Journal of Viral Hepatitis, May 20, 2019
Neuroscience Letters, Aug 1, 2005
Due to the character of the original source materials and the nature of batch digitization, quali... more Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.Includes bibliographical references (leaves 66-72).Issued also on microfiche from Lange Micrographics.Six experiments are reported that explore the relation between a learning/performance deficit observed in signalized rats and the phenomenon of learned helplessness. Previous research in signalized rats has demonstrated that exposure to aversive events that cannot be controlled (noncontingent events) has a deleterious effect on instrumental learning, much like exposure to inescapable shock affects escape/avoidance learning in intact animals. Experiment 1 showed that noncontingent tailshock has an effect similar to noncontingent legshock, inducing a learning deficit in spinal rats. Experiment 2 showed that 6 min of intermittent tailshock at an intensity of 1.5 mA was required to induce the deficit. Previous research demonstrated that the learning deficit observed following noncontingent legshock lasted for at least 20 hrs. Experiment 3 demonstrated that the learning deficit resulting from noncontingent tailshock decays between 48 and 96 hrs. Experiment 4 demonstrated that 360 s of 1.5 mA tailshock does not induce a deficit if subjects are signalized 2 hrs after shock exposure, suggesting that brain-mediated mechanisms can inhibit the induction of the learning deficit. Experiments on learned helplessness using intact rats have demonstrated that the learning deficit can be counteracted by prior exposure to contingent shock (an "immunization" experiment) or by shaping animals to learn to respond following noncontingent shock (a "therapy" experiment). Experiments 5 & 6 showed that these procedures also attenuate the learning deficit in spinal rats
Physiology & Behavior, 2002
Neuroscience Letters, 2005
Molecular Pain, 2008
Background: Safe and effective treatment for chronic inflammatory and neuropathic pain remains a ... more Background: Safe and effective treatment for chronic inflammatory and neuropathic pain remains a key unmet medical need for many patients. The recent discovery and description of the transient receptor potential family of receptors including TRPV1 and TRPA1 has provided a number of potential new therapeutic targets for treating chronic pain. Recent reports have suggested that TRPA1 may play an important role in acute formalin and CFA induced pain. The current study was designed to further explore the therapeutic potential of pharmacological TRPA1 antagonism to treat inflammatory and neuropathic pain. Results: The in vitro potencies of HC-030031 versus cinnamaldehyde or allyl isothiocyanate (AITC or Mustard oil)-induced TRPA1 activation were 4.9 ± 0.1 and 7.5 ± 0.2 μM respectively (IC50). These findings were similar to the previously reported IC50 of 6.2 μM against AITC activation of TRPA1 [ 1 ]. In the rat, oral administration of HC-030031 reduced AITC-induced nocifensive behaviors ...
The Journal of Pain, 2008
Experimental Neurology, 2012
Effective treatments for patients suffering from chronic pain remain an area of intense focus wit... more Effective treatments for patients suffering from chronic pain remain an area of intense focus within the pharmaceutical industry, as the development of novel therapies would help to treat an area of significant unmet medical need. The successful development of pharmacological agents to treat inflammatory and neuropathic pain conditions relies on a thorough understanding of the mechanisms that underlie the development and maintenance of chronic pain states. The goal of this review is to highlight recent discoveries regarding the intracellular signaling mechanisms that appear to play a critical role in persistent inflammatory and neuropathic pain. The review will focus on the mitogen activated protein kinase family of enzymes and the data suggesting that treatments designed to inhibit the activation of these enzymes may lead to significant advancements in the treatment of chronic pain. The review will also highlight the important interplay between neurons and non-neuronal cells (i.e., microglia and astrocytes) within the dorsal horn of the spinal cord in the generation and maintenance of chronic inflammatory and neuropathic pain.
Experimental Neurology, 2007
Experimental Neurology, 2005
Brain Research Reviews, 2009
Behavioural Brain Research, 2007
Behavioral Neuroscience, 2003
Previous work has demonstrated that the spinal cord, isolated from higher neural structures, can ... more Previous work has demonstrated that the spinal cord, isolated from higher neural structures, can support a simple form of instrumental learning. Furthermore, preexposure to uncontrollable (noncontingent) shock to the leg or tail inhibits this form of learning. The present study explores the role of GABA(A) receptor modulation on this inhibitory effect in spinal cord-transected rats. Intrathecal administration of the GABA(A) receptor antagonist bicuculline blocked induction and expression of the inhibition. The GABA(A) receptor agonist muscimol inhibited learning in a dose-dependent manner. However, this effect was transient and showed no additivity with shock. The findings suggest that GABA(A) receptor activation may work like a pharmacological switch that is activated by noncontingent shock to inhibit instrumental conditioning within the spinal cord.
Gut and Liver, Nov 15, 2021
Brain Research Reviews, Apr 1, 2009
Journal of Viral Hepatitis, May 20, 2019
Neuroscience Letters, Aug 1, 2005
Due to the character of the original source materials and the nature of batch digitization, quali... more Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.Includes bibliographical references (leaves 66-72).Issued also on microfiche from Lange Micrographics.Six experiments are reported that explore the relation between a learning/performance deficit observed in signalized rats and the phenomenon of learned helplessness. Previous research in signalized rats has demonstrated that exposure to aversive events that cannot be controlled (noncontingent events) has a deleterious effect on instrumental learning, much like exposure to inescapable shock affects escape/avoidance learning in intact animals. Experiment 1 showed that noncontingent tailshock has an effect similar to noncontingent legshock, inducing a learning deficit in spinal rats. Experiment 2 showed that 6 min of intermittent tailshock at an intensity of 1.5 mA was required to induce the deficit. Previous research demonstrated that the learning deficit observed following noncontingent legshock lasted for at least 20 hrs. Experiment 3 demonstrated that the learning deficit resulting from noncontingent tailshock decays between 48 and 96 hrs. Experiment 4 demonstrated that 360 s of 1.5 mA tailshock does not induce a deficit if subjects are signalized 2 hrs after shock exposure, suggesting that brain-mediated mechanisms can inhibit the induction of the learning deficit. Experiments on learned helplessness using intact rats have demonstrated that the learning deficit can be counteracted by prior exposure to contingent shock (an "immunization" experiment) or by shaping animals to learn to respond following noncontingent shock (a "therapy" experiment). Experiments 5 & 6 showed that these procedures also attenuate the learning deficit in spinal rats
Physiology & Behavior, 2002
Neuroscience Letters, 2005
Molecular Pain, 2008
Background: Safe and effective treatment for chronic inflammatory and neuropathic pain remains a ... more Background: Safe and effective treatment for chronic inflammatory and neuropathic pain remains a key unmet medical need for many patients. The recent discovery and description of the transient receptor potential family of receptors including TRPV1 and TRPA1 has provided a number of potential new therapeutic targets for treating chronic pain. Recent reports have suggested that TRPA1 may play an important role in acute formalin and CFA induced pain. The current study was designed to further explore the therapeutic potential of pharmacological TRPA1 antagonism to treat inflammatory and neuropathic pain. Results: The in vitro potencies of HC-030031 versus cinnamaldehyde or allyl isothiocyanate (AITC or Mustard oil)-induced TRPA1 activation were 4.9 ± 0.1 and 7.5 ± 0.2 μM respectively (IC50). These findings were similar to the previously reported IC50 of 6.2 μM against AITC activation of TRPA1 [ 1 ]. In the rat, oral administration of HC-030031 reduced AITC-induced nocifensive behaviors ...
The Journal of Pain, 2008
Experimental Neurology, 2012
Effective treatments for patients suffering from chronic pain remain an area of intense focus wit... more Effective treatments for patients suffering from chronic pain remain an area of intense focus within the pharmaceutical industry, as the development of novel therapies would help to treat an area of significant unmet medical need. The successful development of pharmacological agents to treat inflammatory and neuropathic pain conditions relies on a thorough understanding of the mechanisms that underlie the development and maintenance of chronic pain states. The goal of this review is to highlight recent discoveries regarding the intracellular signaling mechanisms that appear to play a critical role in persistent inflammatory and neuropathic pain. The review will focus on the mitogen activated protein kinase family of enzymes and the data suggesting that treatments designed to inhibit the activation of these enzymes may lead to significant advancements in the treatment of chronic pain. The review will also highlight the important interplay between neurons and non-neuronal cells (i.e., microglia and astrocytes) within the dorsal horn of the spinal cord in the generation and maintenance of chronic inflammatory and neuropathic pain.
Experimental Neurology, 2007
Experimental Neurology, 2005
Brain Research Reviews, 2009
Behavioural Brain Research, 2007
Behavioral Neuroscience, 2003
Previous work has demonstrated that the spinal cord, isolated from higher neural structures, can ... more Previous work has demonstrated that the spinal cord, isolated from higher neural structures, can support a simple form of instrumental learning. Furthermore, preexposure to uncontrollable (noncontingent) shock to the leg or tail inhibits this form of learning. The present study explores the role of GABA(A) receptor modulation on this inhibitory effect in spinal cord-transected rats. Intrathecal administration of the GABA(A) receptor antagonist bicuculline blocked induction and expression of the inhibition. The GABA(A) receptor agonist muscimol inhibited learning in a dose-dependent manner. However, this effect was transient and showed no additivity with shock. The findings suggest that GABA(A) receptor activation may work like a pharmacological switch that is activated by noncontingent shock to inhibit instrumental conditioning within the spinal cord.