1. Integumentary system (skin). 

2. Muscular system. 

3. Skeletal system. 

4. Nervous system. 

5. Excretory system (nitrogenous wastes). 

6. Digestive system. 

7. Immune system. 

8. Cardiovascular system. 

9. Reproductive system. 

10. Lymph (atic) system. 

11. Endocrine system (hormones).

Neurons and muscle fibers are excitable cells that conduct impulses--for our model we will 

consider a neuron as our excitable cell.

A. Neurons conduct impulses and have the following structure. 

1. Dendrites are cell process that “receive” impulses --there may be numerous 

dendrites. 

2. The soma is the “cell body” that contains the nucleus and the bulk of the 

cytoplasm. 

3. The axon is a process that carries impulses “away” from the soma--there is 

typically a single axon although it may have many branches called axon 

collaterals.  

4. Impulse conduction is functionally, “one way” from dendrite to axon.

Before an impulse can be generated, a resting potential across the cell membrane must be 

established.

1. Excitable cell membranes contain active transport systems known as the Na

+

 /K

+

pumps. 

2. Sodium is transported (“pumped”) across the cell membrane from inside the cell to the 

outside, and potassium from outside to inside in an unequal ratio of approximately 3 

Na ions to 2 K ions--this requires ATP. 

3. The Na/K pump establishes a concentration gradient of the two ions across the 

membrane. 

a) Na ions are concentrated outside. 

b) K ions are concentrated inside. 

c) This not only establishes a concentration gradient, but a charge gradient 

(voltage) as well. 

(1) There are more Na ions outside the cell, than K ions inside the cell, and 

Na ions have a greater mass. 

(2) This makes the inside of the cell relatively negative to the outside, even 

though both particles are cations. 

(3) Some K can also diffuse back out of the cell through ungated channel 

proteins—this adds to the intracellular negativity, because anions cannot 

diffuse through the membrane as readily. 

4. This charge gradient is known as the resting potential of the cell, and is measured at -

70mV (millivolts)--the cytoplasm is 70 mV more negative than the extracellular 15

solution (interstitial fluid) when measured by microelectrodes placed on either side of 

the cell membrane. 

5. The gradient stabilizes at -70 mV because at some point the pumping of ions is offset 

by their diffusion through ungated channel proteins (discussed below). 

a) The membrane is has some ungated K channel proteins so some K will follow 

its concentration gradient out. 

b) This leaves an excess of Cl- and other anions which hold the remaining K more 

strongly. 

c) The Na/K never turns off, but there will be fewer K to pump out because the 

anions and holding them within the cytoplasm so strongly. 

6. The establishment of the resting potential is crucial to function and is one of the 

important qualities of excitable tissues. 

a) The concentration (voltage) gradient stores energy. 

b) The movement of charged particles generates a current, and current has the 

power to do work of some kind.

1. Channel proteins are pore proteins through which ions may diffuse. 

2. Ungated channel proteins are freely permeable to K, and to a lesser degree Na. 

3. Most channel proteins are gated channels. 

a) Na gated channel proteins are normally “closed” preventing dialysis of Na 

across the cell membrane, although if the gates are “opened” Na diffuses rapidly 

through them. 

b) K gated channel proteins are normally “closed” preventing dialysis of K across 

the cell membrane, although if the gates are “opened” K diffuses rapidly through 

them. 

c) The gated channels are opened by two means. 

(1) Ion (chemical) gated channel proteins are opened by binding an ion or 

chemical (neurotransmitter) of some type. 

(2) Voltage gated channel proteins are opened by changes in magnetic fields 

created by changes in the membrane voltage (current generated by 

movement of Na and K).  

d) Excitable cell membranes have high densities of Na and K gated channel 

proteins--particularly the voltage gated channel proteins. 

1. Something (a chemical, possible chemical, physical stimuli, etc.) will alter gated Na 

channel proteins at a specific location on a neuron--this area is typically the dendrite--

opening the gates, making them permeable to Na. 

2. Na “leaks” across the membrane into the cell (following their concentration gradient). 

a) As Na moves into the cell this affects the membrane resting potential. 

b) The cytoplasm becomes more positive. 

3. When the membrane potential reaches -55 mV, a “threshold” potential is reached. 

a) When the resting potential reaches the threshold potential of -55 mV, the local 

voltage gated Na channel proteins fully open, allowing a “flood” of Na into the 

cell at that spot (following their concentration gradient). 

b) This is the beginning of an action potential. 

c) Once the threshold potential is reached, initiating an action potential, an impulse 

will be generated. 

4. As Na rushes into the cell (following their concentration gradient), the membrane 

potential changes dramatically, going from -55 mV to +40 mV in a fraction of a 

millisecond (msec). 

a) The Na voltage gated channel proteins close immediately. 16

b) This influx of Na ions is known as membrane depolarization. 

5. The current generated by movement of the Na ions opens adjacent K voltage gated 

channels, allowing K ions to “flood” out of the cell. 

a) The out flux of K makes the cytoplasm relatively negative again, driving the 

membrane potential down to approximately -70 mV. 

b) The K voltage gated channel proteins close immediately. 

c) This is known as repolarization of the membrane. 

6. The Na/K pump will reestablish the resting potential at that site, in what is called the 

after potential. 

a) The resting potential is reestablished at -70 mV. 

b) This ends the action potential. 

7. The action potential is a local event. 

a) The action potential is the dramatic ionic change in membrane potential that 

occurs at a specific site due to the movement of the Na and K ions. 

b) Another action potential cannot be generated at that site until the resting 

potential is reestablished. 

8. An action potential is an “all or nothing” event--either an action potential occurs or it 

does not, there is no partial action potential (once threshold potential is reached, an 

action potential takes place). 

9. The entire action potential takes about 1msec.

1. The current generated by an action potential (first the influx of Na ions, followed by 

the out flux of K ions) opens adjacent voltage gated Na channel proteins. 

2. This triggers an action potential adjacent to the original action potential. 

3. This, in turn, triggers an action potential adjacent to that spot, and so on and so on. 

4. An impulse, then, is an action potential that is propagated throughout an excitable cell 

membrane. 

a) An impulse is generated by initiation of an action potential at a specific site on 

an excitable cells membrane. 

b) Once generated, the action potential radiates out in all directions until the entire 

membrane has experienced the action potential. 

c) This propagation of the action potential is the impulse.  

5. Like the action potential, and impulse is likewise an “all or nothing” event, in that 

once an action potential is generated, it will produce an impulse--there are no partial 

impulses.

1. Neurons as we have hopefully discussed previously, are functionally directional in 

impulse conduction. 

a) We describe impulses as being conducted from dendrite to axon. 

b) The reality is that impulses are conducted in all directions from the site of action 

potential initiation. 

c) The seeming contradiction is discussed below. 

2. An impulse can be generated almost anywhere on a neuron, but typically occurs on a 

dendrite. 

3. The impulse is conducted throughout the membrane including the length of the axon. 

4. When the impulse reaches the end of the axon there is a space between the neuron 

(presynaptic cell) and the next cell (postsynaptic cell). 

a) The next (post synaptic) cell could be the dendrite of another neuron, forming a 

neuronal synapse (junction). 

b) The next (post synaptic) cell could be a muscle fiber (cell), forming a neuromuscular synapse (junction).

5. The axon terminal (end of the axon) contains numerous synaptic vesicles that contain 

chemicals called neurotransmitters. 

6. The impulse causes the vesicles to fuse with the neurilemma spewing the contents into 

the synapse. 

7. The neurotransmitters rapidly diffuse across the synapse and bind to receptor proteins 

in the postsynaptic membrane, producing one of two general effects (if the post 

synaptic cell is excitable). 

a) Excitation--increases Na ion permeability leading to the threshold potential and 

action potential generation. 

b) Inhibition-- decreases Na ion permeability preventing action potential 

generation. 

c) Excitation or inhibition of the postsynaptic cell depends on the combination of 

neurotransmitter secreted by the presynaptic cell, and the receptor protein of the 

postsynaptic cell. 

d) The postsynaptic cell may not be excitable, in which case the neurotransmitter 

may produce some other effect when bound by a receptor protein, such as 

causing secretion of a hormone. 

e) Examples of neurotransmitters: acetylcholine, epinephrine, norepinephrine, 

endorphins, enkephalins, dopamine, seratonin, etc. 

8. Postsynaptic cell enzymes degrade the neurotransmitters. 

9. The altered neurotransmitters are reabsorbed by the presynaptic axon terminal, 

reactivated, and repackaged into synaptic vesicles. 

10. The reason neurons are functionally unidirectional is that axons have 

neurotransmitters which will initiate an action potential in the dendrites of the post 

synaptic neuron, so impulses are typically generated in the dendrites and propagate to 

the axon terminals--dendrites lack neurotransmitters but the dendritic neurilemma has 

neurotransmitter receptor proteins. 

11. What is the purpose of the synapse? 

a) If neurons were in direct contact impulses would travel from cell to cell--any 

action potential would be conducted throughout all nervous and muscle tissue. 

b) The synapse allows for control of impulses and the effects they generate--each 

synapse permits a decision to be made--should this impulse go on to the next 

cell or not? 

How do neurotransmitters trigger effects in post synaptic cells--example: the neuromuscular 

junction.

1. Neurons that innervate skeletal muscles have synaptic vesicles that contain the 

neurotransmitter, acetylcholine (Ach). 

2. In response to an impulse, the presynaptic vesicles bind to the axon neurilemma and 

spew Ach into the synapse. 

3. Ach binds to its membrane receptor protein in the postsynaptic sarcolemma. 

4. In response to binding Ach, the membrane protein binds and activates the cytoplasmic 

enzyme, adenyl cyclase. 

5. The activated adenyl cyclase converts ATP into cyclic AMP (cAMP). 

6. cAMP binds to and activates a kinase enzyme. 

7. The activated kinase phosphorylates (adds a phosphate) an ion gated Na ion channel 

protein. 

8. Phosphorylating the ion gated Na channel protein opens its gate, increasing the 

membrane’s permeability to Na ions. 

9. Enough acetylcholine will cause the membrane to reach threshold potential, generating 

an action potential.

Some neurons exhibit saltatory (jumping) conduction, which is a more rapid impulse 

conduction than the “normal” impulse described above.

1. Some neurons that form the peripheral nervous system (PNS) have myelinated axons 

or dendrites. 

a) Peripheral nerves exit/attach to the brain or spinal cord, which make up the 

central nervous system (CNS). 

b) Nerves are composed of fascicles (latin for bundles) of axons and or dendrites. 

(1) Each neuron is separated from another neuron by a layer of connective 

tissue known as the endoneurium--connective tissue is not excitable and so 

prevents the impulse conduction from one axon to another. 

(2) Bundles of axons/dendrites form fascicles surrounded by still more 

connective tissue called the perineurium 

(3) The fascicles form the nerve, which is encapsulated in still more 

connective tissue called the epineurium. 

(4) The epineurium, perineurium, and endoneurium are continuous with one 

another. 

2. Myelinated peripheral nerves have specialized glial cells, called Schwann cells that 

associate with an axon or dendrite as it grows. 

3. The Schwann cells attach to a dendrite or axon and grow around it in a spiral fashion, 

covering the neurilemma (neuron cell membrane), and generating several layers of 

Schwann cell plasma membranes around the axon. 

a) Imagine wrapping electrician’s tape around a wire--the wire is an axon, and the 

tape is a Schwann cell growing around the axon. 

b) You end up with several layers of tape around the wire, representing several 

layers of Schwann cell membranes around the axon. 

4. The Schwann cell membranes have large quantities of a white, fatty substance called 

myelin. 

5. Myelin prevents Na and K ion channels from functioning. 

6. Gaps between Schwann cells, called Nodes of Ranvier, expose the neurilemma, and 

these gaps have extremely high concentrations of Na and K voltage gated channel 

proteins.

7. How do these factors lead to saltatory conduction that is faster than normal impulses? 

a) When Na ions flood into the cytoplasm in depolarization they repel other 

positively charged ions creating magnetic flux. 

b) This flux passes through cytoplasm to the next node of Ranvier. 

c) This flux opens the highly concentrated Na voltage gated channel proteins at a 

node of Ranvier. 

d) An action potential is generated at the node, creating another cytoplasmic 

magnetic flux, which affects the Na voltage gated channel proteins at the next 

node, triggering an action potential at that node, and so on, and so on. 

e) The impulse “jumps” from node to node for two reasons: 

(1) Myelin prevents impulse conduction along the membrane--axon potentials 

can occur only at exposed neurilemma sites, i.e. the nodes of Ranvier. 

(2) The highly concentrated voltage gated channel proteins create a stronger 

cytoplasmic flux than is generated in a normal neurilemma. 

f) The cytoplasmic flux proceeds more rapidly than does an impulse moving along 

a normal neuron membrane. 

g) This brings up an important question and answer. 

(1) Question: Why doesn’t the cytoplasmic flux generated in a normal 

impulse affect voltage channels ahead of the impulse making it just as 

fast?   19

(2) Answer: The voltage gated channel protein density is not so concentrated 

as to produce a cytoplasmic flux strong enough to induce action potentials 

ahead of the impulse. 

Skeletal muscles produce movement by using the leverage generated by contraction 

(physically shortening), around a joint.

Connective tissue surrounds and runs through skeletal muscles, forming tendons at each end, 

attaching to bones (typically).

1. The non-moving (or the attachment site on a bone that does not move) attachment site 

is known as the origin of the muscle. 

2. The moving attachment site (or the attachment site on a bone that moves) is known as 

the insertion.

1. The muscle cell is known as a muscle fiber, and the muscle fiber cell membrane is the 

sarcolemma--the sarcolemma has deep invaginations called transverse tubules (ttubules), which penetrate, deep into the interior of the cell contacting sarcoplasmic 

reticula. 

2. The muscle fibers run the length of the muscle. 

3. Each muscle fiber is encased in a thin layer of dense irregular connective tissue called 

the endomysium. 

4. Muscle fibers are bundled into groups called fascicles, and the fascicles are 

encapsulated in connective tissue known as perimysium. 

5. The fascicles are bundled together, forming the muscle, within a layer of connective 

tissue known as the epimysium. 

6. The epimysium, perimysium, and endomysium are continuous with one other, run the 

length of the muscles, and form the tendons at the ends of each muscle. 

7. Additional sheets of connective tissue connect muscles to one another and muscles to 

skin--these are known as fascias. 

8. The muscle fiber contains bundles of proteins known as myofibrils. 

9. These myofibrils are covered with sarcoplasmic reticula, which sequester Ca ions. 

10. The myofibrils are composed of contractile proteins that form myofilaments. 

a) Thin myofilaments are composed of the globular subunits of the protein actin, 

which associate to form a double helix, the troponin- tropomyosin complex is 

also helical and overlays the myosin binding sites of the actin subunits. 

(1) The actin proteins have mysosin binding sites to which myosin heads will 

bind. 

(2) The troponin-tropomyosin complex normally covers the myosin binding 

sites of the actin proteins. 

(3) When the troponin-tropomyosin complex binds Ca ions, it changes the 

shape of the helix exposing myosin-binding sites. 

b) Thick myofilaments are composed of the protein myosin. 

(1) The myosin protein has a part known as the myosin head. 

(2) The myosin head will bind to actin. 

(3) It also has two pivot points. 

(4) When bound to ATP it will be in a power position. 

(5) When ATP is released, and the heads spring forward. 

11. The smallest functional unit of the muscle is the sarcomere; in thin myofilaments 

surround the thick myofilaments.

1. A neuron innervating a muscle (neuromuscular junction) conducts and impulse, and 

initiating an action potential in the sarcolemma of a muscle fiber. 

2. The impulse is conducted throughout the sarcolemma, including down the t-tubules 

into the interior of the fiber to the membrane of the sarcoplasmic reticulum (SR). 

3. The impulse is conducted through the sarcoplasmic reticulum membrane, opening 

voltage gated Ca ion channel proteins. 

4. Ca floods out of the SR and binds to the troponin-tropomyosin complex.  

5. When the troponin-tropomyosin complex binds Ca ions, it changes the shape of the 

helix exposing myosin-binding sites. 

6. Myosin heads having already bound ATP, and in a power position, bind to actin. 

7. Binding to actin causes the myosin heads to release ADP and phosphate. 

8. This causes a change in shape of the myosin head--it pivots “forward” in two 

positions, pulling the actin (thin filaments) over the myosin myofilaments. 

9. This sliding of thin myofilaments past thick myofilaments shortens the physical length 

of the muscle fiber, and muscle as a whole. 

10. The sarcoplasmic reticulum has a Ca pump that will actively transport Ca ions back 

into the sarcoplasmic reticulum. 

11. Calcium released by the troponin-tropomyosin complex is also pumped back into the 

SR. 

12. Without free Ca ions to bind, the troponin-tropomyosin complex covers the myosin 

binding sites on the actin protein, ending the contraction until the next impulse comes 

through. 

13. Muscle fiber contraction is an “all or nothing” event; there are no partial muscle fiber 

contractions.

1. Each muscle fiber contraction is an “all or nothing.” 

2. Each muscle fiber is separated from the others by the endomysium. 

3. The endomysium is dense irregular connective tissue and will not conduct impulses. 

4. The endomysium acts as insulation between muscle fibers. 

5. The strength of contraction of a muscle is dependent on how many muscle fibers are 

recruited (stimulated to contract)--the more fibers recruited the stronger the muscle 

contraction. 

6. A motor unit consists of a neuron and the muscle fibers it innervates (axons may 

branch to innervate numerous muscle fibers). 

7. The more motor units recruited, the greater the strength of contraction.