Physiology 501

The lag between the stimulus and initiation of the action potential is called latency. When thestimulus strength is increased above threshold, the time to reach threshold, the latency, decreases.

rapid depolarization

hyperpolarization

1- Depolarization -> Na+ Channel opens -> increase gNa -> shift of Em towards ENa2- Na+ channel inactivation and K+ channel opens -> decrease gNa and increase gK3- K+ Channel Closes

synaptobrevin

syntaxin is on pre-synaptic membrane

block acetylcholine receptors

D-tubucurareis used surgically.

Non competitive AchR activator keeps the channelopen, succinylcholine produces paralysisby depolarization block

physostigmine inhibit acetylcholinesterase and potentiates acetylcholine action in persons with weakNMJ responses(myasthenia gravis)

effects on autonomic nervous system (meant to use in warfare but now arebanned)

SalivationLacrimationUrinationDefecationEmesis

muscle weakness

•Acquired autoimmunedestruction of acetylcholine receptors

•SNMG – sero negative myasthenia gravis haveantibodies against MUSK – muscle specific kinase - involved in formation of the NMJ

small synaptic vesicles and large dense core vesicles

simultaneous EPSP & IPSP input summation

repetitive EPSP or IPSP

constant length vs. constant tension (hence, the lifting of afterload can occur)

Pennationallows more force to be developed from a muscle that will still fit into thebody – but the trade-off is slowervelocity of contraction

Muscle pennation increases force but reduces velocity

Special proteins span the sarcolemma atthe costameresand transfer force from the cytoskeletonto the extracellular matrix

The costamere is a structural-functional component of striated muscle cells which connects the sarcomere of the muscle to the cell membrane.

bulged areas in nerve cells where neurotransmitters are accumulated within

A channel protein that is embedded within gap junction

A point where contractile fibers are anchored at. When the structure is located at the cell membrane, it is called the membrane dense area or attachment plaque.

Thesurface membrane is coveredwith small invaginations calledcaveolae. These may serve aslocal sources of Ca2+ foractivation of the muscle.

myosin light chain kinase (contraction)/phosphatase (relaxation)

the part of the time that the muscle is activated, increases withintensity because the period of activation decreases less than the period of rest. This describes the situationwhen we increase the speed of a repetitive action such as walking.

higherintensity exercise:

higher duty cycle

less time for metabolism to recover theresting state

At the highest intensity of exercise, there is no rest phase

5mM / 15-20mM

Type 1: slow oxidative

Type 2a: fast oxidative

Type 2b: fast glycolyic

surrounds single muscle fiber / a primary bundle of fibers (fascicle) / the whole muscle fiber

high intensity / short duration = build up of Pi + H+

medium intensity / long duration = depletion of glycogen

constant activation vs. activation by trigger

activates SERCA upon phosphorylation

•formedby sphingomyelinand cholesterol.

•Lipidrafts:

•Segregatesignaling mechanisms

•Segregatemolecules.

GPI (glycosylphosphophatidylinositol), farnesyl, myristyl, palmitosyl

14 + 28 = 42

plasma + ISF + ICF = TBW

Deuterium oxide = all

Inulin = ECF

Tracer = plasma protein (plasma)

•Ionophores aremolecules that allow ions to cross membranes.

•Ionophores areof two types: carriers and channel formers.

Na+/Ca2+ exchanger

Three sodium in / one calcium out; hence, one net positive charge enters the cell

Can reverse its direction upon physiological change in cell potential. eg. depolarization of the heart

0.9%

5% D-glucose

Gs = epi binds b1 or b2 -> ↑ [cAMP] -> activates PKA

Gi = epi binds a2 -> ↓[cAMP]

= epi binds M2 receptor -> alpha inhibits adenylyl cyclase and beta-gamma activates K channel

Gq = epi binds a1 -> alpha activates PLC -> ↑ IP3 -> ↑[Ca2+]

= epi binds a1 -> alpha activates PLC -> ↑ DAG -> DAG activates PKC

G12 = Gα12-GTP -> activates GEF -> activate small G proteins

Gαt-GTP -> activates cGMP phosphodiesterase -> ↓ [cGMP] -> ↓ gNa -> hyperpolarization

can act as a steroidal hormone

PCl > PK > PNa

inhibitor of SERCA; stops inhibition upon phosphorylation by PKA or PKG