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Central nucleus of the amygdala

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The central nucleus of the amygdala (CeA or aCeN) is a nucleus within the amygdala.[1] It "serves as the major output nucleus of the amygdala and participates in receiving and processing pain information."[2]

Amigdale1

CeA "connects with brainstem areas that control the expression of innate behaviors and associated physiological responses."[3] CeA has dopaminergic projections.

CeA is responsible for "autonomic components of emotions (e.g., changes in heart rate, blood pressure, and respiration) primarily through output pathways to the lateral hypothalamus and brain stem.". CeA is also responsible for "conscious perception of emotion primarily through the ventral amygdalofugal output pathway to the anterior cingulate cortex, orbitofrontal cortex, and prefrontal cortex." [4]

Amygdala subdividisions and outputsEdit

The regions described as amygdala nuclei encompass several structures with distinct connectional and functional characteristics in humans and other animals.[5] Among these nuclei are the basolateral complex, the cortical nucleus, the medial nucleus, and the central nucleus. The basolateral complex can be further subdivided into the lateral, the basal, and the accessory basal nuclei.[6][7]

File:Gray 718-amygdala.png

The amygdalofugal pathway (Latin for "fleeing from the amygdala" and commonly distinguished as the ventral amygdalofugal pathway) is one of the three principal pathways by which fibers leave the amygdala. The other main efferent pathways from the amygdala are the stria terminalis and anterior commissure. The anterior commissure also serves to connect the two amygdala.[How to reference and link to summary or text]

The ventral amygdalofugal pathway carries output from the central and basolateral nuclei and delivers it a number of targets; namely, the medial dorsal nucleus of the thalamus, the hypothalamus, the basal forebrain, the brain stem, septal nuclei and nucleus accumbens.[How to reference and link to summary or text]

ResearchEdit

  • "psychological stressor induced an increase in both CRH mRNA levels and CRH content in the CEA. Exposure to the psychological stressor also caused a significant increase in CRH mRNA levels with a trend for an increase in CRH content in the dorsolateral subdivision of the bed nucleus of the stria terminalis (BNST) which is anatomically associated with the CEA."[8]
  • "oxytocin in the CeA exerts a facilitatory role in the maintenance of hydroelectrolyte balance"[9]
  • "the central nucleus of the amygdala (CeA) and its connections with the nigral dopamine system have been reported to modulate cognitive processes dependent substantially on attentional allocation. CeA dopamine function is involved in modulation of disengagement behavior."[10]
  • "Opioid mechanisms are involved in the control of water and NaCl intake and opioid receptors (ORs) are present in the central nucleus of the amygdala (CeA)" μ-opioid receptors "in the CeA increases hypertonic sodium intake, whereas antagonizing these sites inhibits hypertonic sodium intake. …μ-ORs in the CeA in a positive regulation of sodium intake."[11]
  • CeA "is essential for acquiring and expressing conditional fear after overtraining"[12]
  • "glucocorticoids can facilitate CRH mRNA expression in the CEA, a site implicated in anxiety and fear"[13]

See alsoEdit

ReferencesEdit

  1. (2004). The Role of the Central Nucleus of the Amygdala in Mediating Fear and Anxiety in the Primate. Journal of Neuroscience 24 (24): 5506–15.
  2. (2008). GABAA receptors in the central nucleus of amygdala (CeA) affect on pain modulation. Brain Research 1241: 36–41.
  3. (2008). Amygdala. Scholarpedia 3 (4): 2698.
  4. "Limbic System: Amygdala" Homeostasis and Higher Brain Function, University of Texas Health Science Center at Houston.
  5. (2012). An investigation of the structural, connectional, and functional subspecialization in the human amygdala. Human Brain Mapping: n/a.
  6. Best, Ben The Amygdala and the Emotions. The Anatomical Basis of Mind.Template:Self-published inline
  7. (2010). Diffusion tensor imaging segments the human amygdala in vivo. NeuroImage 49 (4): 2958–65.
  8. (1999). Psychological stress increased corticotropin-releasing hormone mRNA and content in the central nucleus of the amygdala but not in the hypothalamic paraventricular nucleus in the rat. Brain Research 850 (1–2): 136–43.
  9. (2013). Oxytocin in the central amygdaloid nucleus modulates the neuroendocrine responses induced by hypertonic volume expansion in the rat. Journal of Neuroendocrinology: n/a.
  10. (2013). The Role of Central Amygdala Dopamine in Disengagement Behavior. Behavioral Neuroscience.
  11. (2013). Activation of μ-opioid receptors in the central nucleus of the amygdala induces hypertonic sodium intake. Neuroscience 233: 28–43.
  12. (2007). The central nucleus of the amygdala is essential for acquiring and expressing conditional fear after overtraining. Learning & Memory 14 (9): 634–44.
  13. (1994). Corticosterone effects on corticotropin-releasing hormone mRNA in the central nucleus of the amygdala and the parvocellular region of the paraventricular nucleus of the hypothalamus. Brain Research 640 (1–2): 105–12.
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