Gnarly Nervous Physiology Chapter 48 & 50 Notes

I. Nerve Structure Review

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

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 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 -)

Nerve Signal Details (cont) Undershoot: Inside gets extra – 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 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)

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 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 *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 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

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 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!!