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Furthermore, acute estrogen administration decreases 5-HTT mRNA levels (Pecins-Thompson et al., 1998) and 5-HT1A mRNA levels and binding. For instance, 5-HT1B autoreceptor mRNA in dorsal raphe (Hiroi and Neumaier, 2009) and MAO-A mRNA and activity (Gundlah et al., 2002) are decreased after estrogen treatment. Estrogen has been reported to have potent serotonin-modulating properties from the level of neurotransmitter synthesis via the regulation of tryptophan hydroxylase (Lu et al., 1999) and degradation of 5-HT to the density and binding of 5-HT receptors (Bethea et al., 2002). Furthermore, the serotonergic system is a main target of steroid hormones, cytokines, neuropeptides and trophic factors, all of which impact the generation and efficacy of serotonergic neurotransmission (McEwen, 2002; Bethea and Reddy, 2012). Several neuropsychiatric pathologies that display a substantial sexual dimorphism have been linked to abnormal dopaminergic function, such as schizophrenia (Brunelin et al., 2013), Parkinson's (Dluzen and Horstink, 2003; Horstink et al., 2003; Sanchez et al., 2010) or Alzheimer's disease (Reeves et al., 2009). Most experts agree that estrogen has an overall facilitating effect on dopaminergic neurotransmission (Sanchez et al., 2010; Jacobs and D'Esposito, 2011; Uban et al., 2012; Rey et al., 2014).
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Estradiol suppresses the 5-HT1A receptor signaling resulting in an increase in the firing activity of the 5-HT neurons (Riad et al., 2001; Raap et al., 2002; Mize et al., 2003) suggesting a negative correlation between E2 and 5-HT1A activity. Additionally, E2 has been shown to affect serotonin receptors 5-HT1A and 5-HT2A, both of which have been implicated in neuropsychiatric disorders due to their ability to be activated by 5HT. Several studies suggest that under OVX conditions SERT binding density, expression intensity, and 5-HT-positive cells were significantly decreased (Bertrand et al., 2005; Bethea et al., 2011). While the effects of E2 on SERT remain inconclusive there have been several reported cases suggesting a correlation between E2 and [git.violka-it.net](https://git.violka-it.net/jeremyhumble21/2037509/wiki/Testosterone-Replacement-Therapy:-Injections%2C-Patches%2C-and-Gels) SERT expression and function in OVX animals suggesting E2 plays a role in the reuptake of serotonin in the presynaptic terminal. Estradiol is a steroid hormone that influences the serotonergic, dopaminergic, and glutamatergic systems.
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However, in proestrus, which E2 levels are high, spinal endomorphin 2 antinociception was facilitated independently of mERα, namely, through glutamate-activated mGluR1 (Liu et al., 2019). Additionally, in diestrus where E2 levels are low, mERα-mediated activation of mGluR1 suppressed spinal endomorphin 2 antinociception. Within 5 min of introducing E2 into the pyramidal neurons, there was a significant increase in cAMP, response element-binding protein (CREB; Boulware et al., 2005), a transcription factor that has been implicated in addiction within the NAc (Lonze and Ginty, 2002), phosphorylation created by the MAPK/ERK. Boulware et al. used CA3-CA1 hippocampal pyramidal neurons from male and female rat pups to better understand how E2 is affecting mGluRs. Collectively, these findings suggest that estrogen augments excitatory synaptic transmission by increasing the release of the neurotransmitter glutamate.
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