Answer:
characterized by presence or absence of antigens
the blood types are A, B, O, AB
Explanation:
There are two antigens and two antibodies that are mostly responsible for the ABO types. The specific combination of these four components determines an individual's type in most cases. Erythrocytes and serum were related to the presence of antigens on these erythrocytes and antibodies in the serum. these antigens are A and B, and depending upon which antigen the erythrocytes express, blood either belonged to blood group A or blood group B. A third blood group contained erythrocytes that reacted as if they lacked the properties of A and B, and this group was later called "O" blood group. The fourth blood group AB, was added to the ABO blood group system. These erythrocytes expressed both A and B antigens.
Blood group Antigen present on RBC Antibodies in serum Genotype(s)
A antigen A anti-B AA or AO
B antigen B anti-A BB or BO
AB both A and B antigen none AB
O none anti-A and anti-B OO
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.
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Answer:
The correct answer is: geography and UV radiation.
Explanation:
Skin variation occurred thanks to evolution, and was driven as a consequence of the geographical location of different populations of humans.
The humans that lived in hot and sunny places, closer to the equator, where much more exposed to the sun's ultraviolet radiation. In order to survive the amount of UV lights that they were exposed to, new humans in those regions were being born with a darker skin tone, which was rich in melanin (a brown pigment that protects us from the sun radiation).
Contrary to these humans that lived in the tropical areas, the humans that populated the areas that were closer to the poles, developed much lighter skin as a result of lower amounts of melanin in their skin. Since sun exposure in the poles is very limited, humans needed to receive as much as they could for the production of Vitamin D, and thus, their skins got lighter and less protected.
