fight or flight is controlled by the adrenal medulla part of the brain.
fight or flight is controlled by the adrenal medulla part of the brain.
fight or flight controlled by which part of the brain?
the adrenal medulla
nicotine is a parasympathomimetic stimulant that binds to and activates nicotinic acetylcholine receptors in the brain, which subsequently causes the release of dopamine and other neurotransmitters, such as norepinephrine, acetylcholine, serotonin, gamma-aminobutyric acid, glutamate, endorphins, and several neuropeptides, including proopiomelanocortin-derived α-msh and adrenocorticotropic hormone. corticotropin-releasing factor, neuropeptide y, orexins, and norepinephrine are involved in nicotine addiction. continuous exposure to nicotine can cause an increase in the number of nicotinic receptors, which is believed to be a result of receptor desensitization and subsequent receptor upregulation. long-term exposure to nicotine can also result in downregulation of glutamate transporter 1. long-term nicotine exposure upregulates cortical nicotinic receptors, but it also lowers the activity of the nicotinic receptors in the cortical vasodilation region. these effects are not easily understood. with constant use of nicotine, tolerance occurs at least partially as a result of the development of new nicotinic acetylcholine receptors in the brain. after several months of nicotine abstinence, the number of receptors go back to normal. the extent to which alterations in the brain caused by nicotine use are reversible is not fully understood. nicotine also stimulates nicotinic acetylcholine receptors in the adrenal medulla, resulting in increased levels of adrenaline and beta-endorphin. its physiological effects stem from the stimulation of nicotinic acetylcholine receptors, which are located throughout the central and peripheral nervous systems. the α4β2 nicotinic receptor subtype is the main nicotinic receptor subtype. nicotine activates brain receptors which produce sedative as well as euphoric effects. chronic nicotinic acetylcholine receptor activation from repeated nicotine exposure can induce strong effects on the brain, including changes in the brain's physiology, that result from the stimulation of regions of the brain associated with reward, pleasure, and anxiety. these complex effects of nicotine on the brain are still not well understood. nicotine interferes with the blood-brain barrier function, and so raises the risk of brain edema and neuroinflammation. when nicotine enters the brain, it stimulates the midbrain dopaminergic neurons situated in the ventral tegmental area and pars compacta, among other activities. it induces the release of dopamine in different parts of the brain, such as the nucleus accumbens, amygdala, and hippocampus. ghrelin-induced dopamine release occurs as a result of the activation of the cholinergic–dopaminergic reward link in the ventral tegmental area, a critical part of the reward areas in the brain related with reinforcement. ghrelin signaling may affect the reinforcing effects of drug dependence.
electronic cigarette
section::::competition.:classes.









































for competitive purposes, there are three classes of hang glider: 









































bullet::::- class 1 the "flexible wing" hang glider, having flight controlled by virtue of the shifted weight of the pilot. this is not a paraglider. class 1 hang gliders sold in the united states are usually rated by the hang gliders manufacturers' association.









































bullet::::- class 5 the "rigid wing" hang glider, having flight controlled by spoilers, typically on top of the wing. in both flexible and rigid wings the pilot hangs below the wing without any additional fairing.
hang gliding