Muscle Physiology and Neurons

Main functions of nervous system

Receive information about the environment around us, generating responses to that information, and integrate sensory input with memories, emotional state, or learning

Sensory (Afferent) Function

detect stimuli that registers a change from homeostasis or a particular event in the environment

Response function (Motor/Efferent) Division)

produce a response (voluntary or involuntary) based on the stimuli perceived by sensory structures

Integration function

CNS translate sensations from neural impulses into perception

Cell body

consists of cytoplasm (called axoplasm in neurons) filled with organelles

Dendrites

are axoplasm filled extension of the cell body used to receive communication with other neurons

Axon

extends from a thickening of cell body called the axon hillock

Axolemma

the plasma membrane in a neuron

Myelin sheaths

enclose larger axons to increase speed of nerve impulse.

The Axon terminal or synaptic knob

used to communicate to target cells, to include other neurons

Resting membrane potential

The membrane at its negative membrane potential (before stimulation), -70mV for neurons

Depolarization

Gain of positive charges makes the inside of the cell less negative, -60 mV

Hyperpolarization

Loss of positive charge (or gain of negative charges) makes the inside of the cell more negative, -80 mV

Action potential

rapid depolarization and repolarization of the membrane potential of a cell (trigger zone of axon hillock)

axons and the synaptic knob

experience action potentials

Dendrites and cell bodies

generate local potentials that spread to the axon hillock

Leak Channel

Stimulus non, Always open

Ligand-gated channel

Stimulus binding of ligand to a receptor associated with the channel

Voltage-gated channel

Stimulus voltage changes across the plasma membrane (axoplasm)

Mechanically gated channel

Stimulus mechanical deformations of the channel (by pressure stretch, etc.)

Voltage gated channels

are in the axons and axon terminals of neurons

Voltage gated potassium channel has two states:

resting – activation gate is closed; channel is closed

activated – activation gate is open; channel is open

Voltage gated sodium channel has three states

resting – channel is closed

inactivated – inactivation gate is closed; activation gate is open

activated – both the inactivation and activation gates are open, and the channel is open

Action Step 1: Threshold

Local potential depolarizes axolemma close to the exon hillock to threshold (-55 mV)

Action Step 2: Depolarization

Activation gate for voltage-gated Na+ channels open in the axon hillock

Action Step 3: Repolarization

Inactivation gate for voltage-gated Na+ channels close; activation gate for K+ voltage gated channels open

Action Step 4: Repolarization continued

voltage-gated Na+ channels at resting stage; voltage gated K + channels still open

Action Step 5: Hyperpolarization

voltage-gated K+ channels may release additional K+ ions before returning to at resting stage

Action Step 6: Resting polarization

is restored in this segment of the axolemma

Absolute refractory period

Rising and slow falling on graph (Above -55 mV), no stimuli can produce action potential

Relative refractory period

Rise and slow falling on graph (Below -55 mV), only strong stimulus can produce an action potential

End of a motor neuron close to sarcolemma

a synapse or axon terminal (outlined)

Acetylcholine (ACh)

Motor neuron communicates with many muscle fibers using neurotransmitter ligands

Voltage-gated Ca2+ channels

will need to be activated for the vesicles to bind to the axon terminal and perform exocytosis of their cargo

neuromuscular junction

The synapse of a motor neuron with a skeletal muscle fiber

synaptic cleft

Space between synapse and skeletal muscle fiber

Motor end plate

region of sarcolemma (outlined) with numerous ligand-gated receptors

The ligand shape on the receptors are specific to ACh

Phase 1: Excitation

Neural impulse (fluorescent green) reaches axon terminal (or synaptic knob)

Release of acetylcholine into synaptic cleft

Binding of acetylcholine to the ligand-gated sodium channel

Influx of sodium produces a motor endplate potential

Phase 2: Excitation-Contraction coupling

Acetylcholinesterase degrades excess ACh in synaptic cleft (not shown), so multiple neural impulses are necessary to stimulate end-plate potentials in the target muscle fibers

Action potential (dark green) spreads to and down the T-tubule’s sarcolemma (fluorescent green) and penetrate the triads

Recall – T tubule is an invagination of the sarcolemma

Depolarization of T-tubules allows voltage-gated calcium channels in the terminal cisterna of the SR to open and Ca2+ to enter the cytosol

Preparing for contraction

Calcium entering the myocyte cytosol is needed for exposure of actin binding sites

Phase 3: Contracting sarcomeres rely on multiple crossbridge cycles

The thick and thin filaments will slide in between each other in the A zone of the contracting sarcomere as the myosin head pulls on actin

Showcases the ability of muscle cells to be distensible.

Phase 4: Relaxation

Acetylcholinesterase (blue ball; shown) continues to degrades excess ACh in synaptic cleft

Concurrently, no additional neuronal action potentials are occurring

Sarcolemma repolarizes back to the resting potential (note the decrease of the “fluorescent green”)

Calcium protein pumps return Ca2+ to SR

Actin binding sites are recovered by tropomyosin as calcium leaves the cytosol

Several stimuli activate smooth muscle fiber contractions

Activation of stretch receptors (mechanical)

Hormonal and neural stimuli

Pacemaker cells

Calcium ions come from two sources in a smooth muscle cell

Released from the sarcoplasmic reticulum

Enter from the extracellular fluid

Role of Calcium ions is different than with skeletal muscle because smooth cells lack troponin

Calcium ions bind a cytosol protein called calmodulin (Cam)

Ca2+/Cam complex activates an enzyme associated with myosin called myosin light-chain kinase (MLCK).

MLCK activates myosin ATPase to hydrolyze ATP for myosin to bind to actin and create a crossbridge.

Crossbridge cycles occur followed by same relaxation techniques as previously discussed.