Mechanism of action of steroids anti inflammatory

Gliquidone Mechanism of action on insulin secretion In the basal state, the plasma membrane of the β cell is hyperpolarized, and the rate of insulin secretion from the cell is low. When glucose is available, it enters the cell via GLUT2 transporters in the plasma membrane and is metabolized to generate intracellular ATP . ATP binds to and inhibits the plasma membrane K+/ATP channel. Inhibition of the K+/ATP channel decreases plasma membrane K+ conductance; the resulting depolarization of the membrane activates voltage-gated Ca2+ channels and thereby stimulates an influx of Ca2+ . Ca2+ mediates fusion of insulin-containing secretory vesicles with the plasma membrane, leading to insulin secretion.

Under normal circumstances the prefrontal cortex regulates attention, behavior and emotion. Deficits in prefrontal cortex functioning have been linked to ADHD symptoms such as: poor impulse control, weak sustained attention and heightened distractibility [1] . Norepinephrine (NE) and dopamine (DA) are key neurotransmitters for prefrontal functioning, there is an inverted-U dose-response relationship for catecholamines and prefrontal abilities. The images below show the relationship between levels of catecholamine release and prefrontal abilitites in fatigued, alert and stressed states.

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Mechanism of action of steroids anti inflammatory

mechanism of action of steroids anti inflammatory

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