Ontogeny of the Human Amygdala

Abstract

Data on the fetal development of the human amygdala is reviewed with special reference to major ontogenetic events. In the fifth gestational month, the inferior portion of the amygdala reveals cell‐dense columns merging with the ganglionic eminence (proliferative zone) in Nissl‐stained sections. These columns contain vimentin‐positive fibers and can therefore be regarded as migrational routes. In the sixth and seventh months, distinct reorganization of the cytoarchitectonics takes place. The sequential occurrence of afferens can be visualized using anti‐GAP‐43; moreover, outgrowing axons appear to reach the periphery of the ganglionic eminence. The latter may thus represent an intermediate target for growing axons using anti‐calbindin and anti‐calretinin. Migrating and immature amygdaloid neurons can be shown in the fifth month. From the eighth month onwards, various nonpyramidal neurons and pyramidal neurons are immunolabeled. Transient expression of calretinin in pyramidal neurons is observed. When punctate calbindin and calretinin immunostaining in the fifth and eighth months is compared, distinct redistribution is observed. On the whole, it is apparent that the amygdala has reached a high degree of maturity in the eighth month. At this developmental stage, AKAP79, being enriched in postsynaptic densities, shows a characteristic nuclear‐specific distribution pattern. The latter largely corresponds to the expression pattern of NMDAR1. Thus, AKAP79 may have a preference for anchoring enzymes to glutamate receptors. The aforementioned results provide a basis for investigations on subtle changes in pathologically altered material, such as hemorrhage, in the ganglionic eminence of preterm infants.

The neurobiology of Williams syndrome: Cascading influences of visual system impairment?

“…The medial, lateral, and caudal ganglionic eminences populate different regions of the mouse brain with GABAergic interneurons [80]. For example, medial ganglionic eminence neurons migrate to the striatum, thalamus, and cortex [78], while the caudal ganglionic eminence contributes neurons to the amygdala [81]. Each region of the ganglionic eminence appears to be genetically distinct based on studies of knockout of homeobox precursors (e.g.…”

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“…Although the basic architecture of the human amygdala is present at birth (Humphrey, 1968;Ulfig et al, 2003), it does appear to undergo significant structural and functional remodeling and refinement across the infancy, childhood, and adolescent stages of development (see Tottenham, 2014;Tottenham and Sheridan, 2009 for a review). Although the most rapid postnatal volumetric growth occurs soon after birth (eg, over 100% increase in volume in 0-1 year followed by a 9% increase from years 1 to 2; Gilmore et al, 2012; also see Payne et al, 2010;Uematsu et al, 2012), the amygdala continues to increase in volume until 4 years of age in females and 18 years of age in males (Giedd et al, 1996;Mosconi et al, 2009;Nordahl et al, 2012;Schumann et al, 2004).…”

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