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Predict The Consequence of a Reduced Intracellular K+ Concentration on The Resting Membrane |, Assignments of Physiology

Material Type: Assignment; Class: Anatomy & Physiology; Subject: Biology / Biological Sciences; University: Southwestern Illinois College; Term: Forever 1989;

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Uploaded on 12/14/2009

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PredicttheconsequenceofareducedintracellularK+concentrationontherestingmembrane
potential.
Iftheintracellularconcentrationofpotassiumionsdecreased,theneuronwouldbecome
hyperpolarized.Inotherwords,therestingmembranepotentialwouldbelowerwithrespecttowhatit
isnormally.Thepotassiumionsarepositivelychargedandmanynegativelychargedproteinsandother
moleculesexistintheneuron.Asthepositivelychargedmoleculesdiffuseoutoftheneuronthen,the
netintracellularchargeoftheneuronbecomesmorenegative.
OnecanalsousetheGoldmanequationtopredicttheactualeffectontherestingmembranepotential.
PK+representsthepermeabilityofthepotassiumionthroughthemembrane.
[K+]outrepresentstheextracellularconcentrationofpotassiumions.
[K+]inrepresentstheintracellularconcentrationofpotassiumions.
Rrepresentstheidealgasconstant.
TrepresentsthetemperatureinKelvin.
FrepresentstheFaradayconstant.
Theratiobetweentheintracellularandextracellularionsshouldalwaysresultinavaluelessthanone(it
willbegreaterthanoneiftheoverallextracellularconcentrationofionsisgreaterthantheoverall
intracellularconcentrationofions).Therefore,astheintracellularconcentrationofpotassium
decreases,theoverallvaluefortheratioincreasestoavaluemorenearone.Ifweignorethefactthat
we’renotconsideringtheotherions(thisisveryimportant),thistrendwillindicatethattheresting
membranepotentialbecomesmorenegative.
TheNernstequationwouldordinarilybeused,butduetothepresenceofsodiumpotassiumpumps,the
systemisnotinequilibriumandthereforetheequationisinvalid.
Studentsinaveterinaryschoolweregiventhefollowinghypotheticalproblem.Adogingests
organophosphatepoison,andthestudentsareresponsibleforsavingtheanimal’slife.
Organophosphatepoisonsbindtoandinhibitacetylcholinesterase.Severalsubstancestheycould
injectincludethefollowing:acetylcholine,curare(whichblocksacetylcholinereceptors),and
potassiumchloride.Ifyouwereastudentintheclass,whatwouldyoudotosavetheanimal?
Acetylcholinewouldnotbeusedbecauseacetylcholinewouldalreadybeinexcess.Excessacetylcholine
atnerveendingsisaclinicalsignoforganophosphatepoisoning.Asacetylcholinebuildsup,thiscauses
thepostsynapticcelltokeepfiringwhichinturncausesmuscles,organsandglandstobecomeover
stimulated.
IfIwereoneofthestudents,I’dusethecurare.Curarebindstooneofthetwotypesofacetylcholine
receptors(nAChR).dtubocurarine,themain“poison”incurare,willtendtooccupythesameposition
onthesamereceptorsasacetylcholine,butwithanequalorgreateraffinitythanacetylcholineitself.
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Predict the consequence of a reduced intracellular K+ concentration on the resting membrane potential. If the intracellular concentration of potassium ions decreased, the neuron would become hyperpolarized. In other words, the resting membrane potential would be lower with respect to what it is normally. The potassium ions are positively charged and many negatively charged proteins and other molecules exist in the neuron. As the positively charged molecules diffuse out of the neuron then, the net intracellular charge of the neuron becomes more negative. One can also use the Goldman equation to predict the actual effect on the resting membrane potential. P (^) K+ represents the permeability of the potassium ion through the membrane. [K+]out represents the extracellular concentration of potassium ions. [K+]in represents the intracellular concentration of potassium ions. R represents the ideal gas constant. T represents the temperature in Kelvin. F represents the Faraday constant. The ratio between the intracellular and extracellular ions should always result in a value less than one (it will be greater than one if the overall extracellular concentration of ions is greater than the overall intracellular concentration of ions). Therefore, as the intracellular concentration of potassium decreases, the overall value for the ratio increases to a value more near one. If we ignore the fact that we’re not considering the other ions (this is very important), this trend will indicate that the resting membrane potential becomes more negative. The Nernst equation would ordinarily be used, but due to the presence of sodium‐potassium pumps, the system is not in equilibrium and therefore the equation is invalid. Students in a veterinary school were given the following hypothetical problem. A dog ingests organophosphate poison, and the students are responsible for saving the animal’s life. Organophosphate poisons bind to and inhibit acetylcholinesterase. Several substances they could inject include the following: acetylcholine, curare (which blocks acetylcholine receptors), and potassium chloride. If you were a student in the class, what would you do to save the animal? Acetylcholine would not be used because acetylcholine would already be in excess. Excess acetylcholine at nerve endings is a clinical sign of organophosphate poisoning. As acetylcholine builds up, this causes the post‐synaptic cell to keep firing which in turn causes muscles, organs and glands to become over‐ stimulated. If I were one of the students, I’d use the curare. Curare binds to one of the two types of acetylcholine receptors (nAChR). d‐tubocurarine , the main “poison” in curare, will tend to occupy the same position on the same receptors as acetylcholine, but with an equal or greater affinity than acetylcholine itself.

When occupying the receptor site, d‐tubocurarine elicits no response. The curare provides competition (acting as a competitive antagonist) for acetylcholine. This, in effect, blocks the response to an excess of acetylcholine. Explain whether an axon stimulated in the middle could propagate an action potential in both directions. If an axon is stimulated in the middle, an action potential travels in both directions, but can only be propagated in one direction. The action potential is only propagated in one direction because the initial site of stimulation is depolarized. During its refractory period, that portion of the axon stays depolarized for a sufficient amount of time that, as a result, forces the action potential to travel to a polarized (activated) site. At each increment that the action potential travels, the site “behind” the action potential is depolarized and prevents “back flow.” A patient exhibits enlargement of the lateral and third ventricles, but no enlargement of the fourth ventricle. What would you conclude? I would conclude, after an MRI to delineate the patient’s anatomy and demonstration by the patient of signs and symptoms, that the patient is suffering from hydrocephalus. This is an increased amount of CSF in the ventricles which results in an increase in intracranial pressure. Usually, this is treated surgically with the placement of a ventricular catheter (basically, a shunt). This allows the CSF to drain more freely. Perhaps you have heard someone say that eating carrots is good for the eyes. What is the basis for this claim? Carrots are high in beta‐carotene, which the body converts to Vitamin A. Vitamin A is modified to produce retinal. Retinal combines with opsin (converts photons of light into electrochemical signals) to produce rhodopsin. Rhodopsin, in turn, is responsible for monochromatic vision in the dark. Retinal combines with opsin and a chromophore (the part of a molecule responsible for its color; resulting from a conjugated pi bonding system) to produce photopsin, photoreceptor proteins that are responsible for color vision. Rhodopsin and photopsin are very important for the quality of vision. Without Vitamin A (considering beta‐carotene as a precursor), the visual cycle of the human would not be possible. Vitamin A produced from beta‐carotene (other sources are available) is essential for human eyesight. It does go a long way to helping night‐vision (preventing night‐blindness). However, many people have the notion that eating beta‐carotene will actually improve their eyesight and this is not true.