It is not surprising that a compound with such unique properties as NH3/NH4+, should have a large variety of biochemical and neurological effects and to find itself implicated in many pathological conditions. Its undissociated (NH3) or dissociated (NH4+) forms, having different physicochemical properties, enter neurons and other cells through differing pathways. These two forms then change internal pH in opposite directions, and initiate a variety of regulatory processes that attempt to overcome these pH changes. In addition, ammonia has a central role in normal intermediary metabolism, and when present in excess, it can disturb reversible reactions in which it participates. The challenge in interpreting these various observations lies in the difficulty in assigning to them a role in the generation of symptoms seen in experimental and clinical hyperammonemias. In this review we have attempted to summarize information available on the effects of ammonium ions on synaptic transmission, a central process in nervous system function. Evidence has been presented to show that ammonium ions, in pathologically relevant concentrations, interfere with glutamatergic excitatory transmission, not by decreasing the release of glutamate, but by preventing its action on post-synaptic AMPA receptors. Furthermore, NH4+ depolarizes neurons to a variable degree, without consistently changing membrane resistance, probably by reducing [K+]i. A decrease in EK+ may also be responsible for decreasing the effectiveness of the outward chloride pump, thus explaining the well known inhibitory effect of NH4+ on the hyperpolarizing IPSP. There is a consensus of opinion that chronic hyperammonemia increases 5HT turnover and this may be responsible for altered sleep patterns seen in hepatic encephalopathy. There does not seem to be a consistent effect on catecholaminergic transmission in hyperammonemias. However, chronic hyperammonemia causes pathological changes in perineuronal astrocytes, which may lead to a reduced uptake of released glutamate and a decreased detoxification of ammonia by the brain. Chronic moderate increase in extracellular glutamate results in a down-regulation of NMDA receptors, while the decreased detoxification of ammonia makes the central nervous system more vulnerable to a sudden hyperammonemia, due, for instance, to an increased dietary intake of proteins or to gastrointestinal bleeding in patients with liver disease. Clearly, data summarized in this review represent only the beginning in the elucidation of the mechanism of ammonia neurotoxicity. It should help, we hope, to direct future investigations towards some of the questions that need to be answered.
Low calcium ion levels can have several negative effects on the nervous system. Calcium is essential for proper nerve conduction, and low levels can impair the ability of neurons to transmit signals effectively. This can lead to symptoms such as muscle cramps, numbness or tingling sensations, and even affect the normal functioning of the brain. Severe calcium deficiency can also result in seizures or convulsions.
Calcium
The answer is that you will never be nervous again and that you have to much caffeine causing your body losing calcium.
When calcium levels increase, parathyroid hormone decreases. When calcium levels decrease, parathyroid hormone increases. This is known as a negative feedback system.
true
Parasympathetic
Central nervous system cells are most likely to be affected by these changes in sodium levels.
Your nervous system Will speed up.
deflex affects the nervous system by not allowing it to work properly
Nerve agents affect the transmission of nerve impulses in your nervous system. Nerve agents can affect the central nervous system, the respiratory system as well as cholinergic nervous system.
Nervous system
no
no
the nervous system
central nervous system
Ariel
Calcium
they affect the nervous system.