ap ch 48 49 powerpoint - Pregitzersninjascienceclasses
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Transcript ap ch 48 49 powerpoint - Pregitzersninjascienceclasses
Gnarly Nervous
Physiology
Chapter 48-49 Notes
I. Nerve Structure Review
II. Nerve Signals
Membrane Potential
• Electrical charge difference across the plasma
membrane
• Anions (-): Concentrated inside the cell
• Cations (+): Concentrated in extracellular
matrix
II. Nerve Signals
• Resting potential: Membrane potential of an
unstimulated neuron
• Action potential: A nerve impulse that can be
transmitted to another nerve
Nerve Signals Details
1. Resting: Na+ and K+ gates closed (resting
potential)
2. Threshold: Na+ gates open
3. Depolarization: Na+ rushes into the cell
(interior more +)
4. If signal is strong enough – generates an
ACTION POTENTIAL
5. Repolarization: Na+ gates close, K+ channels
open. K+ leaves cell (interior more -)
Nerve Signal Details (cont)
6. Undershoot: Inside gets extra –
7. Refractory Period: Na+ / K+ pump gets
things back to normal.
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
Neuron Communication at the
Synapses
1. Ca+ gates open. Ca+ enters the cell
2. Synaptic vesicles merge with presynaptic
nerve’s membrane
3. Releases neurotransmitter into synapse.
Neurotransmitter binds with receptors on next
neuron (postsynaptic)
4. Neurotransmitter bound to ion channel, opens
it which allows ions to rush in (depolarize)
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.
IV. Common Neurotransmitters
A. 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
Mighty Muscular Physiology
• I. Mighty Muscular
• *Muscles only shorten or contract
Mighty Muscular
•
•
•
•
•
A. Muscle Structure
*Muscle Cell= muscle fiber
*Cell Membrane= sarcolemma
*Cytoplasm= sarcoplasm
*Endoplasmic Reticulum= Sarcoplasmic
Reticulum
Mighty Muscular
1. Muscle fibers are made up of myofilaments
2. Myofilaments are made of actin (thin) and
myosin (thick) microfilaments.
3. Repeating units along a muscle fiber are called
sarcomeres--they are the contractile unit of the
muscle.
4. Note on diagram: Z line, H zone, I band, A
band, M line
Muscle contractions
• *Length of sarcomere is reduced (distance
between Z lines gets smaller)
• *I band shortens, A band stays the same, H zone
disappears
Sliding Filament Model
1.
2.
3.
4.
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)
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!!