Question

Contrast the role of calcium cations in action potentials and muscle contractions Mention how their levels in cytosol are regulated and which molecules or interac with the cations. Also explain the similarities of the calcium regulation in both mechanisms.

Answer 1

It is suggested that calcium and sodium ions can make an additive contribution to the overshoot potential by carrying the inward current. ... Barium ions nad depolarizing currents affect the neurones in a manner indicative that one role of calcium is to stabilize the membrane structure.

Importance of Calcium Ions. Ca2+ ions play an important role in muscle contraction by creating interactions between the proteins, myosin and actin. The Ca2+ ions bind to the C component of the actin filament, which exposes the binding site for the myosin head to bind to in order to stimulate a muscle contraction.

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Calcium ions play a critical role in most if not all cellular processes. It has even been demonstrated that Ca2+ currents in root tips, in combination with gravity, are responsible for their downward growth.Most of these effects are mediated by both temporally and spatially tightly controlled changes in cytosolic free Ca2+ brought about by activation of Ca2+ influx pathways in the cell membrane or by activation of intracellular Ca2+ release channels, and countered by transporters acting as Ca2+ pumps. Voltage-gated Ca2+ channels are a preeminent class of plasma membrane proteins providing regulated Ca2+ influx, and the remainder of the volume is dedicated to their many different facets. In this introductory chapter, we will briefly review other aspects of cellular Ca2+ homeostasis. We will review some of the chemical properties of Ca2+ that are important to its role in biology, we will review intracellular Ca2+ stores, and we will review other Ca2+ handling proteins. Due to space limitations we will not be able to refer to the original literature in most cases, but have to limit ourselves to a relatively small number of recent reviews that could provide the reader further guidance into the many exciting and sometimes controversial topics of current research in Ca2+ transport and storage in cells.

Similaritis :

The sequence of events that result in the contraction of an individual muscle fiber begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP . As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.

The hypothesis that the mitochondria contributes to calcium homeostasis at low resting cytosolic free calcium concentration ([Ca2+]i) in synaptosomes has been tested; it has been found that in fact this is the case. Intrasynaptic mitochondria actively accumulates calcium at [Ca2+]i around 10(-7) M, and this activity is necessary for the regulation of [Ca2+]i. When compared with other membrane-limited calcium pools, it was found that depending on external concentration the calcium pool mobilized from mitochondria is similar or even greater than the IP3- or caffeine-sensitive calcium pools. In summary, the results presented argue in favor of a more prominent role of mitochondria in regulating [Ca2+]i in presynaptic nerve terminals, a role that should be reconsidered for other cellular types in light of the present evidence.