1. The glutamate causes an influx of ca2+ ions into the nerve cell akin to what occurs during depolarization. However, this occurs excessively without regulation (due to excessive stimulation by the glutamate) that eventually causes nerve injury through cytotoxic edema.
2. When the ca2+ levels are lowered during stroke, then nerve cell injury would be obviated hence enabling the chances of restoration of nerve cell function. This would happen because there would be no excess calcium ions to influx when the NMDA receptors are excessively stimulated by the glutamate molecules.
The organism that has all the adaptations listed above is C. polar bear.
Answer:
relaxes
Explanation:
Acetylcholine is the substance responsible for the transmission of nerve impulses from pre-postganglionic neurons, in the ganglia of the autonomic nervous system. At the level of the parasympathetic nervous system, the transmission between the postganglionic neuron and the effector organ also mediates. In addition, it is the mediator of the nerve transmission of the terminal motor plate.
There are large differences in the effects that Acetylcholine triggers at different cholinergic transmission sites
Intra-arterial injection near Acetylcholine produces muscle contraction similar to that caused by motor nerve stimulation. Decreased resting potential in isolated intestinal muscle and increased frequency of spike production, accompanied by increased tension. In the cardiac conduction system, nodes S-A and A-V, it produces inhibition and hyperpolarization of the fiber membrane; and pronounced decrease in depolarization speed. Central regulation of extrapyramidal motor function. Exciting effect of the basal ganglia that counteracts the inhibitory action of Dopamine. Although cholinergic innervation of blood vessels is limited, cholinergic muscarinic receptors occur in sympathetic vasoconstrictor nerves. The vasodilator effect on isolated blood vessels requires the presence of an intact endothelium. The activation of muscarinic receptors causes the release of a vasodilator substance - <u>relaxing factor derived from the endothelium - that diffuses to the smooth muscle producing </u><u>relaxation</u><u>.</u>
The answer to your question: cause of death.
