Beta Gamma Protein Summary

Acetylcholine is found at the peripheral nervous system and synapses in the central nervous system within the human body. Acetylcholine is an excitatory neurotransmitter that conducts electrical impulses, allowing nerve cells to communicate with muscle cells and generate muscle contractions. However, acetylcholine produces an inhibitory effect in cardiac muscle. (Waymire, 1997) Therefore, once the Daphnia are exposed to acetylcholine, their heart rate is expected to decline. In contrast, epinephrine, also known as adrenaline, is a hormone which binds to the beta adrenergic receptors in the heart leading to increases in the firing rate of the pacemaker cells. (Meyers, 2011) Therefore, the Daphnia’s heart rate is expected to increase with exposure to

Voltage gated channels are necessary components of life processes, in many organisms. One in particular, is the calcium voltage gated ion channel. Often lodged within the phospholipid bilayer, the imbalance of the calcium, or, the inside vs outside concentration, creates a gradient. The channel proteins often undergo conformations, states that which allow or block calcium ions from passing through. As ions move inside the cell, this creates a depolarization, or surge in the voltage. Clinically, this is associated with the heart and how it allows the heart to contract, which can be read in the

When beta-1 receptors are turned on it leads to elevated heart rate and increased contractual force. Beta-blockers are medications used in the treatment of high blood pressure.These medications inhibit the negative effects caused by the sympathetic nervous system on the heart muscle. They act by capping off beta-receptors, and thus inhibit the stimulating affects on the heart caused by adrenaline (Aschenbrenner & Venable, 2012). The medication in-effect lowers blood pressure, by decreasing contractual force on the myocardium and reducing heart beat (Mayo Clinic,

Agus ZS, Morad M. Modulation of cardiac ion channels by magnesium. Annu Rev Physiol 1991; 53:299.

When both NA and Praz act on GPCR in VSM membrane, NA induces production of IP3 and Praz does not. Therefore, to produce same level of contraction from NA only by using NA with Praz, higher concentration of NA is necessary to occupy more receptor. Theoretically, the maximum (100%) concentration should be achieved with high concentration of agonist with antagonist (1 p10). 82.61% of contraction was observed in this experiment. it could be due to tissue damage from experimental process or could be influenced by more than five days storage of prepared tissue (3). 5HT2 receptor is located in the CNS and also located in the periphery (1 p196). The subtypes of 5HT2 are linked to colonic motility (5-HT2A), heart (5-HT2B), and central nervous system (5-HT2c) (1 p196). Meth act as antagonist to 5-HT2A, partial agonist to 5-HT2B, and antagonist to 5-HT2C (1 p199, 4). Both 5HT, and Meth works as agonist, but binding of 5HT to receptor give full response (full agonist), and Meth give less than full response (partial agonist). Meth act as agonist in presence of low concentration of 5HT with Meth. Meth act as antagonist in presence of high concentration of 5HT with Meth. Meth disturbs 5HT binding to receptor to give full response. Therefore, crossover of 5HT only trend line and 5HT with Meth should be observed. Absence of crossover might be due to different efficacies, as Meth is known

Characteristic of this family, each KCNJ11 subunit has 2 transmembrane domains. This KATP channel exists as an octamer, consisting of both KCNJ11 (Kir6.2) and SUR1 together, which are present in a 4:4 ratio in every channel [3]. It is KCNJ11 that has the pore forming region, and that sets the resting potential of the cell at -70 mV, as this is the equilibrium potential for K+ [3][6]. ATP binding to the KCNJ11 subunit is what causes the characteristically important closing step of the KATP channel, and the depolarizing of the cell, along with the rest of the cascade leading to insulin release [3]. This is intuitive, as increased glucose uptake will cause increased ATP production, and thus high ATP levels cause the insulin releasing cascade. However, an alternate mechanism exists to control the open vs. closed state of the channel. SUR1 is a regulatory subunit, whose role can be seen during interactions with MgADP (ADP bound to Mg for stabilization) [3]. When MgADP interacts with SUR1, it counteracts the effect from ATP binding to the KCNJ11 subunit, and causes stimulation of the channel, such that it will allow for the current of K+ to resume [3]. This is intuitive as well, as increasing levels of MgADP would indicate a shift in the [ATP]/[ADP] ratio towards ADP, meaning the cell is not taking up enough glucose to create sufficient ATP. The cellular stores of ATP are

cell affects the beta-goblin subunit and is given the name HBB gene. This gene mutation causes in a change in the beta-goblin structure by replacing glutamic acid with valine in the sixth position in the polypeptide chain. This gene is found on chromosome 11. This change results in an abnormal version of the beta-goblin which is called haemoglobin S (HbS).

The PNS decreases heart rate by transmitting its impulses onto long, myelinated preganglionic neurons that trigger the release of ACh onto nicotinic cholinergic receptors found on the postganglionic cell. The impulse then travels along short, unmyelinated cholinergic postganglionic neurons, and triggers the release of ACh onto muscarinic cholinergic receptors found on the effector target cells. The speed and duration of response by the PNS is quicker because most of its axonal journey is done upon long myelinated fibers. The PNS release of ACh can also be easily broken down by acetycholinesterase, so its effect only last for a short period of time. The speed and duration of response by the SNS is slower and longer due to most of its axonal journey being done upon long

(c) Estimate the EC50 values for the effects of acetylcholine and nitroprusside in both types of arterial ring, and present these in a table.

"The calcium-sensing- gate mechanism discovered here is an entirely novel concept with potential to shift our general understanding of ion channel gating, cardiac arrhythmogenesis, and the treatment of calcium-triggered arrhythmias”

The physiological function of each receptor subtype has not been established and is currently the subject of intensive investigation (1).

Catalytic receptors are characteristically dimeric cell surface proteins that contain a single transmembrane domain which separates an extracellular ligand binding site and an intracellular enzymatic activity. Receptors with extrinsic tyrosine kinase activity and intrinsic protein serine/threonine kinase activity form minor subfamilies in this group2.

I chose this paper because it discusses the human cardiac troponin complex and how it facilitates the contraction of cardiac muscle. I found it interesting how the troponin complex in the cardiac muscle is made up of three subunits called troponin I, C and T (TnI, TnC, TnT), and how the phosphorylation of the troponin I subunit by the enzyme protein kinase A increases the rate of cardiac muscle relaxation to regulate the heartbeat.

Cys-loop receptors are characterized by pentameric ligand-gated ion channels. Some other members of this superfamily are nicotinic acetylcholine (nACh), 5-hydroxytryptamine (type 3, 5HT3) and glycine receptors 1, 2 and 3. nACh receptors and 5HT3 receptors contain cation-selective channels that depolarize or excite neurons, whereas GABAA/B receptors and glycine receptors contain anion-selective channels that, in most cases, hyperpolarize or inhibit neurons. Exception occurs during early postnatal development when these channels are excitatory.5, 3 Neuropathic pain can occur if these channels become excitatory in adults.16 The unique feature of GABA receptors that distinguish it from other cys-loop receptors is its activating ligand GABA (or accurately γ-aminobutyrate). There are two types of GABA receptors- A & B. GABAB receptor was originally found due to their insensitivity to bicuculline which is GABAA antagonist1. They are G-protein-coupled receptors and differ strongly in structure, function, and sequence from GABAA receptors and will not be discussed further in this

intracellular potassium ion gradient is fundamental to the establishment of the resting membrane potential in excitable cells (neurons and muscle cells) is necessary in order to appreciate how hyperkalemia (excess extracellular K) disrupts this delicate balance. Because of the loss of this potassium gradient, excitable cells become hypopolarized, and are therefore less responsive to stimuli (action potentials). This results in muscle weakness and flaccid paralysis that progresses in an ascending pattern. The main concern with hyperkalemia is its implication on the cardiac system (Copstead & Banasik, 2013). Hyperkalemia that exceeds 6.0 mEq/L can be fatal because of its depressant effects on myocardial activity. This is demonstrated on an ECG tracing with the disappearance of the P wave, extended T wave and QRS segment, and depressed ST segment. Should this happen, the client is an emergent situation and immediate measures must be taken to reduce serum potassium to prevent cardiac arrest (Osborn, et al. 2014). This patient’s serum potassium was 6.1 mEq/L on arrival, which placed at an extremely high risk for cardiac dysfunction. He was immediately given a combination of immediate and longer-acting medications to lower his serum potassium (calcium, D50, insulin, bicarbonate, and