Answer:
ureter, or ureters, are what Connect the kidneys to the bladder
Answer:
All made of cells, All have the DNA-->RNA-->Protein method of information transfer(can't think of exact word)
Explanation:
<h2>Membrane potential </h2>
Explanation:
- Membrane potential represents charge difference across the membrane, all biological cells are negative inside (cytoplasm) and positive outside (due to difference in ionic distribution)
- In a typical neuron cell membrane potential of cytoplasm is negative at rest (when no stimulus is applied) hence called resting membrane potential
- Resting membrane potential of excitable cells is established by Na+ and K+pump
- Repolarization starts with the efflux of K+ by the opening of voltage gated K+ channels
- Voltage gated K+ channels starts to open when voltage gated Na+ channels becomes inactive
- Hyperpolarization occurs due to excessive efflux of K+ by voltage gated K+ channels
- Additional efflux of K+ occurs due to slow inactivation of voltage gated K+ channels
The tricuspid valve shuts. This prevents blood from flowing backward into the right atrium while the ventricle contracts. So, your answer will be the Tricuslid Valve. Hope I helped!
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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