Clc-2 Case Study

Next, to determine if contraction via the EMC pathway requires extracellular or intracellular calcium, the second type of stimulus was used and the tissue was stimulated using calcium free K+-depolarising solution. The bathing solution in this experiment was calcium free solution to make sure all extracellular calcium was eliminated, as without calcium, the EMC pathway is expected to produce no response.

Contractility of ASM requires an increased levels of intracellular Ca2+. When surface receptors are not activated, Ca2+ levels are low. Upon activation of these cell surface receptors by contractile agonists e.g. acetylcholine, serotonin and histamine, intracellular Ca2+ increases causing a contraction (9). Smooth muscle cell contraction is controlled by both receptor and mechanical activation of proteins actin and myosin and also changes to membrane potential.

If the calcium and sodium channels remain open, it would cause a uncontrolled muscle twitch.

Both electrical and chemical forces combine to determine the resting membrane potential of the cell. Although the resting membrane potential of most cells is normally negative, the selective permeability of the membrane allows certain ions in and out, causing the neuronal membrane voltage to become depolarized (more positive), or hyperpolarized (more negative). Key ions involved in muscle membrane potential are sodium, potassium, and chloride, which move via passive or active diffusion through ion channels and transporter pumps (Baierlein et al. 2011). The Nernst equation predicts the membrane voltage based on the assumption that the membrane is only permeable to one type of ion. In this investigation, we are seeking to understand the basis for how different ions interact to produce the membrane potential of DEM, DEL1, and DEL2 crayfish muscle

While completing CLDE 5160 I began to develop a deeper understanding of the history of bilingual education. For standard 5.a I have selected the completed case study as my artifact. The reason I selected my case study as the artifact for this standard was because we developed it over the course of the semester and now it shows my growth as an educator. I completed this artifact prior to starting my first year as a teacher of record on the school that I had been hired to teach at.

Starting from the top with Group I ACs, this includes ACs 1, 3, and 8, this group is stimulated by the Ca2+/calmodulin signaling pathway via direct binding of calmodulin (CAM) to the ACs.9 A majority of the evidence of stimulation comes from overexpression system studies, but current evidence on the mechanism by which the binding of CAM to AC1, 3, or 8 stimulates activity has yet to be deciphered in a cohesive manner.9 However, on the other end of the spectrum exists Group III ACs, which includes ACs 5 and 6. The Ca2+/CAM signaling pathway inhibits their activity. Structural analyses done on ACs 5 and 6 provide evidence indicating that the Ca2+ ion displaces Mg2+ ions in the active site.10 Figure 3 shows the active site with emphasis on the Asp396 and Asp440, but also shown is their interactions between a Mn2+ ion and a Mg2+ ion. The

Chloride channels are a structurally diverse superfamily of transmembrane proteins that facilitate the transport of negative anions across the cell membrane. These channels are involved in a plethora of physiological processes such as neurotransmission, excitation of skeletal, cardiac, and smooth muscle, salt transport, cell volume regulation, and acid production in internal and external compartments. Families of these channels include the voltage-gated CLC family, calcium-activated CaCC family, GABAA receptors, glycine receptors, and the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR is an ATP-binding cassette (ABC) transporter that is responsible for proper fluid transport across the epithelial membrane of various cells

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

Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disorder found prominently in horses that occurs due to an inherited genetic mutation [1]. Specifically, a point mutation in the sodium channel gene, found in the muscle of affected horses, is passed on to offspring [1]. Sodium channels found in the muscle cell membrane primarily control muscle fiber contraction [1]. According to research summarized by UC Davis, when this defective sodium channel gene is present, the channels “leak” due to fluctuation of blood potassium levels, causing the muscle to depolarize and to contract involuntarily [4]. These fluctuating potassium levels may result from a period of fasting, followed by intake of high potassium feed, such as alfalfa [1]. Ultimately, the depolarization causes the muscles to lose their effectiveness, and myopathy eventually develops [4]. All horses positive for the HYPP gene mutation are affected for their entire lives [2].

What played the biggest role in my decision to apply to CMC was its large array of resources. From its top research institutions to the numerous amount of classes provided throughout the Claremont colleges, CMC provides its students with some of the best resources and opportunities that a undergraduate school has to offer. However, out of all the opportunities and resources that CMC could provide, I believe that the Athenaeum caught my attention the most.

Cystic fibrosis (CF) is the most commonly inherited, autosomal recessive disease in the UK with approximately 1 in 2500 people being affected (6). The disease stems from a mutation in the protein forming the Cystic Fibrosis transmembrane conductance regulator (CFTR), a chloride channel regulating the transport of ions across epithelial cell membranes. Dysfunctional CFTR channels are incapable to transporting chloride ions to the luminal surface and consequently water doesn’t follow osmotically. Coupled

Today is the beginning of our first CLC assignment. Collaboratively working together to accomplish this week’s task alongside the other CLC assignment weekly assignment going forward. The focus as a whole needs to factor: Making a point of contact, aligning individual’s strengths in areas to complete the assignments, and individual responsibilities. These assignments require weekly leadership, and a submitter. Please let’s text, or call one another today to get this ball on the roll. Looking forward to speaking and working with you all and together I believe we will succeed. I will initiate today’s point of contact to the team through text please feel free to call me any time after 3:45pm (Arizona time zone).

Excitation-contraction coupling (ECC) is the connection between the electrical action potential and the mechanical muscle contraction. Physiologically, it is a mechanism whereby an electrical signal detected by the dihydropyridine receptor is converted into an increase in calcium via activation of ryanodine receptors (RyRs). Per the article, mutations in RYR1, the gene encoding, are the underlying cause of various congenital myopathies including central core disease, multiminicore disease (MmD), which is a disorder that primarily affects muscles used for movement, as well as some forms of centronuclear myopathy (CNM), a condition characterized by muscle weakness, and congenital fibre-type disproportion. Patients with recessive, but not dominant,

While contraction in skeletal muscle is triggered by motor neurons under central control, certain cardiac muscle variants exhibit autorhythmicity. This means that that they are capable of producing their own depolarizing electrical potential. The cardiomyocytes that are capable of producing their own electrical potentials are found in what is referred to as the electrical condition system of the heart. This system is comprised of specializes cardiomyocytes that are autorhythmic and are able to conduct electrical potentials rapidly. These specialized structures include the sinoatrial node, atrioventricular node and bundle, and Purkinje fibers.

The Na-K-Cl cotransporter is a group of ubiquitous membrane transport proteins. This secretory cotransporter maintains electroneutrality by transporting ions with the stoichiometry of 1Na+: 1K+: 2Cl-. Two different gene isoforms of the Na-K-Cl cotransporter have been found. Both varieties of the symporter act to regulate and maintain cell volume and intracellular Cl- concentrations. However, the two different isoforms of NKCC vary structurally as although NKCC2 is around 60% homologous to NKCC1, it is lacking exon 21 (Delpire et al., 1994). The loss of this exon leads to the differential sorting of the two isoforms therefore they are targeted to different membrane domains (Carmosino et al., 2008). The first isoform, NKCC1, is a major component in mediating Cl- influx in the basolateral membrane. Contrastingly, NKCC2 is selectively expressed in the apical membrane of cell such as in thick ascending limb of Henle and primarily involved in NaCl reabsorption (Darman and Forbush, 2002).