Identify – fasicle, epimysium, perimysium, endomysium, myofibril, myofilament

Banding pattern: I-band , A-band, H zone, m line, Z line, Myosin and actin

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Know the structure of Myosin, Actin, Troponin and Tropomyosin – must recognize these structures

Identify, Sarcoplasm, Sarcolemma, Sarcoplasmic reticulum, Transverse tubule.  Should know structure and how this plays a role in muscle contraction.  What do they contain?

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Identify the two deep muscles in the back – Erector spinae and quadratus lumborum

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1. Quad

2. Erector

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[image] The arrival of a nerve signal at the synaptic knob opens voltage-gated calcium channels.

[image] Ca²⁺ enters the knob and triggers exocytosis of the synaptic vesicles, releasing ACh.

[image] Empty vesicles drop back into the cytoplasm to be refilled with ACh, while synaptic vesicles in the reserve pool move to the active sites and release their ACh—a bit like a line of Revolutionary War soldiers firing their muskets and falling back to reload as another line moves to the fore.

[image] Meanwhile, ACh diffuses across the synaptic cleft and binds to ligand-gated channels on the postsynaptic neuron. These channels open, allowing Na⁺ to enter the cell and K⁺ to leave. Although illustrated separately, Na⁺ and K⁺ pass in opposite directions through the same gates.

[image] As Na⁺ enters, it spreads out along the inside of the plasma membrane and depolarizes it, producing a local voltage shift called the postsynaptic potential. Like other local potentials, if this is strong and persistent enough (that is, if enough current makes it to the axon hillock), it opens voltage-gated ion channels in the trigger zone and causes the postsynaptic neuron to fire.

employs γ-aminobutyric acid (GABA) as its neurotransmitter.

Amino acid neurotransmitters work by the same mechanism as ACh—binding to ion channels and causing immediate changes in membrane potential. The release of GABA and binding to its receptor are similar to the preceding case. The GABA receptor, however, is a chloride channel. When it opens, Cl⁻ enters the cell and makes the inside even more negative than the resting membrane potential. The neuron is therefore inhibited, or less likely to fire.

An Excitatory Adrenergic Synapse

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[image] The unstimulated NE receptor is bound to a G protein.

[image] Binding of NE to the receptor causes the G protein to dissociate from it.

[image] The G protein binds to adenylate cyclase and activates this enzyme, which converts ATP to cAMP.

[image] Cyclic AMP can induce several alternative effects in the cell.

[image] One effect is to produce an internal chemical that binds to a ligand-gated ion channel from the inside, opening the channel and depolarizing the cell.

[image] Another is to activate preexisting cytoplasmic enzymes, which can lead to diverse metabolic changes (for example, inducing a liver cell to break down glycogen and release glucose into the blood).

[image] Yet another is for cAMP to induce genetic transcription, so that the cell produces new enzymes leading to diverse metabolic effects.

Use the diagrams below to learn the adrenergic and cholinergic neurons.  What NTs do they produce and what effects do they bring about by binding to nicotinic, muscarinic, alpha, alpha2, beta or beta2 receptors?

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Cholinergic: Produces Acetycholine (ACh)

- When binded to Muscarinic: inhibits cardiac muscle by binding to a different type

- When binded to Nicotinic: opens ligand gated ion channels and produce postsynaptic potential  in the target cell

Adrenergic: Produces Norepinephrine (NE)

- When binded to a1&a2: promotes labor contraction, stimulates piloerection, constricts blood vessels but inhibits intestinal motiliry (

- When binded to B1&b2: NE relaxes and dialates the bronchioles  (excitatory effect)

How does substance P, serotonin and enkephalins modulate pain? See figure on the right 

pg. 586

Should be able to identify parts of ear and function.                

Parts of the eye & function

How does the eye detect light via Rod and Cones?

Should know basic physiology of vision – role of rhodopsin, glutamate, etc

pg. 619