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A crude model was automatically traced using the program RESOLVE 40

Increased release of glutamate from presynaptic terminals activates N -methyl-D-aspartate (NMDA) receptors on postsynaptic terminals to lead to a widespread neuronal depolarization or spreading depression, further disrupting the sodium ion, potassium ion, and calcium ion equilibria (Bouley et al., 2019)

5F, G) but also restored cell growth inhibited by the ER antagonist Fulvestrant (Fig

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Evidence on GLP-1 receptor-based drugs and ED are scant and have been mostly accrued in animal models and people with diabetes

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