A decrease in E2 levels correlates with the decrease of glutamate concentrations within the medial PFC (Yap et al., 2021). The postsynaptic effects of E2 on these actions is necessary to understand the synaptic plasticity capabilities of estradiol. Treatment with E2 enhanced NMDA glutamate receptor-mediated excitatory postsynaptic potential, hippocampal long-term potentiation (Foy et al., 1999), increase in dendritic spine density (Woolley and McEwen, 1994), and increased the number of NMDA receptor binding sites (Weiland, 1992; Gazzaley et al., 1996). Amphetamine-induced DA response increased in the striatum (Becker, 1990; Castner et al., 1993) and K + -stimulated DA release increased in both the striatum and NAc (Becker, 1990; Thompson and Moss, 1994) in vivo, vitro, and OVX females when treated with E2, but not in males. Future studies should not only be replicated to ensure accuracy among findings of the relationship of E2 and DA, but also should include males as they are severely underrepresented in this line of research. Other studies observed no change in D2 availability in the striatum during both the high and low-estrogen phases of the menstrual cycle (Petersen et al., 2021). Similar to TPH, TH is the rate-limiting enzyme in dopamine synthesis indicating that E2, ERα, and ERβ influence dopamine transcription.
Testosterone is an androgen hormone primarily produced in the testes (in men) and ovaries (in women), with small amounts made in the adrenal glands. This article will help you explore how testosterone interacts with these neurotransmitters, including some effective ways to balance them. Testosterone is a major sex hormone that helps regulate various physiological and neurological functions. Low testosterone levels can contribute to fatigue, decreased drive, and emotional flatness. That’s a question for a thoughtful discussion with your gynecologist or psychiatrist, but there’s no doubt that hormones and mood are deeply intertwined. The serotonergic system integrates sex steroid information and plays a central role in mood and stress regulation, cognition, appetite and sleep.
A study examined PC12 cells, a type of catecholamine cells that synthesize, store and release dopamine, transfected with the reporter construct p5’TH (−773/+27)/Luc and expression vectors for mouse ERα and ERβ, investigating ERs’ influence on TH transcription. In ERβ knockout mice, 5-HT levels are lower in various brain regions compared with controls (Imwalle et al., 2005). It is theorized that after 5-HT2A receptor activation, 5-HT1A receptors become unable to reduce 5-HT production, resulting in an increase in 5-HT concentrations (Rybaczyk et al., 2005). Activation of 5-HT2A receptors induces transient desensitization of 5-HT1A receptor signaling (Zhang et al., 2001).
Estrogens are among the wide range of endocrine-disrupting compounds because they have high estrogenic potency. The name estrogen is derived from the Greek οἶστρος (oîstros), literally meaning "verve" or "inspiration" but figuratively sexual passion or desire, and the suffix -gen, meaning "producer of". With the years, American English adapted the spelling of estrogen to fit with its phonetic pronunciation. In 1929, Adolf Butenandt and Edward Adelbert Doisy independently isolated and purified estrone, the first estrogen to be discovered.
GPER and 5-HT1A receptors were found to be co-expressed in the hypothalamus in rats, further supporting this concept (Lu et al., 2009; Xu et al., 2009; Akama et al., 2013). Moreover, it was shown that the desensitization of 5-HT1A receptors that is necessary for SSRI therapeutic efficacy in the paraventricular nucleus of the hypothalamus in rats, depends on GPER (McAllister et al., 2012). Using SH SY5Y neuroblastoma cells, known for expressing TPH-2 and 5-HT1A, it was shown that E2 downregulated the presence of 5-HT1A and upon withdrawing E2, 5-HT1A levels returned to normal.

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