Receptors
Receptors specifically bind to target molecules and initiate a response in the target cell. In most cases, these receptors are transmembrane proteins on the cell surface. When an extracellular signal molecule binds to them, they release a cascade of intracellular signals that alter the behavior of the cell1. In this experiment, we will be adding compounds, such as eserine and acetylcholine to a muscle cell bath and measuring its effect, in this case being force of contraction. These compounds target muscarinic acetylcholine receptors to produce their response, which will be made into a concentration/effect curve.
Muscarinic acetylcholine receptors
The muscarinic acetylcholine receptor (MAR) is a G protein– coupled receptor whose activation leads to opening of K+channels and subsequent hyperpolarization of the plasma membrane2. The binding of acetylcholine leads to the activation of a G protein, which binds to and releases ion channels. These ion channels can allow a varity of ions to move in or out of the cell, including K+, Na+ and Ca2+. There are five different types of MAR, M1-M5. Contraction of the bladder involves direct contraction of the M3 and an indirect re-contraction by the M2-receptors3. These are the receptors that we will be
…show more content…
The effect is produced as the ligand binds to the receptor. Therefore, the more ligand you have, the more receptors you are able to stimulate/inhibit. As concentration of the drug increases, its effect will also increase5. However, once all carrier sites become occupied, further increases in drug concentration will not produce further increments in drug influx5. In this experiment, we will be determining the effect of increasing concentration of drugs like eserine and acetylcholine on muscle tissue response, at what concentration levels effect increases fastest, as well as where a further increase will yield no further
C4564 Description: IC50: 3-AP is a ribonucleotide reductase inhibitor and iron chelator with antitumor activity. Ribonucleotide reductase, the rate-limiting enzyme for de novo DNA synthesis, is an excellent target for chemotherapy. Its increased activity in cancer cells is associated with malignant transformation and proliferation.
C3220 Description: IC50: N/A XAP044 is a mGluR7 antagonist. The function of metabotropic glutamate receptor subtype 7 (mGlu7), an critical presynaptic regulator of neurotransmission in the mammalian CNS, has been linked to drug abuse, anxiety, autism, as well as depression. However, it is difficult to develop specific blockers of native mGlu7 signaling in relevant brain areas such as limbic cortex and amygdala.
It binds and stabilizes actin filaments, as well as regulating actin-myosin interaction in a calcium (Ca2+)/calmodulin (CaM)- and/or phosphorylation-dependent manner.(17) The domain of this protein includes binding activities to Ca++-calmodulin, actin, tropomyosin, myosin, and phospholipids. As
So, the result was presented as the emergence of paralysis in the affected areas. Initial blockage of sodium ion channel totally deactivated an entire process in the neuromuscular junction. In other words, sodium ions mainly influence to the action potential generated in muscle cells, so TTX may inhibit muscle activity
Research has found that enkephalins are scattered in GABAergic interneurons, with MORs and DORs inhibit granule cells because they are in very distinct subpopulations of GABAergic interneurons (11). On the other hand, dynorphins are in granule cells and dendrites and KOR agonists, which will consist of endogenous dynorphins, decrease long-term potentiation. KORs have also been found to regulate GABA release at the presynaptic sites of the neurons (K- opioid). GABA, being the main inhibitory
c. The secondary amines (e.g. imipramine) is typically metabolized by
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction
Activity 1 Increasing extracellular K+ reduces the net diffusion of K+ out of the neuron through the K+ leak channels because it caused to decrease in the concentration gradient. Increasing extracellular K+ causes the membrane potential to change to a less negative value because extracellular K+ is increasing, which it will cause intracellular K+ to be less. A change in extracellular Na+ did not alter the membrane potential in the resting neuron because there are a lot of K+ leak channels than Na+ leak channels The relative permeability of the membrane to Na+ and K+ in a resting neuron is that Na+ leak channel is less, but K+ leak channels has more so the membrane become less permeable to Na+.
Examples of directly acting agonist are apomorphine which binds to dopamine receptors. However, direct-acting antagonist is taking up the space on receptor, so that inhibit the binding of neurotransmitter. The result is that neurotransmitters almost are blocked binding to the receptors. The most common example of a drug is atropine.
Background: Explain on the cellular level how dropping warm Ringers solution on the frog’s heart would affect the cells of the SA node. Dropping warm Ringers solution on the frog’s heart would increase the heart rate because the calcium channels open faster. Explain on the cellular level how dropping warm Ringers solution on the frog’s heart would affect the cells of the contractile muscle of the ventricles. Dropping warm Ringers solution on the frog’s heart would increase the heart rate because the actin binds to the myosin more quickly due to the calcium channels opening faster leading to faster contraction of the heart.
The effects of alcohol on Biological Membranes. Introduction In this experiment it will be analysed the damage alcohols can have on biological membranes. Membranes are made up of lipids and proteins. Membranes usually help maintain the balance in a cell as it holds all the cellular materials.
Then we calculated for (ED50) and (ECR) with the help of the graph. RESULTS FOR ACETYLCHOLINE AND NON
Later, 5ml of 1 x 10-6 M of mepyramine was added into the reservoir containing 1000ml of Krebs-Henssleit solution to produce a FBC of 5.0 x 10-9M. It was equilibrated with tissue for 10 minutes by flushing into the organ bath. After that, the steps above were repeated to test tissue response using 5ml of 1 x 10-5M and 1 x 10-4M of mepyramine. The experiment was repeated by replacing mepyramine with SIPBSDrug A as the antagonist. Lastly, concentration-response curve with Hill-Langmuir equation and Schild Plot were plotted using Bio-Graph. KB and pA2 values for mepyramine and SIPBSDrug A were calculated based on Schild plots and Gaddum
through proteins called RANKL and its receptor RANK” (n.p).
When a receptor becomes adjacent active receptors are inhibited highlighting edges and as a result creating