Unlabelled: Cognitive-behavioral treatments for chronic pain typically target pain-related fear; exposure in vivo is a common treatment focusing on disconfirming harm expectancy of feared movements. Exposure therapy is tailored on Pavlovian extinction; an alternative fear reduction technique that also alters stimulus valence is counterconditioning. We compared both procedures to reduce pain-related fear using a voluntary joystick movement paradigm. Participants were randomly allocated to the counterconditioning or extinction group. During fear acquisition, moving the joystick in 2 directions (conditioned stimulus [CS+]) was followed by a painful electrocutaneous stimulus (pain-unconditioned stimulus [US]), whereas moving the joystick in 2 other directions was not (CS-). During fear reduction, 1 CS+ was extinguished, but another CS+ was still followed by pain in the extinction group; in the counterconditioning group, 1 CS+ was extinguished and followed by a monetary reward-US, and another CS+ was followed by both USs (pain-US and reward-US). The results indicate that counterconditioning effectively reduces pain-related fear but that it does not produce deeper fear reduction than extinction. Adding a reward-US to a painful movement attenuated neither fear nor the intensity/unpleasantness of the pain. Both procedures changed stimulus valence. We contend that changing the affective valence of feared movements might improve fear reduction and may prevent relapse.
Perspective: This article reports no immediate differences between counterconditioning and extinction in reducing pain-related fear in the laboratory. Unexpectedly, both methods also altered stimulus valence. However, we cautiously suggest that methods explicitly focusing on altering the affective valence of feared movements may improve the long-term effectiveness of fear reduction and prevent relapse.
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http://dx.doi.org/10.1016/j.jpain.2015.09.007 | DOI Listing |
Alzheimers Dement
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
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Background: Neurodegenerative disorders such as Alzheimer's Disease (AD) are increasingly associated with irregular lipid accumulation. Dysfunction in the catabolism of sphingolipids leads to many neurodegenerative disorders but has only recently garnered interest in AD. Excess ceramide deposition has been observed in Aβ-plaques, plasma, and cerebrospinal fluid in AD patients and AD mouse models.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Iowa, Iowa City, IA, USA.
Background: Sorbs2 is a cytoskeletal adaptor protein that is expressed in hippocampal neurons, but its mechanistic role in these cells is not yet fully understood.
Method: We created two groups of mice for our study: whole-body Sorbs2-Knockout (KO) mice and Sorbs2-Flox mice, which had neuronal knockout via AAV-PHP.eB-hSyn1-Cre virus injection.
Alzheimers Dement
December 2024
Edith Cowan University, Perth, Western Australia, Australia.
Background: Our research group is currently exploring the potential of Butyric acid (NaB), a Short Chain Fatty Acid (SCFA), as a novel therapeutic agent for Alzheimer's disease (AD).
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Centre for Brain Research, Indian Institute of Science, Bangalore, Karnataka, India.
Background: F-actin plays crucial roles in establishment and maintenance of synapses including post synaptic density organization, facilitation of vesicle trafficking, anchoring of postsynaptic receptors, and involvement in translational machinery. Proteomic analysis of actin-interacting proteins revealed the interaction of PSD-95 with actin in synaptosomes from brain cortex of APP/PS1 mice. PSD-95 functions as a critical scaffold for the assembly of neurotransmitter receptors at the synapse, playing a pivotal role in regulating synaptic strength and plasticity.
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