There are conflicting reports on the impact of antidepressants on neural reactions for positive information. We thus hypothesized that there would be clinically important individual differences in neural reactivity to positive information during SSRI therapy. We further predicted that only those who responded to SSRIs would show increased amygdala reactivity to positive information following treatment to a level similar to that seen in healthy participants. Depressed individuals (n = 17) underwent fMRI during performance of a task involving rating the self-relevance of emotionally positive and negative cue words before and after receiving 12 weeks of SSRI therapy. At post-treatment, SSRI responders (n = 11) had increased amygdala activity in response to positive stimuli, and decreased activity in response to negative stimuli, compared to non-responders (n = 6). Results suggest that normalizing amygdala responses to salient information is a correlate of SSRI efficacy. Second line interventions that modulate amygdala activity, such as fMRI neurofeedback, may be beneficial in those who do not respond to SSRI medications.
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http://dx.doi.org/10.1016/j.nicl.2020.102388 | DOI Listing |
Rev Neurosci
January 2025
School of Medical Sciences, Henan University of Chinese Medicine, Zhengzhou 450046, Henan Province, China.
Cholecystokinin (CCK) is a major neuropeptide in the brain that functions as a neurotransmitter, hormone, and growth factor. The peptide and its receptors are widely expressed in the brain. CCK signaling modulates synaptic plasticity and can improve or impair memory formation, depending on the brain areas studies and the receptor subtype activated.
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January 2025
Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences (CAS), Beijing, the People's Republic of China.
Background: Psychotherapeutic memory plays an important role in maintaining therapeutic effects; however, the neural mechanisms of therapeutic metaphor promoting long-term memory were still unknown.
Objective: This study used metaphorical micro-counseling dialog scenarios to investigate the memory effect of therapeutic metaphor and correlated neural mechanisms.
Methods: At first, 31 participants read a mental distress problem, followed by a metaphorical or a literal solution, while undergoing functional magnetic resonance imaging scanning during the encoding phase.
Neuroimage
January 2025
Neuropsychology and Functional Neuroimaging, Universitat Jaume I, Castelllón de la Plana, Spain. Electronic address:
Introduction: Chronic exercise has been linked to structural and functional changes in the hippocampus and surrounding areas. However, less is known about how a single session of exercise can induce immediate effects that may contribute to these longterm changes.
Objective/methods: Resting-state fMRI was used to investigate changes in brain networks 19 minutes after a 20-minute bout of vigorous-intensity acute exercise.
Epilepsy Behav
January 2025
Epileptology Unit Reference Center for Rare Epilepsies Department of Neurology AP-HP Pitié-Salpêtrière Hospital Paris France; Rehabilitation Unit AP-HP Pitié-Salpêtrière Hospital Paris France; Paris Brain Institute (ICM), Sorbonne-Université, Inserm U1127, CNRS 7225, Paris F-75013 France; Université Paris Sorbonne, Paris, France. Electronic address:
This narrative review aims to identify and summarize existing research to better understand the pathophysiological and neuroanatomical bases of social cognition deficits in people with epilepsy. The neuroanatomical basis of social cognition was primarily examined in healthy subjects. In healthy individuals, social cognition is supported by a complex network of interconnected brain regions.
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January 2025
Department of Biological Sciences, Southern Methodist University, Dallas, TX 75275, USA.
Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related death, likely stemming from seizure activity disrupting vital brain centres controlling heart and breathing function. However, understanding of SUDEP's anatomical basis and mechanisms remains limited, hampering risk evaluation and prevention strategies. Prior studies using a neuron-specific conditional knockout mouse model of SUDEP identified the primary importance of brain-driven mechanisms contributing to sudden death and cardiorespiratory dysregulation; yet, the underlying neurocircuits have not been identified.
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