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Delayed-Rectifier Potassium Channel

Allow ions one way and takes some time to open. It is responsible for the recovery of the membrane potential to the starting level, or even more negative than the starting level Only two states: open and closed One Gates m gate: Location inside the channel where amino acids on opposite ends will join together blocking any ion movement into the channel --- It opens in response to membrane depolarization, but with a slight delay compared to the voltage-gated sodium channel. Stages At rest (no axon activity [-70 mV]) • m gate is closed • No flow of K+ Immediately after Depolarization • m gate is closed • No flow of K+ • no change even though there was a change in membrane potential from the Na+ entering the cell (recall this is a delayed pathway) 2 ms after Depolarization • m gate is OPEN • change in membrane potential had a delayed effect • K+ flows out of the cell -- the cell depolarizes • often the cell is depolarized to below the starting level (undershoot)

Flow of Na+ in vertebrate photoreceptor cells (rods/cones) in response to varying light intensity?

As light intensity increases, conductance/permeability (aka flow) of Na+/K+ decreases Seems fishy since the flow of Na+ is needed to form an action potential

Interaction of myosin with actin to produce the sliding of the thin filament

1) ATP is hydrolyzed activating myosin (attaches ADP+P) causing the myosin head to angle down 2) Actin binds to myosin on its myosin-binding site 3) Myosin get deactivated (loses ADP+P) 4) Swiveling of myosin heads as it returns to its relaxed state causes movement in actin towards the M line 5) Only after a new ATP binds to the myosin can the actin detach from the myosin N.B. the energized myosin is ADP bound

How are action potentials initiated?

1) The dendrites on the cell body receive inputs from the axons of presynaptic neurons at the synapse --- The inputs into a neuron from another axon can be either excitatory (favors forming action potential) or inhibitory (disfavors forming action potential), depending on the ion channels that are opened at the synapse. 2) The axon releases a chemical messenger at the synapse that binds to receptors on the postsynaptic cell and opens ions channels. --- In general, the opening of Na+ channels or Ca+ channels is excitatory, while the opening of Cl channels is inhibitory 3) Information from the other neurons get collected in the spike-initiating zone and either creates an action potential or doesn't --- adds up the signals from excitatory presynaptic neurons (favors forming action potential) and inhibitory presynaptic neurons (disfavor forming action potentials) and if the AP threshold is met then an AP will occur --- if the threshold is not met, the change in membrane potential will not continue down the axon --- adds up all the EPSP (signals that favor forming an action potential) and all the IPSP (signals that disfavor forming an action potential)

Ways EPSP and IPSP can contribute to reaching action potential threshold

1) spatial summation 2) temporal summation

Basic structure of action potential curve

1. Resting stage (baseline) 2. depolarization (massive spike) 3. repolarization (spike goes down) 4. Undershoot (hyperpolarization; goes below the baseline) 5. resting stage (return to baseline)

Anatomy of Rod Cell

3 Major Segments Outer segment Inner Segment Synaptic terminal Outer Segment: where the sensors that detect changes in light are located Inner Segment: integrate information coming from the outer segment --- contains lots of mitochondria Synaptic terminal: causes the changes in membrane potential that gets carried on by the subsequent cells in the retina

myelin

A layer of fatty tissue segmentally encasing the fibers of many neurons; enables vastly greater transmission speed of neural impulses as the impulse hops from one node to the next. --- produced by Schwann cells

Voltage-gated Sodium Channel

A membrane protein forming a pore that is permeable to Na+ ions and gated by depolarization of the membrane. The channel exists in three states A) Closed (m gate) B) Open (m gate) C) Inactive (h gate; only last a few milliseconds) Two Gates m gate: Location inside the channel where amino acids on opposite ends will join together blocking any ion movement into the channel h gate: Cluster of amino acids at the very end of the intracellular part of the membrane Stages At rest (no axon activity [-70 mV]) • m gate is closed but h gate remains open --- m gate is opened in response to a change in membrane potential (voltage-gated pathway • Does NOT allow Na+ inside the cell Opening of the channel (immediately after depolarization) • m gate and h gate are open • Na+ flows into the cell Inactivation (5 ms after depolarization) • m gate is open but h gate is closed • Does NOT allow Na+ inside the cell • While inactivated, the channel cannot be opened, regardless of the membrane potential. • This is the basis of the refractory period of an axon that follows an action potential, which is the time during which another action potential cannot be elicited • Lack of the flow of Na+ leads to repolarization and eventually hyperpolarization

straited (skeletal) muscle

A muscle that appears banded --- distinct pattern of light and dark bands across the tissue --- distinct cube structures cross section of myofibril" large blots are myosin, small blots are actin

Acetylcholine (ACh)

A neurotransmitter that triggers muscle contraction

myosin filament

A protein that works synergistically with actin, responsible for muscular contraction. A single myosin molecule consist of a globular head and a flexible tail that are connected by a hinge region. --- globular head head will move along with the sliding of actin during contraction Two myosin molecules will wrap their tails together and will function as a two-headed unit. Then, multiple of these pairs will aggregate together to form the thick filaments of the sacromere --- globular head regions in the filament are in pairs --- the globular heads left of the M line face left, and the globular heads right of the M line face right

Interplay between voltage-gated sodium channels and delayed-rectifier potassium channels

A) Resting Potential: both sodium and potassium channels are closed ---- Sodium channel: m gate closed and h gate open --- Potassium channel: m gate closed B) Depolarization phase: sodium channel is open; potassium channel remains closed (due to delayed response) ---- Sodium channel: m gate open and h gate open --- Potassium channel: m gate closed C) Repolarization Phase: sodium channel is closed; potassium channel is open ---- Sodium channel: m gate open but h gate closed [inactive state] --- Potassium channel: m gate open (activated by Na+ entering the cell and changing the membrane potential) D) Hyperpolarization phase (Undershoot): sodium channel is closed; potassium channel is open ---- Sodium channel: m gate open but h gate closed [inactive state] --- Potassium channel: m gate open E) Return to Resting Potential: sodium channel is closed (i think, this one weird here???); potassium channel is closed ---- Sodium channel: m gate closed but h gate opens up [no longer in the inactive state] • The inactivation (h) gate must open before the channel returns to the resting state. Until that occurs, an action potential cannot be generated --- Potassium channel: m gate closed

Steps in Sensory Transduction (simple)

A. Stimulus arrives at the sensory receptor B. Action Potential generated which pass on information to interneurons that pass it along to the CNS Sensors Taste - taste buds Smell - receptors in nose Somatosensory (skin) - pressure Muscle - receptors that detect tension in muscle Heearing - receptors to sound waves Vision - photons detected by rods (amount of light) and cones (wavelength/color)

Following the Action Potential entering the muscle cell, it travels down T tubule [get better title]

ACh depolarizes the muscle cell membrane, inducing an action potential in the muscle membrane, which spreads throughout the muscle membrane, including into the T-tubules. AP travels from the membrane to T tubule As the AP travels, it activates receptors along the T tubule and the sarcoplasmic reticulum, causing the release of ions that are critical for myofibril contractions

What activates Myosin? How?

ATP (myosin is an ATPase; it binds ATP and catalyzes the hydrolysis of ATP to ADP) Myosin is a machine that converts the energy released by ATP hydrolysis into mechanical force activated myosin is connected to an ADP+P; once activated it will cause the head to swivel which leads to muscle contraction

alternative view of the term above (get better title)

Action Potential travels along the sarcolemma (muscle cell plasma membrane) AP travels down the T tubule AP reaches the Dihydropyridine receptor (DHPR) and activates it DHPR then activates the Ryanodine receptor (RyR) which induces the releases of Ca2+ so it can be available for contraction --- terminal cistern: area near the channel of RyR where most of the Ca2+ is stored To stop the release of calcium, the protein SERCA gets hydrolyzed by ATP and starts shuttling Ca2+ back into the SR

Effect of Sodium Removal on the Squid Action Potential

Action potential 1: After the first action potential, the solution housing the axon was replaced with one that contained no sodium Action Potential 2-5: As the sodium near the axon membrane declined, the height of the AP declined, and by AP 5, no AP existed. After AP 5, the sodium-containing medium was re-introduced, and the normal AP could be fired (AP 6) Big Picture: sodium plays a critical role in depolarization

Why do vertebrate photoreceptor cells (rods/cones) hyperpolarize [decrease membrane potential (more negative)] in the presence of light?

At baseline levels, all the Na+/K+ channels are open; Na+ is coming in and K+ is coming out. (-40 mV) At Dim light, some of the channels begin to close (Causes a little hyperpolarization.) At bright light, nearly all the channels are closed (massive hyperpolarization.) [-70 mV] The membrane potential of a vertebrate photoreceptor cell becomes more negative in proportion to light

Why does the action potential only move away from the cell body?

Because once the action potential has occurred in a region, the refractory period in the sodium channels occur (inactive state [h gate]) and so sodium cannot be transported across the membrane where the action potential had already passed through for a couple milliseconds (movement of sodium is time-dependent)

What regulates the interaction of myosin with actin?

CALCIUM

Hodgkin and Huxley Experiment [recap]

Hodgkin and Huxley had two microelectrodes embedded at different points along the axon to see if a disturbance at an earlier point on the axon could be sensed by the farther end of the axon. They found that 1) If an electrical stimulation is introduced, it causes a major depolarization in that region of the axon. The depolarization only last a short while and in a fraction of a second it goes back to its resting potential [goes positive very quickly, then goes right back down to normal] 2) If the electrical stimulation is large enough, then, a few milliseconds after, the region further along the axon will have a similar depolarization and they just as quickly return to resting potential 3) If sodium (Na)is removed from the system, action potential does not occur

Change in Membrane Potential of Muscle Cell following ACh receptor activation

Equilibrium Membrane Potentials (MPs it would be if a certain element was at equilibrium on both sides) Na+: +50 mV Ca2+: +100 mV K+: -100 mV Resting: -70 mV (due to a combination of Na+, K+, and Ca2+) ACh receptor Opens: -25 mV (since Na+ is rushing in, the membrane potential move towards Na+ equilibrium potential [though doesn't reach it])

Santiago Ramón y Cajal

Father of neuroscience (one person) Created incredibly detailed drawings of neurons and neural structure --- won Nobel Prize in 1906 --- played chess in that one pic

Inhibitory Presynaptic Neuron

Hyperpolarizes and makes it more difficult for an impulse to cross synapse. The influx of Cl- decreases the membrane potential. --- initiate inhibitory signals (disfavor action potential) Mechanism (see term above for pic) • The inhibitory presynaptic axon targets the inhibitory synaptic current on the dendrite of the postsynaptic neurons. • This activates the opening of Cl- channels at the synapse. • The opening of these channels stimulate hyperpolarization which disfavors the formation of action potential

spatial summation

If two different inputs arrive at the same time, their effects on the membrane potential of the spike initiating zone are cumulative. If enough different inputs arrive at the same time, the spike initiating zone's membrane potential can be brought to the threshold. Determined by the combined effect of EPSPs or IPSPs produced nearly simultaneously by different synapses. --- if each of the charges occurred individually, none of them would be strong enough to form an action potential. But, if they are done at the same time, they can be added and can then overcome the threshold.

What happen if the Ca2+ is never removed by SERCA?

If you don't remove calcium, then the contraction will keep on going which leads to stiff muscles. When people die, they can no longer produce ATP which means SERCA cannot remove calcium, so contractions will continue. We call this rigor mortis.

IPSP

Inhibitory postsynaptic potential --- negative charge a slight hyperpolarization of the postysynaptic cell, moving the membrane potential of that cell further from threshold.

Structures in the muscle cell

Plasma Membrane T tubule Myofibril: long structures in the cell that contain the proteins that cause muscle contraction Sarcoplasmic reticulum: flat sacs that extend around the surface of he microfibril; source of important ions that promote myofibril contactions

Excitatory Presynaptic Neuron

Presynaptic neurons that favor depolarizes and generating a new action potential. The influx of Na+ increases membrane potential. Mechanism (see term above for pic) • The excitatory presynaptic axon targets the excitatory synaptic current on the dendrite of the postsynaptic neurons. • This activates the opening of Na+ or Ca+ channels at the synapse. • The opening of these channels stimulate depolarization which will favor the formation of an action potential

saltatory conduction

Rapid transmission of a nerve impulse along an axon, resulting from the action potential jumping from one node of Ranvier to another, skipping the myelin-sheathed regions of the membrane. --- no Na+ or K+ channels present in the myelinated areas --- action potential/refractory period only occurs at Nodes of Ranvier Myelination allows axons to have small diameters, yet transmit action potentials rapidly

movement of info in the retina [get better title]

Rods and Cones detect light which initiates a change in the membrane potential. Horizontal cells integrate information from the rods and cones and feeds it into the bipolar cells. Amacrine cells integrate information from the bipolar cells and feeds it into the ganglion cells. Ganglion cells group together forming the optic nerve and take this information in the form of action potentials out of the eye to the visual cortex of the brain. In short, bipolar cell takes information from the sensory cells to the ganglion cells. Ganglion cell takes the information in the form of action potentials to the brain. --- horizonal and amacrine cells are used to integrate information from sensory cells

Overcoming undershoot

The inactivation (h) gate of the sodium channel must open before the channel returns to the resting state. Until that occurs, an action potential cannot be generated --- idk if this depolarizes back to resting potential since i think the sodium channel is still closed???

synaptic inputs on a neurons

The mapping of a portion of the actual inputs to a single neuron. Some of these inputs will be excitatory, some inhibitory. The neuron integrates the totality of the inputs, and if the spike initiating zone is depolarized to threshold, an action potential is produced.

The mechanism of sarcomere shortening

The myosin molecules pull the actin filaments toward the center of the sarcomere, which causes the z lines to move closer together When contractions occur, the globular heads of the myosin (which are attached to the actin filaments) swivel towards the M line causing the actin filaments to move towards the center of the sarcomere. The I band, Z line, and the sarcomere in general reduce in size. The A band remains the same size

microanatomy of rod cell

The outer segment consist of intercellular disks made of lipid bilayer (essentially flattened vesicles) piled atop each other. Visual pigments called Rhodopsin are located throughout these vesicle membrane s.

undershoot

The part of an action potential when the membrane potential is more negative than at rest --- hyperpolarization

The conductance (permeability) of the membrane to Na and K during an action potential

The permeability to a particular ion is determined by the number of open channels for that ion. Na channels peak during the depolarization of the action potential K channels peak during the repolarization of the action potential

action potential threshold (aka all or nothing principle) [recap]

The principle that once the electrical impulse reaches a certain level of intensity (its threshold), it fires and moves all the way down the axon without losing any intensity. Once it crosses the threshold, there is a massive increase in membrane potential (see pic). After the membrane potential drops, there are a few milliseconds where it actually goes below the resting potential (more negative than the baseline), though only temporarily and it quickly returns to resting potential.

Santiago Ramón y Cajal's drawing of the retina

The retina, as drawn by Ramón y Cajal from a stained cross- section view through a microscope Very top Rods are long tubes Cones are soda-bottle shaped Middle Bipolar cells are the red circles with the a dot in the middle Bottom Ganglion are the large brown circles that are connected to the red lines --- mike wazowski Flow of light: from bottom of the pic to the top [past the ganglion to rods/cones] Flow of information: from the top of the pic to the bottom [from rods/cones to the ganglion]

temporal summation

The synaptic potential decays slowly, so if a the second pulse arrives soon after the first, its effect on membrane potential is additive. Differs from spatial summation in that the signals are not occurring at the exact same time, but in succession after one another, though still fast enough for the change in the potential to not go back down before the next stimulation starts. --- the same amount of stimulation, but they happen so quickly after one another --- minuscule difference in time between stimulation

Retina

Thin layer of several different types of cells that extends from the very bottom to the very top of the eye. contains sensory receptors that process visual information and sends it to the brain. Types of Cells in the Retina in order Ganglion cell Amacrine cells Bipolar cells Horizontal cells Rods (sensory cell) Cones (sensory cell) Epithelial Cells (grounding cells that holds the rods and cones in place) - NOT one of the main cells N.B. sensory cells are in the back, which seems counterintuitive since light will reach them last.

Motor unit

a motor neuron and all the muscle fiber it stimulates --- junction between the motor neuron and the muscle fiber is the neuromuscular junction • Every motor neuron in the spinal cord innervates one muscle fiber. • An action potential generated in the neuron leads to the contraction of the muscle. • The axon of the motor neuron may be a meter long. We are studying the processes that lead to the creation of a action potential in the neuron and the spread of the AP down the axon

hyperpolarization

action potential becomes more negative

depolarization

action potential becomes more positive

spike-initiation zone

aka axon hillock A region of the neuronal membrane near the base of the axon where action potentials are normally initiated, characterized by a high density of voltage-gated sodium channels. Several dendrites will send either excitatory or inhibitory signals. The signals will congregate at the spike-initiated zone and be added up. If the AP threshold is met then an AP will occur. If not the change in membrane potential will not continue down the axon. --- adds up all the EPSP (signals that favor forming an action potential) and all the (signals that disfavor forming an action potential)

acetylcholine receptor

aka the nicotinic ACh receptor, nAChR Receptor for ACh neurotransmitter found on skeletal muscle cells that is partly responsible for muscle contraction Consist of 5 protein subunits (2 alpha units, 2 beta units, and 1 delta unit) that come together to form a barrel that can open and close. When ACh in the synapse binds to the ACh-binding site on the alpha subunits, it changes the conformation of the receptor allowing Na+ to rush in causing depolarization. K+ is also released in a relatively smaller quantity Change in Membrane Potential of Muscle Cell onceResting: -70 mV Resting: -70 mV

muscle fiber

cellular unit of skeletal muscle --- formed by the end-to-end fusion of many muscle cells (contain myofibrils) during embryonic development

status of m and h gate in sodium channels When the axon is at rest (not sending a signal), m gate is (open/closed) and h gate is (open/closed) When the sodium channel permitting the flow of Na+, m gate is (open/closed) and h gate is (open/closed) During the refractory period, m gate is (open/closed) and h gate is (open/closed)

closed; open open; open open; closed

axon terminal

end of axon that is near the synapse

How does the arrival of an action potential at the neuromuscular synapse cause the muscle to contract?

excitation-contraction coupling

retinal

eye chromophore (molecule that respondds to a photon of light) --- found at lysine 296 (domain 7) in rhodopsin in the outer segment of rod cells --- aldehyde of vitamin A (this is why they thought carrots were good for your eyes) When it absorbs a photon, it transforms from 11-cis retinal to All-trans retinal

this took way lon

ger than it should have

connective tissue

holds muscle fiber in place

retina dagram (simple)

light flows from the bottom of the pic to the top [ganglion to the photoreceptors] information flows from the photoreceptors to the ganglion

myofibrils

long protein structures that make up muscle fibers --- contain actin and myosin proteins that are responsible for muscle contraction contractile unit of muscle fibers

motor neuron [recap]

multipolar neurons that carry outgoing information from the brain and spinal cord to the muscles that use them to contract. Neural cells have their cell bodies in the ventral part (towards the stomach) of the spinal cord and send long neurites to the muscles. They are not derived from neural crest cells but from the neural tube. Dendrites receive information from other neurons. Information is collected up in the cell body. Axon sends the signal to the periphery tissues (in this case, muscle tissues) Information goes from spinal cord to periphary

Muscles are made of ______________________, which are made of ____________________, which are made of _____________________

muscle fibers myofibrils sacromeres

postsynaptic neuron

neuron that receives the signal

presynaptic neuron

neuron that sends the signal

EM of actin and myosin filament

once the actin filament polymerizes, it is very very long Myosin filament consist of several pairs of myosin molecules that congregate together; much smaller than actin filament --- can see the golf club shape

Steps in Sensory Transduction (complex)

overview; don't need to know all parts What you do need to know is that the sensory response ALWAYS involve s a change in the membrane potential of the sensory cell (the generator, or receptor, potential) [process of promoting or inhibiting an action potential]

sarcolemma

plasma membrane of a muscle cell

sarcoplasm

plasma membrane of a muscle cell

Flow of action potential from motor unit to the muscle fiber

pretty much incorporate everything we learned above that's a lot of writing and i don't want to do it

Cones

retinal receptor cells that give rise to color sensations --- concentrated near the center of the retina and that function in daylight or in well-lit conditions.

Rods

retinal receptors that detect the amount of light

What regulates the opening of the photoreceptor ion channel?

short answer, cyclic GMP cGMP is required to open to photoreceptor ion channel When in the dark, the channel is open b/c cGMP binds to a receptor on the channel to keep it open When light exposure occurs it lowers the cGMP closing the channel leading to hyperpolarization

Action Potential [recap]

the change in membrane potential associated with the successful passage of an impulse along a nerve cell [implies that the threshold has been surpassed] --- action potential is undiminished as it continues down an axon

Strength ofa stimulus is determined by...

the frequency of the action potential

Characteristics of Action Potential

• Action potentials are triggered by depolarization • A threshold level of depolarization must be reached to trigger an action potential • Action potentials are all-or-none events • An action potential propagates undiminished throughout an axon •After a neuron fires an action potential, there is a brief period, called the refractory period, during which it is impossible to cause another action potential to be produced. This is due to the inactivation of the sodium channels (by the h gate)

Myofibril structure

Consist of units call sarcomeres laid end to end Sarcomeres consist of two proteins: actin and myosin --- actin filament [blue twist]: thin, elongated structures that consist of two actin twisted around each other --- myosin filament [red structure]: thick filament formed from multiple golf club-structured myosin Actin and Myosin are held in place by the Z line: protein that binds to the actin; act as anchors and establish boundaries of the sarcomere --- from one Z line to the other consist of one sarcomere --- name comes from it's morphology Titin filament: protein originating from the Z line that holds the myosin filament in place in the center of the sarcomere M band: web of sticky proteins right in the center of the sarcomere that also helps hold the myosin filaments in place A band: distance within a sarcomere from one end of the myosin filament to the opposite end --- length of the A band doesn't change even when it's contraction (b/c the myosin filaments don't go anywhere) H Zone: distance within a sarcomere between from one end of the actin filament and the end of the opposing actin filament --- size of H zone contracts when the actin filament contracts I band: distance between myosin filaments in adjacent sarcomeres --- used as an indicator of whether the muscle has contracted or not Contraction of muscle is the result of the sliding of actin towards the center of the sarcomere

Mechanism behind the reaction to pain

Ex. holding a finger over a flame [recap] There are sensory neurons (formed from the neural crest cells) that take information from the environment back to the CNS. Conversely, the motor neurons (formed from the neural tube; Shh) take information from the CNS to peripheral parts of the body. When you feel pain from the heat, pain receptors in your finger are stimulated causing an action potential to travel to the dorsal root ganglia to reach the spinal cord. In the spinal cord, an excitatory interneuron receives the signal and transmits this information to two different neurons: flexor motor neurons and inhibitory interneurons. The flexor motor neuron will have an action potential travel down it and have the flexor muscle contract (pull back at the sensation of pain.) At the very same time, the excitatory interneuron connects with another excitatory interneuron which then connects to an inhibitory interneuron that inhibits the extensor motor neuron (inhibits the depolarization; prevents an action potential.) Because the extensor motor neuron was inhibited, the extensor muscle relaxes so the arm doesn't stay still and prevent movement. [at the same time, the flexor muscle is activated and the extensor muscle is inhibited]

How does the membrane potential of a vertebrate photoreceptor cell (rods/cones) change in response to light?

Ex. rod cell exposed to different amounts of light When exposed to a bright light, the membrane potential decreases dramatically (hyperpolarization) --- membrane potential is higher in dark than in bright light (we expected the opposite) When exposed to a dim light, there is also hyperpolarization though not as extreme

EPSP

Excitatory postsynaptic potential --- positive charge a slight depolarization of a postsynaptic cell, bringing the membrane potential of that cell closer to the threshold for an action potential.

Human Eye Structure

Sclera: tough outer-covering surrounding the eye made of collagen that acts as a protective layer Cornea: part of the eye that interfaces with light and allows light to come in Iris: colored part of the eye that regulates how much light enters through either contracting or dilating --- split in two parts so there can be an opening for the lens (see pic) Lens: flexible structure that bends light at different angles so it can be focus onto the back of the retina Ciliary muscles: muscles connected to the lens that change the shape of the lens to control the angle and orientation with which light hits the retina Retina: comes the cells that are going to sees the light (rods & cones) Optic nerve: group of nerves on the back of the eye that transmits information/action potentials from the eye to the visual cortex of the brain Ocular muscles (not depicted): muscle on the surface of the eye that move the eye in different directions

intercellular disks (in rods)

Several flattened membranes stacked on top of each other in the outer segment of rod cells --- disks are derived from the plasma membrane --- contain rhodopsin There are 2 million rod cells per frog retina. Within a single frog rod cell, there are 1700 disk in the counter segment, 2.5 billion rhodopsin molecules.

muscle synapse

Space between plasma membranes of the axon tip of the sending neuron and the dendrite or cell body of the receiving neuron --- where neurotransmitters that act on receptors are released In muscle cells, it is found in the neuromuscular junction

sacromeres

The Actin and Myosin filaments in skeletal muscles are organized into sections

How does calcium regulate the interactions between myosin and actin

The actin filament consist of the long strands that run anti-parallel to each other. Between the two strands are the proteins Troponin and Tropomyosin. --- Troponin is a globular protein that contains the Ca2+ binding site --- Tropomyosin is an elongated protein that interacts with actin and covers the Myosin binding site; so, in a relaxed state, these will prevent the binding of myosin to actin When calcium levels are increased, it bind to troponin which slightly changes the conformation of tropomyosin such that the myosin binding sites are revealed and myosin can bind to actin.

Schwann cells

Type of glial cell (neural supporting cell) that surrounds the axon by producing an insulating later of myelin --- important for increasing the speed with which neural signals travel through saltatory conduction Structure: Wraps around axons in circular layers Node of Ranvier: segments of the axon not covered by Schwann cells

refractory period

Very short time frame when the sodium channel cannot be opened and so another action potential cannot be elicited ---the channel remains closed regardless of membrane potential Occurs b/ the h-gate is closed 5 ms after depolarization Refractory period ends once the h-gat opens up agains

Typical Action Potential [recap]

Vm depolarizes from the resting level of -70 mV to +50 mV and then repolarizes to a level below the original resting level. --- the episode lasts a few milliseconds --- the disturbance is propagated undiminished down the axon

Transferring Action Potential from one Cell to the Other

When the action potential reaches the end of the axon (near the synapse) • Na+ (continuation from the flow of action potential) flows into the axon terminal causing a depolarization change in membrane potential in that region • The change in membrane potential in the axon terminal activate calcium transporters which cause Ca2+ to flow INTO the axon terminal • Ca2+ promotes vesicle fusion; vesicles contain neurotransmitters such as Acetylcholine (Ach) • Vesicles with neurotransmitters fuse with the plasma membrane and get released into the synapse • In the synapse, then neurotransmitters bind to their specific receptors on the membrane of the postsynaptic cell (Ex. Ach receptors) • Leads to the transport of Na+ ions into the postsynaptic cell which causes an action potential in that cell

flow of action potential down the axon

Yellow = sodium channel Blue = potassium channel Stimulation from electrical current changes the shape of a Na+ channel (opening the m gate) allowing Na+ to rush inside the axon Na+ accumulates inside the membrane and travels down the axon, which causes a change in the electrical properties leading to depolarization in further parts of the axon. When these areas undergo depolarization, Na+ against rushes into the axon causing an action potential further along the axon. That increased Na+ continues traveling further down the axon Once the Na+ accumulation has passed on down the axon, the K+ channels begin their delayed activation in the area where the Na= accumulation just was. K+ channels push K+ out of the axon contribution to repolarization/hyperpolarization. Eventually these close and that area returns to baseline potential. This process keeps on continuing down the axon

Boundary between sarcomeres

Z line

Where does the calcium for myosin/actin functioning come from and how is it regulated? [calcium release in muscle cells]

[recap] ACh depolarizes the sarcoplasm [muscle cell membrane], inducing an action potential in the sarcolemma [muscle membrane], which spreads throughout the muscle membrane, including into the T-tubules. When the action potential that is caused by ACh spreads along the muscle cell membrane and reaches the T tubules, where it activates the Dihydropyridine receptor, membrane receptor on the interface between the T tubule and the sarcoplasmic reticulum which stores calcium. The Dihydropyridine receptor causes a change in the Ryanodine receptor, the calcium channel in the SR, which induces the release of calcium from the SR. To stop the release of calcium, the protein SERCA gets hydrolyzed by ATP and starts shuttling Ca2+ back into the SR

neuromuscular synapse

the junction between the axon of a neuron and a muscle cell --- see "Transferring Action Potential from one Cell to the Other" for how the action potential gets from the neuron axon into the muscle cell top: presynaptic cell (neuron) bottom: postsynaptic cell (muscle) synapse is 50 nm [recap] In order to transfer the action potential to the muscle cell, calcium channels in the presynaptic cell open which lead to the formation of synaptic vesicles that contain ACh. The vesicles fuse with the plasma membrane releasing ACh into the synapse; ACh binds the receptors on the muscle cell which lead to Na+ entering the muscle cell and forming an action potential. Active Zone (Dense Bar): Area in the presynaptic plasma membrane where the synaptic vesicles fuses with the presynaptic plasma membrane to get released into the synapse --- happens in specific areas so there is a higher concentration of ACh there so there can be a greater probability that they reach the the ACh receptor The membrane of the postsynaptic cell is not straight; instead, there are several folds along the interface underneath rich areas of ACh receptors. --- somehow this increases the liklihood that the ACh reaches the ACh receptors Basement Membrane: number of different extracellular matrix proteins that make it easier for ACh to bind the its receptor; matrix for cells to function properly System is set up so that ACh has the most optimal chance of reaching its receptor

synapse

the junction between the axon tip of the sending neuron and the dendrite or cell body of the receiving neuron --- the site where an axon makes contact with another cell

Rhodopsin

the pigment in rod cells that causes light sensitivity --- a seven transmembrane domain protein (7TD) --- type of G protein --- found in the disk membranes of photoreceptor cells. --- at a particular amino acid (lysine 296), rhodopsin has a chromophore, called retinal, which can be excited by photons and cause it to change conformation

sensory transduction

the process by which sensory stimuli are transduced into action potentials that are sent to the CNS • A sensory stimulus ALWAYS results in a change in the membrane potential of the receptor cell. • Information about a sensory stimulus is always carried to the central nervous system by ACTION POTENTIALS. The cell that makes action potentials may or may not be the receptor cell. • Information about the strength of the stimulus is encoded in the FREQUENCY of the action potentials.

Actin filament

thin filaments of the sarcomere that are responsible for cell contraction. --- consist of actin monomers Actin monomers polymerize to form the filaments (recall the acrosome reaction) --- attached to the z-lines of the sarcomere --- Each actin monomer has a myosin binding site