Answer:
If there is homologous chromosomes (metaphase I) or duplicated chromosomes/sister chromatids (metaphase II) in the middle of the cell.
Explanation:
Meiosis involves two series of nuclear divisions grouped into meiosis I and meiosis II. Each division has the same number of stages i.e prophase, metaphase, anaphase, telophase etc. Meiosis I involves the separation of homologous chromosomes i.e similar but non-identical chromosomes from each parent.
On the other hand, meiosis II involves the separation of sister chromatids (duplicated chromosome). Since METAPHASE is generally characterized by the alignment of chromosome at the middle of the cell for separation in the anaphase stage, it means that the difference between metaphase in meiosis I and II will be whether it is homologous chromosomes that are in the middle or sister chromatids.
Therefore, according to this question, I would know if the cartoon is in metaphase I or II if:
- there are homologous chromosomes in the middle of the cell (metaphase I)
- there are sister chromatids in the middle of the cell (metaphase II).
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: Genetic drift may result in the loss of some alleles (including beneficial ones) and the fixation, or rise to 100% frequency, of other alleles.Once it begins, genetic drift will continue until the involved allele is either lost by a population or is the only allele present at a particular gene locus within a population. ... Genetic drift can result in the loss of rare alleles, and can decrease the size of the gene pool.
Explanation:
Answer:
Near the outer edge of the galaxy!
These are signs of amniotic fluid embolism, a rare emergency that can occur during the very last stages of labour. This is caused by the circulation of amniotic fluid in the blood stream of the pregnant woman. The nurse should administer oxygen using a facemask, in order to increase the oxygen intake of the woman.
