Term
| What can be found in muscle nerves? |
|
Definition
| Axons of: alpha/gamma motor neurons, proprioceptors |
|
|
Term
| What is the difference between extra/intrafusal muscle cells |
|
Definition
Extra - normal contractile
Intra- within spindle |
|
|
Term
| how do muscle cells hypertrophy? |
|
Definition
| Their satellite cells respond to stimulus and divide, then fuse with muscle cells to form larger muscle cell. |
|
|
Term
| what muscle fiber types can be interconverted? |
|
Definition
|
|
Term
| what type of neuron innervates skeletal muscle? |
|
Definition
|
|
Term
| what is the difference between the muscle spindle and the golgi tendon organ? What sort of nerve fibers exit these? |
|
Definition
1) Spindle conveys stretch info, while golgi tendon organ conveys force info
2) GSA's. type Ia and II innervate spindles; type Ib innervates golgi tendon organs |
|
|
Term
| What does a gamma motor neuron do? |
|
Definition
| Adjusts the lengths of spindle cells (muscle) |
|
|
Term
| which organelles are not located in the periphery of a muscle fiber? |
|
Definition
| Glycogen granules, mitochondria, smooth ER |
|
|
Term
| What are the various components of the sarcomere? |
|
Definition
A band - the area of myosin
M line - down the middle of the myosin
H band - the area of myosin w/ no actin overlap
I band - the area of actin w/ no myosin overlap
Z line - the plate connecting sarcomeres |
|
|
Term
| 1) Does troponin or tropomyosin bind Ca++? What are its subunits? 2) Does troponin or tropomyosin actually interfere with actin-myosin binding? |
|
Definition
1) Troponin - its subunits are Tn T (binds tropomyosin), Tn I (inhibits actin/myosin interaction), and Tn C (binds Ca ++)
2) Seems to be a combination of both, mostly tropomyosin |
|
|
Term
| what is the z disc composed of ? |
|
Definition
|
|
Term
what are the functions of
1) dystrophin and
2) desmin? |
|
Definition
dystrophin links the actins to integrins
desmin links z disks together in ADJACENT myofibrils (this is why striations are |
|
|
Term
| which signal stimulates satellite cell proliferation? |
|
Definition
|
|
Term
| at which point in the muscle powerstroke cycle is Pi bound to the actin head? |
|
Definition
| Only when the myosin head is returning to its pre-actin-bound conformation |
|
|
Term
| what type of receptors couples t-tubule depolarization to Ca++ release from SR? |
|
Definition
| Dihydropyridine receptor responds to voltage change, causes ryanodine receptor to be an open Ca++ channel |
|
|
Term
| what is the equation for muscle power? Muscle load of maximum efficiency? |
|
Definition
P= v*F
P_max at 30% F_max |
|
|
Term
| what are the differences between ventricular and purkinje cardiac cells? |
|
Definition
| Purkinjes are longer, fatter, have less striations and more glycogen. |
|
|
Term
| what is the mechanism of actin-myosin cross bridge activating in cardiac muscle? |
|
Definition
| Troponin-C binding Ca removes troponin I and tropomyosin from locations where they inhibit actin-myosin cross bridges. |
|
|
Term
| what is the difference between between t-tubules in skeletal and cardiac muscle? |
|
Definition
| in cardiac, t-tubules are located at z-line instead of the A/I |
|
|
Term
| how are dhydropiridine and ryanodine receptors coupled in cardiac muscle? |
|
Definition
| by Ca++, which enters sarcoplasm via dhp and activates rdn. Note that this makes the Ca++ pumps much more important to get Ca++ outside the cell so the SR Ca++ channels don't activate. |
|
|
Term
| what is the effect of norepinephrine on cardiac tissue? |
|
Definition
| Increases PKA activity, which phosphorylates myosin, phospholambin (SR pump) and dihydropiridine receptor, increasing activity of all - increasing both contractile force and velocity while shortening contractile time. |
|
|
Term
| how does increasing rate of cardiac contraction increase contractility? |
|
Definition
| It increases lingering Ca++ in sarcoplasm |
|
|
Term
| What is the effect of digitalis on 1) heart contractility and 2) heart rate? |
|
Definition
1) increases contractility
2) no effect on rate - doesn't increase rate of Ca exiting sarcoplasm (no phospholambin phosphorylation), doesn't increase cross-bridge cycling (no myosin phosphorylation). |
|
|
Term
| what is a positive inotropic agent? |
|
Definition
Increases contractility
inos=fiber |
|
|
Term
| which sorts of muscle cells exhibit gap junctions? |
|
Definition
| Cardiac and smooth muscles |
|
|
Term
|
Definition
| An axonal enlargement where the axon contacts a smooth muscle |
|
|
Term
| Which neurotransmitters are used in smooth muscle? What are their effects? |
|
Definition
| Both epinephrine and Ach are used in smooth muscle (depending on autonomic innervation) |
|
|
Term
| what is stress relaxation in a smooth muscle? |
|
Definition
| Increases length w/o increasing tension |
|
|
Term
| how are actin/myosin crossbridges stimulated in smooth muscle? |
|
Definition
| Calmodulin/Ca++ causes myosin phosphorylation via myosin light-chain kinase |
|
|
Term
| what is the effect of epinephrine on smooth muscle contraction? |
|
Definition
| If B2 adrenergic receptors are present, the MLCK is phosphorylated and thus inactivated, so the muscle relaxes. |
|
|
Term
| Which receptor does norepinephrine agonise in cardiac muscle? In smooth? |
|
Definition
| Cardiac - B1, leading to PKA phosphorylating myosin light chains and phospholambin, among other things. Smooth - a1, leading to PLC-mediated IP3 release. Note that B1-AdR isn't present in smooth muscle, but B2 is - so epinephrine causes increase in cAMP, but norepinephrine doesn't |
|
|
Term
| what are chromaffin cells? |
|
Definition
| These are cells of the adrenal medulla that release epinephrine |
|
|
Term
| What is the postsynaptic Ach receptor for parasympathetic 1) preganglionic and 2) pre-effector axon terminals? |
|
Definition
1) nicotinic cholinergic - only goal is to depolarize the post-synaptic neuron. No real 2nd messenger needed.
2) muscarinic - signals something to the cell to upregulate or downregulate its activity. Thus linked to Gq (1,3,5) or Gi (M2,4) systems. |
|
|
Term
what is the axon reflex?
How else can reflexes occur without CNS involvement? |
|
Definition
Injury stimulates an afferent axon to stimulate (efferently) nearby blood vessels to dialate - without any CNS involvement (no interneurons, nothing).
Reflexes can also occur with ganglial organization, especially in the gut. |
|
|
Term
| What is the micturition reflex? |
|
Definition
| full bladder causes parasympathetic stimulation (M1) of ditrusor muscle, and inhibiton (M2) of sphinctor. |
|
|
Term
| What is the nucleus tractus solitarius? |
|
Definition
| Afferent information is processed here - communicates with hypothalamus so afferents evoke and efferent response |
|
|
Term
| which adrenergic receptor has a higher sensitivity to norepinephrine than to epinephrine? |
|
Definition
|
|
Term
| Where are parasympathetic neurons not found? |
|
Definition
| In the limbs - or anywhere there's skin, skeletal muscle, or bone. |
|
|
Term
| What is the mechanism by which NO is secreted? What are its effects? |
|
Definition
| Secreted by endothelial cells in response to Ach (from parasymp). Causes GC receptor to activate in nearby smooth muscle cell, producing cGMP and leading to relaxation (vasodilation). This one way the symp. and parasymp. systems have opposing effects! |
|
|
Term
| What is the mechanism of sildenafil? |
|
Definition
| This inhibits the phosphodiesterase enzymes in corpus cavernosum smooth muscle. As a result, cGMP levels stay elevated in response to NO, and the blood vessels dialate. |
|
|
Term
| Do endothelial cells contribute to constriction or vasodilation of blood cells? |
|
Definition
| Both! Thromboxane A2, endothelins constrict. |
|
|
Term
| What is the typical physiologic stimulus for NO secretion? |
|
Definition
| Sheer stress on endothelial cells from high-pressure fluid flow |
|
|
Term
| What couples activated TK to its downstream substrates? |
|
Definition
| Coupling proteins with SH2 domains that bind to the autophosphorylated tyrosines of the TK |
|
|
Term
| What couples EGFR to RAS activation? |
|
Definition
| GRB2 binds (P)EGFR, and binds SOS which stimulates GDP-RAS to swap in a GTP, becoming active. Ras is a serine/threonine kinase |
|
|
Term
| What are the activators of c-fos and c-jun? |
|
Definition
| c-fos: ERK c-jun: p38 MAPK, JNK |
|
|
Term
| How does the EPO/EPOR pathway function? |
|
Definition
| JAK is bound to EPOR, and becomes active TK upon EPO binding. Phosphorylates STAT, a transcription factor which leads to increased erythopoiesis. |
|
|
Term
| What signalling system does p28^v-sis disrupt? |
|
Definition
| PDGF-B/EGFR binding - PDGF-B is primary growth factor in serum; EGFR is a TK. p28^v-sis mimics PDGF |
|
|
Term
| How does gp65^v-arb B2 interfere with mitogens? |
|
Definition
| The protein is homologous to the TK portion of EGFR and is constitutively active |
|
|
Term
| What is the biological effect of c-fos activation? |
|
Definition
|
|
Term
| What is the biological effect of c-jun activation? |
|
Definition
| differentiation, inflammation, apoptosis |
|
|
Term
| What are the three branches of PDK signalling? |
|
Definition
1) PKC (shared branch with PLC signalling)
2) AKT (PKB) - leads to GLUT4 translocation, cyclin phosphorylation
3) ser-thr kinase that results in ribosome phosphorylation |
|
|
Term
| What are the two branches downstream of IRS-1 ? |
|
Definition
| MAPK signalling via grb-2, PI3K signalling via PI3K->PDK |
|
|
Term
| How is Atrial natriuretic factor released? |
|
Definition
| Its zymogen, atrial peptigen, is cleaved by proteolysis and released |
|
|
Term
What are two possible kinases that target MLCK?
What are two possible ligands for upstream receptor that could result in MLCK phosphorylation? |
|
Definition
1) PKA and PKG
2) Epinephrine and ANF |
|
|
Term
| What is the difference between the NO-activated and ANF-activated guanylyl cyclases? |
|
Definition
| The NO-activated one is cytosolic, soluble |
|
|
Term
| what is the route of activation of the soluble guanylyl cyclase? |
|
Definition
| 1st NO increases affinity for substrate by binding to heme of activator portion, extra NO's bind to other allosteric sites, increasing efficiency |
|
|
Term
|
Definition
| oxygenated HB with NO bound to a cysteine - can release NO in blood if O2 drops to dilate blood vessels. |
|
|
Term
| What is the effect of NO on platelets |
|
Definition
|
|
