Answer:
The answer is Vitamin E or α-tocopherol.
Explanation:
Vitamin E is a <u>fat-soluble</u> vitamin is first absorbed in the small intestine and is then <u>stored at the liver</u>. It is an <u>antioxidant</u> which <u>protects cells from free radicals or reactive oxygen species (ROS)</u>. It can also prevent bad cholesterol from depositing in the blood vessels.
Vitamin E can be <u>naturally found in nuts, seeds, and vegetable oils</u>. As a dietary supplement, it takes the form of α-tocopherol. The RDA depends on the age of the person, as it may range from <u>4 mg to 15 mg per day</u>.
<u>Vitamin E deficiency is so rare</u> that it will only occur if the person has a <u>fat malabsorption illness like Crohn's disease, abetalipoproteinemia</u>, etc. Symptoms of deficiency include <em>muscle weakness, retinal degradation, peripheral neuropathy, and an immunocompromised state</em>.
The cell theory is fundamental to all living things.
Hello!
I believe the correct answer would be: Nonheme Iron.
I really hope my answer helped you! :)
Answer:
Prokareotes have no neucles so false
Explanation:
Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
Learn more about receptors here:
brainly.com/question/11985070
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