Paul J. Shughrue

TL;DR: Comparing the distribution of the classical and novel forms of ER mRNA‐expressing neurons in the central nervous system (CNS) of the rat with in situ hybridization histochemistry provides evidence that the region‐specific expression of ER‐α, ER‐β, or both may be important in determining the physiological responses of neuronal populations to estrogen action.

TL;DR: The widespread distribution of GLp‐1R mRNA‐containing cells strongly suggests that GLP‐1 not only functions as a satiety factor but also acts as a neurotransmitter or neuromodulator in anatomically and functionally distinct areas of the central nervous system.

TL;DR: The results clearly establish that the ERα subtype is a critical mechanistic link in mediating the protective effects of physiological levels of estradiol in brain injury and carry far-reaching implications for the selective targeting of ERs in the treatment and prevention of neural dysfunction associated with normal aging or brain injury.

TL;DR: The results of these studies have demonstrated that (1) ERβ mRNA is translated into immunoreactive protein throughout the rat brain, and (2) ER β resides in the cell nucleus.

TL;DR: It is indicated that estradiol modulates the expression of bcl-2 in ischemic injury, and the data suggest that estrogen receptors may be involved in hormone-mediated neuroprotection.