Stress impairs 5-HT2A receptor-mediated serotonergic facilitation of GABA release in juvenile rat basolateral amygdala.
TLDR
In stressed rats, the 5-HT2A receptor-mediated facilitative actions were severely impaired, which might result in an amygdala circuitry with hyperexcitability, and a lower threshold of activation, and thus be an important mechanism underlying the emergence of stress-associated psychiatric symptoms.About:
This article is published in Neuropsychopharmacology.The article was published on 2009-01-01 and is currently open access. It has received 130 citations till now. The article focuses on the topics: Basolateral amygdala & Agonist.read more
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Synaptic plasticity in depression: molecular, cellular and functional correlates.
TL;DR: Subregions of the prefrontal cortex and hippocampus structural and synapse-related findings seem consistent with a deficit in long-term potentiation (LTP) and facilitation of long- term depression (LTD), particularly at excitatory pyramidal synapses.
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The basolateral amygdala in reward learning and addiction
Kate M. Wassum,Alicia Izquierdo +1 more
TL;DR: Evidence is derived for BLA as a neural integrator of reward value, history, and cost parameters and evidence that experiences with opiates and psychostimulants alter these outcome representations in BLA, resulting in long-term modified action.
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The role of serotonin 5-HT2A receptors in memory and cognition.
TL;DR: It is concluded that the development of selective 5-HT2AR modulators to target distinct signaling pathways and neural circuits represents a new possibility for treating emotional, neuropsychiatric, and neurodegenerative disorders.
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Revisiting the Serotonin Hypothesis: Implications for Major Depressive Disorders
TL;DR: The overarching goal of this review is to present recent findings from studies examining the serotonergic pathway in MDD, with a focus on SERT and the serotonin 1A (5-HT1A), serotonin 1B (5 -HT1B), and serotonin 2A ( 5-HT2A) receptors.
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Serotonin, Amygdala and Fear: Assembling the Puzzle.
TL;DR: The aim of this review is to elucidate the physiological role of 5-HT in fear learning via its action on the neuronal circuits of the amygdala and discuss how recently developed optogenetic tools combined with electrophysiological recordings and behavior could progress the knowledge of the mechanisms underlying5-HT modulation ofFear learning via action on amygdala circuits.
References
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Emotion Circuits in the Brain
TL;DR: The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area, and much of the progress has come from studies of fear, and especially fear conditioning as mentioned in this paper.
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A neurotrophic model for stress-related mood disorders.
TL;DR: Analysis of preclinical cellular and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies, are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation ofBDNF plays a role in the actions of antidepressant treatment.
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Serotonin Transporter Genetic Variation and the Response of the Human Amygdala
Ahmad R. Hariri,Venkata S. Mattay,Alessandro Tessitore,Bhaskar Kolachana,Francesco Fera,David Goldman,Michael F. Egan,Daniel R. Weinberger +7 more
TL;DR: Genetically driven variation in the response of brain regions underlying human emotional behavior is demonstrated and differential excitability of the amygdala to emotional stimuli may contribute to the increased fear and anxiety typically associated with the short SLC6A4 allele.
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The emotional brain, fear, and the amygdala.
TL;DR: Research on the role of the amygdala in fear conditioning, a behavioral procedure used to couple meaningless environmental stimuli to emotional (defense) response networks, concludes that the amygdala plays critical role in linking external stimuli to defense responses.
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Neuroimaging studies of mood disorders.
TL;DR: Findings implicate interconnected neural circuits in which pathologic patterns of neurotransmission may result in the emotional, motivational, cognitive, and behavioral manifestations of primary and secondary affective disorders.