Answer:
The chemical reaction that represents the process of aerobic cell respiration is oxygen + glucose → water + carbon dioxide + energy
Explanation:
Cell respiration occurs in the mitochondria of eukaryotic cells and consists of a series of chemical reactions in which energy in the form of ATP molecules is obtained from a glucose molecule in the presence of oxygen.
<u>Glucose is the main energetic substrate</u> to be able to synthesize energy in the form of ATP, through oxidative phosphorylation. At the end of the process ATP is obtained as products, and as waste compounds water and carbon dioxide, which can be schematized in the following chemical reaction:
<em> C₆H₁₂O₆ + 6O₂ → 6H₂O + 6CO₂ + ATP ↑</em>
<em> Glucose + Oxygen → Water + Carbon dioxide + Energy ↑</em>
This reaction summarizes what happens in aerobic cellular breathing, which is necessary to synthesize energy for cellular functions.
The other reactions:
- <em>oxygen + water </em><em>→</em><em> glucose + lactose
</em>
- <em>glucose + lactose </em><em>→</em><em> oxygen + water
</em>
- <em>water + carbon dioxide + energy </em><em>→</em><em> oxygen + glucose</em>
<em>do not represent the components or the order of the reactions that occur in aerobic cell respiration</em>
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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Answer:
any of numerous complex proteins that are produced by living cells and catalyze specific biochemical reactions at body temperatures
I think Leonardo could have a point but I’m pretty sure it’s just based on genetics even with sea monsters lol
