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Dorsal Raphe Nucleus panic 


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The dorsal raphe nucleus (DRN) is involved in panic-like behaviors and fear-induced antinociception. Activation of DRN 5-HT2A receptors modulates panic attack-like behavior and antinociception organized by brainstem neurons, such as those in the superior colliculus (SC) . Chemical stimulation of the lateral wings subnucleus of the DRN (lwDR) evokes escape responses, suggesting a role in panic-like behaviors . The DRN is also connected to the locus coeruleus (LC) and sends pathways to the medial hypothalamus (MH), where it modulates defensive behaviors . Additionally, DRN 5-HT2A receptors play a critical role in panic attack-like defensive behavior and fear-induced antinociception organized by neurons in the central nucleus of the inferior colliculus (IC) . Different subsets of neurons in the DRN are activated by anxiety- and panic-relevant stimuli/situations, with implications for the pathophysiology of generalized anxiety and panic disorders .

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The study suggests that 5-HT2A receptors in the dorsal raphe nucleus play a critical role in modulating panic-like defensive behaviors.
The study suggests that dysfunction in the mechanisms controlling escape in the dorsal raphe nucleus is critically implicated in the pathophysiology of panic disorder.
The study suggests that 5-HT2A receptors in the Dorsal Raphe Nucleus play a critical role in the modulation of panic attack-like behavior.
The blockade of noradrenergic receptors in the Dorsal Raphe Nucleus impairs the panic-like response organized by medial hypothalamus neurons.

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How does serotonin affects anxiety behaviors through the projections from the raphe to the hippocampus?5 answersSerotonin affects anxiety behaviors through projections from the raphe to the hippocampus. Activation of serotonin neurons in the median raphe nucleus (MRN) promotes an anxiogenic state, and this effect may be mediated by serotonergic signaling within the dorsal hippocampus (dHC). Optogenetic stimulation of MRN serotonin neurons elicits anxiety-like behaviors, and stimulation of serotonin terminals in the dHC recapitulates these anxiety-like behaviors. Deep brain stimulation (DBS) of the dorsal subregion of the dorsal raphe (DRD), which sends serotonergic projections to the ventral hippocampus, induces anxiolytic-like effects. Serotonergic inputs from the raphe nuclei to the hippocampus carry reward and locomotion information, suggesting a role in integrating locomotion and reward information into the hippocampus. The dorsal raphe serotonin system contains parallel sub-systems that differ in input and output connectivity, physiological response properties, and behavioral functions. Serotonin from the dorsal raphe enhances fear and anxiety by activating a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed nucleus of the stria terminalis (BNST).
What is the brain circuitry of PTSD?5 answersThe brain circuitry of PTSD involves dysfunction in several regions. The amygdala is hyperresponsive, while the ventromedial prefrontal cortex (vmPFC) is hyporesponsive, leading to a failure of fear inhibition. The dorsal anterior cingulate cortex (dACC) and insula are hyperresponsive, indicating heightened threat processing. The hippocampus also functions abnormally, although the direction of this abnormality varies. Additionally, there is increased neural activity and functional connectivity between brain regions involved in the innate alarm system (IAS), including the locus coeruleus, superior colliculus, amygdala, and prefrontal cortex. These alterations are observed during both subconscious threat processing and at rest, suggesting increased defensive posturing. Overall, dysregulations in these neurocircuits contribute to the development and expression of key PTSD symptoms.
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