Damani N Bryant

Learn More
Numerous preclinical studies suggest that gonadal steroids, particularly estrogen, may be neuroprotective against insult or disease progression. This paper reviews the mechanisms contributing to estrogen-mediated neuroprotection. Rapid signaling pathways, such as MAPK, PI3K, Akt, and PKC, are required for estrogen's ability to provide neuroprotection. These(More)
Multiple mechanisms mediate the effects of estrogen in the central nervous system, including signal transduction pathways such as protein kinase A, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) pathways. Previously we demonstrated that estrogen regulates a number of PI3K-related genes in the hypothalamus, including the PI3K p55gamma regulatory(More)
Estrogen receptors can activate transcription in the nucleus, and activate rapid signal transduction cascades in the cytosol. Multiple reports identify estrogen receptors at the plasma membrane, while others document the dynamic responses of estrogen receptor to ligand binding. However, the function and identity of membrane estrogen receptors remain(More)
During normal olfaction, stimulation is dependent upon nasal inhalation. When collecting chemosensory event-related potentials (CSERPs), inhalations may produce artifacts such as respiration-related brain potentials that confound interpretation of the data. To avoid this type of artifact, CSERPs have often been collected using stimulation that is(More)
Although most agree that 17β-estradiol is neuroprotective via a variety of mechanisms, less is known about the role that biological sex plays in receptor-mediated estradiol neuroprotection. To address this issue we isolated primary cortical neurons from rat pups sorted by sex and assessed the ability of estradiol to protect the neurons from death induced by(More)
Premature and long-term ovarian hormone loss following ovariectomy (OVX) is associated with cognitive impairment. This condition is prevented by estradiol (E2) therapy when initiated shortly following OVX but not after substantial delay. To determine whether these clinical findings are correlated with changes in synaptic functions, we used adult OVX rats to(More)
Physiological doses of 17-beta Estradiol (E2) rapidly induce mitogen-activated protein kinase (MAPK) phosphorylation in a variety of cell culture and tissue explant preparations. Rapid MAPK phosphorylation has been implicated as a critical step in estrogen's effects on neuronal activity, gene transcription and neuroprotection. The present series of in vivo(More)
  • 1