Comparison of ventromedial hypothalamic nucleus growth hormone-releasing hormone neuron counterregulatory neurochemical marker gene expression in young adult versus middle-aged male and female rats

比较青年成年大鼠与中年雄性和雌性大鼠下丘脑腹内侧核生长激素释放激素神经元拮抗调节神经化学标记基因的表达

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Abstract

Aging impairs glucose counterregulatory function by unknown mechanisms. Ventromedial hypothalamic nucleus/dorsomedial division (VMNdm) growth hormone-releasing hormone (Ghrh) neurons control counterregulation through Ghrh-modulated discharge of structurally diverse co-expressed neurochemicals. Current research used gene silencing and single-cell laser-catapult-microdissection/multiplex qPCR tools to investigate whether aging alters eu- and/or hypoglycemic patterns of co-produced counterregulatory-inhibiting (γ-aminobutyric acid) or -stimulating (Ghrh; glutamate; nitric oxide) neurotransmitter marker genes in this cell population. Data document basal Ghrh mRNA diminution in older, i.e., middle-aged rats of each sex and age-specific Ghrh transcriptional responses to hypoglycemia in females. Older rats showed Ghrh repression of glutamate decarboxylase(67) (GAD(67)) and GAD(65) mRNAs, a gain of inhibitory tone in female. In middle-age male rats, both GAD transcripts were refractory to hypoglycemia, an age-related response loss. In older females, hypoglycemia stimulated GAD(65) gene expression, contrary to Ghrh-mediated repression in young adult animals. Ghrh suppressed glutaminase (GLS) mRNA in middle-aged rats of each sex, like young adults. Unlike young adult males, older males showed no GLS transcriptional response to hypoglycemia; older hypoglycemic females exhibited up-regulated GLS mRNA, differing from down-regulated expression in younger animals. Aging reduced neuronal nitric oxide synthase (nNOS) gene profiles in females only; nNOS transcription was increased by hypoglycemia in middle-aged rats irrespective of sex, but was unopposed by Ghrh, indicating loss of this inhibitory tone. Results bolster the notion that by midde-age, aging may adjust, according to sex, multi-modal transmitter signaling by VMNdm Ghrh neurons to the brain glucose-regulatory network. Further research is justified to ascertain consequences of aging-associated patterns of co-expressed transmitter release on counterregulation in each sex.

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