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Review
. 2008 Sep;213(1-2):73-91.
doi: 10.1007/s00429-008-0176-2. Epub 2008 Feb 19.

The comparative distributions of the monoamine transporters in the rodent, monkey, and human amygdala

Affiliations
Review

The comparative distributions of the monoamine transporters in the rodent, monkey, and human amygdala

Hilary R Smith et al. Brain Struct Funct. 2008 Sep.

Abstract

The monoamines in the amygdala modulate multiple aspects of emotional processing in the mammalian brain, and organic or pharmacological dysregulation of these systems can result in affective pathologies. Knowledge of the normal distribution of these neurotransmitters, therefore, is central to our understanding of both the normal processes regulated by the amygdala and the pathological conditions associated with monoaminergic dysregulation. The monoaminergic transporters have proven to be accurate and reliable markers of the distributions of their substrates. The purpose of this review was twofold: First, to briefly recount the functional relevance of dopamine, serotonin, and norepinephrine transmission in the amygdala, and second, to describe and compare the distributions of the monoamine transporters in the rodent, monkey, and human brain. The transporters were found to be heterogeneously distributed in the amygdala. The dopamine transporter (DAT) is consistently found to be extremely sparsely distributed, however the various accounts of its subregional topography are inconsistent, making any cross-species comparisons difficult. The serotonin transporter (SERT) had the greatest overall degree of labeling of the three markers, and was characterized by substantial inter-species variability in its relative distribution. The norepinephrine transporter (NET) was shown to possess an intermediate level of labeling, and like the SERT, its distribution is not consistent across the three species. The results of these comparisons indicate that caution should be exercised when using animal models to investigate the complex processes modulated by the monoamines in the amygdala, as their relative contributions to these functions may differ across species.

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Figures

Fig. 1
Fig. 1
Representative autoradiograms of [3H]PTT (DAT), [3H]citalopram (SERT), and [3H]nisoxetine (NET; Hipolide et al. 2005) binding sites in the rat brain at the level of the amygdala. Bl basal nucleus, lateral division; Bm basal nucleus, medial division; CEl central nucleus, lateral division; CEm central nucleus, medial division; Co cortical nucleus; L lateral nucleus. [3H]nisoxetine image reproduced from Hipolide et al. (2005) with permission from Elsevier
Fig. 2
Fig. 2
Representative autoradiograms of [3H]CFT (DAT), [3H]citalopram (SERT), and [3H]nisoxetine (NET) binding in the monkey amygdala. ABmc accessory basal nucleus, magnocellular division; ABpc accessory basal nucleus, parvocellular division; Bmc Basal nucleus, magnocellular division; Bpc basal nucleus, parvocellular division; CEl central nucleus, lateral division; CEm central nucleus, medial division; L lateral nucleus; M medial nucleus; PAC periamygdaloid cortex

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