1. Gnarly Nervous Physiology
Chapter 48 & 50 Notes

2. I. Nerve Structure Review

3. Nerve Structure Cell body – includes cell organelles and nucleus
Dendrite – receive signals from other neurons
Axon – transmits signals to other cells
Synapse – gap/junction between neurons
Sensory neurons – carry messages from sensors to brain
Interneurons – neurons in brain that interpret information
Motor neurons – transmit signals to muscle cells

4. II. Nerve Signals Membrane Potential
Electrical charge difference across the plasma membrane
Anions (-): Concentrated inside the cell
Cations (+): Concentrated in extracellular matrix

5. II. Nerve Signals
Resting potential: Membrane potential of an unstimulated neuron
Action potential: A nerve impulse that can be transmitted to another nerve

6. Nerve Signals Details
Resting: Na+ and K+ gates closed (resting potential)
Threshold: Na+ gates open
Depolarization: Na+ rushes into the cell (interior more +)
If signal is strong enough – generates an ACTION POTENTIAL
Repolarization: Na+ gates close, K+ channels open. K+ leaves cell (interior more -)

8. Nerve Signal Details (cont)
Undershoot: Inside gets extra –
Refractory Period: Na+ / K+ pump gets things back to normal.

10. III. Neuron communication at the Synapses
A. The Process
*Cytoplasm at end of axon contains synaptic vesicles
The vesicles contain neurotransmitters
These are chemical messengers

11. Neuron Communication at the Synapses
Ca+ gates open. Ca+ enters the cell
Synaptic vesicles merge with presynaptic nerve’s membrane
Releases neurotransmitter into synapse. Neurotransmitter binds with receptors on next neuron (postsynaptic)
Neurotransmitter bound to ion channel, opens it which allows ions to rush in (depolarize)

13. Nerve Communication at the Synapses
If Na+ gates open, membrane becomes depolarized (more +) and results in excitatory postsynaptic potential. It may generate an action potential if strong enough.
If K+ gates open, membrane becomes polarized and results in inhibitory postsynaptic potential (more - because K+ goes out). No action potential.

14. IV. Common Neurotransmitters
Acetylcholine
*Found at neuromuscular junctions. Stimulates muscle contraction.
B. Epinephrine, Nor epinephrine, Dopamine, & Serotonin
*Secreted between neurons in CNS
*Dopamine and serotonin affect sleep, mood, attention and learning
*Excessive dopamine is linked to schizophrenia
*Some hallucinogenic drugs bind to serotonin and dopamine receptors

15. Mighty Muscular Physiology
*Muscles only shorten or contract

16. Mighty Muscular A. Muscle Structure Muscle Cell= muscle fiber
Cell Membrane= sarcolemma
Cytoplasm= sarcoplasm
Endoplasmic Reticulum= Sarcoplasmic Reticulum

18. Mighty Muscular Muscle fibers are made up of myofilaments
Myofilaments are made of actin (thin) and myosin (thick) microfilaments.
Repeating units along a muscle fiber are called sarcomeres--they are the contractile unit of the muscle.
Note on diagram: Z line, H zone, I band, A band, M line

19. Muscle contractions
Length of sarcomere is reduced (distance between Z lines gets smaller)
I band shortens, A band stays the same, H zone disappears

20. Sliding Filament Model
ATP binds to myosin head
ATP-----> ADP + Pi
Myosin head binds to actin forming cross-bridge
ADP + Pi are released. Myosin head changes shape. This slides the actin toward the center of the sarcomere (Z lines get closer)
Whoo Hoo! Contraction!
5. ATP binds, releases myosin head. We start again.
(Corpse is “stiff” because there is not ATP to undo the contraction)

22. It Can’t Be That Simple 
When muscles are at rest, the myosin binding sites on the actin are blocked by a protein called tropomyosin. The proteins in the troponin complex control the position of tropomyosin on the actin.
For contraction to occur, the binding sites need to be uncovered.
Ca+ to the rescue!! Calcium binds to troponin, it alters the shape and exposes the myosin binding sites on the actin.
So drink lots of milk!! No Ca+ ---no contraction!!