Neuroanatomical Distribution of Aromatase MRNA in the Rat Brain: Indications of Regional Regulation

Abstract

Aromatase, the enzyme responsible for the conversion of testosterone to estradiol, is found in the rat brain and is present in regions of the preoptic area, hypothalamus, and limbic system. Gonadal steroid hormones regulate aromatase activity levels in many brain regions, but not all. Using in situ hybridization, we examined the distribution of aromatase mRNA in the adult male forebrain, as well as the levels of aromatase mRNA in the brains of males and females, and the regulation by gonadal steroid hormones. In the adult male, many heavily labelled cells were found in the encapsulated bed nucleus of the stria terminalis (BNST), the medial preoptic nucleus (MPN), the ventromedial nucleus (VMN), the medial amygdala (mAMY) and the cortical amygdala (CoAMY). The regional distribution of aromatase mRNA was similar in males and females, but males tended to have a greater number of aromatase mRNA-expressing cells in each region compared to females. Aromatase mRNA levels in the BNST, MPN, VMN and mAMY tended to be lower in castrated males than in intact males, whereas aromatase mRNA levels were unaltered by castration in the CoAMY. Further analysis of individual cells expressing aromatase mRNA suggests that aromatase mRNA may be regulated by steroid hormones differentially in specific populations of cells in regions where enzyme activity levels are steroid-hormone-dependent.

Rapid control of male typical behaviors by brain-derived estrogens

“…Together, these observations suggests that if estrogens induce rapid and transient behavioral effects in males, mechanisms must exist to regulate local estrogen concentrations on much shorter time scales. Brain aromatase, which is expressed and active especially in brain regions controlling aggressive and sexual behaviors [14; 49; 93; 137; 226; 227; 229; 233; 234; 280; 282] but also in the hippocampus [14; 226; 229; 233; 239; 240; 260; 282], was thus considered as a potential local source of estrogens. However, due to their lipophilic nature, estrogens cannot be stored in synaptic vesicles before rapid release like classical neurotransmitters or neuropeptides.…”

“…The enzyme is mainly expressed in the ovaries but is also found in many other tissues including the brain. In reptiles, birds and mammals, brain aromatase expression is restricted to specific neuronal populations mainly located in the hypothalamic/preoptic area (HPOA) including the medial preoptic nucleus and in the limbic system [11; 49; 60; 93; 136; 137; 169; 226; 227; 228; 229; 233; 234; 240; 260; 280; 282]. In songbird species, aromatase is found in another neuronal population located in the caudomedial nidopallium NCM, a pallial area (homologous to secondary auditory cortex in mammals) adjacent to the song control nucleus HVC (acronym used as proper name [14; 240; 251]).…”

Local modulation of steroid action: rapid control of enzymatic activity

“…This transformation is catalyzed by the enzyme aromatase, also known as CYP 19 or estrogen synthase. In most vertebrates, central aromatase expression is restricted to specific neuronal populations mainly located in the hypothalamic/preoptic areas including the medial preoptic nucleus and in the limbic system (Roselli et al, 1985 ; Foidart et al, 1995a , b ; Wagner and Morrell, 1997 ; Trainor et al, 2007 ; Metzdorf et al, 1999 ; Roselli and Resko, 2001 ). It should be noted that songbirds have an additional population of aromatase expressing neurons in the caudomedial nidopallium, in the telencephalon (NCM; Shen et al, 1995 ; Saldanha et al, 2000 ).…”

MPTP Neurotoxicity and Testosterone Induce Dendritic Remodeling of Striatal Medium Spiny Neurons in the C57Bl/6 Mouse

“…Indeed, experimental evidence has shown that estrogen also protects against nigrostriatal degeneration in the male striatum. However, while circulating estrogen is abundant in females, striatal estrogen available in males is minimal due to the low levels of aromatase in the striatum [63–66]. Therefore, the inability of testosterone to act through estrogenic mechanisms effectively prevents hormone-driven neuroprotection in the striatum.…”