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66 Cards in this Set
- Front
- Back
Afferent division of nervous sytem
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input back to CNS
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Efferent division of nervous system
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input away from CNS
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Autonomic nervous system divisions
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Sympathetic (thoracolumbar)
Parasympathetic (craniosacral) Enteric (gut brain) |
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Somatic motor system events/structure
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1. CNS command
2. lower motor neuron 3. NMJ excitation/contraction coupling 4. skeletal muscle contraction 5. movement |
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Autonomic system events/structure
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1. CNS command reflex to periphery
2. tonic control 3. preganglionic fiber 4. ganglia/postganglionic fiber 5. organ 6. response + or - |
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Sympathetic Nervous system pre/post ganglionic lengths
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pre- short
post- long |
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Parasympathetic nervous system pre/post ganglionic lengths
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pre-long
post-short |
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Implications of dual innervations of target organs by PNS and SNS
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reciprocal effects- one inhibits while other stimulates - fine control of organ functions (heart rate and intestinal motility)
cooperative effects- promote same goal (salivary gland secretion and male sexual response) |
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Neurotransmitters of PNS and SNS
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Acetylcholine (ACh) and Norepinephrine (NE)
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Acetylcholine-where
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cholinergic nerves.
all sympathetic and parasympathetic preganglionic nerves. sympathetic postganglionic nerves innervating sweat glands in skin and some skeletal muscle blood vessels. all parasympathetic postganglionic nerves. |
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Norepinephrine
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adrenergic nerves.
most sympathetic postganglionic nerves. adrenal medulla releases some into blood stream |
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Epinephrine
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hormone of sympathetic nervous system.
released from adrenal medulla |
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Adrenal medulla
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modified postganglionic neuron of sympathetic nervous system. releases EPI, NE, and dopamine (catecholamines).
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Parasympathetic neurotransmitters
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pre- ACh
post- ACh |
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Sympathetic neurotransmitters
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pre- ACh
post- NE, ACh adrenal medulla- EPI, NE, dopamine |
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Acetylcholine synthesis/degradation/function
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synthesized from AcCoA + choline by choline acetyl transferase (Chat).
stored in vesicles which are released when AP increases Ca2+ entry into nerve ending binds to receptor and broken down in synaptic cleft by acetylcholinesterase (AChE). AChE inhibitors used to treat glaucoma, increase GI motility, and myasthenia gravis. |
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Norepinephrine synthesis/degradation (presynaptic and target cells)/diffusion
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tyrosine enters nerve terminal > DOPA > dopamine > NE
NE stored in vesicles complex with ATP and released when AP increases Ca2+ entry into nerve ending. binds to receptor. presynaptic: uptake by active pump mechanism (uptake-1) which is inhibited by cocaine and tricyclic antidepressants. NE metabolized by enzyme MAO target cells: uptake-2 pump that is not sensitive to cocaine. NE metabolized by enzyme COMT. diffusion-detectable in plasma (also metabolized in liver) |
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Cholinergic receptors (4)
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muscarinic M1-increase intracellular Ca2+
muscarinic M2-inhibit adenylyl cyclase muscarinic M3- increase intracellular Ca2+ nicotinic Nn-open Na+ and K+ channels, depolarization |
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Adrenergic receptors (5)
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a1- increase intracellular Ca2+
a2- decrease cAMP b1- increase cAMP b2- increase cAMP b3- increase NO (nitric oxide) |
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Dopaminergic receptors (2 groups)
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D1,D5- increase cAMP
D2,D3,D,4- decrease cAMP |
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Tonic activity of autonomic nervous system
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active under resting conditions
fine control-increase or decrease SNS and PNS tonically acticve to most organs they innervate |
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Reflex activity of autonomic nervous system
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response to change in environment (may not require cortical processing)
many basic reflexes modulated by other inputs to CNS or by higher brain sensor |
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Parasympathetic nervous system - Rest & Digest - examples (7)
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constrict pupils,
increase watery saliva enhance GI GU emptying stimulate release of insulin and enhance storage of excess glucose as fat and glycogen slow heart rate constrict airways open resistance vessels of coronary circuit |
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Sympathetic nervous system - Fight or Flight - examples (8)
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dilate pupil
increase thick viscous salive decrease intestinal motility stimulate hepatic glycogenolysis and inhibit insulin release increase heart rate and cardiac contractility dilate bronchial smooth muscle alter blood flow by changing vasoconstriction of blood vessels sweating |
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Heart - reciprocal effects of PNS/SNS
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Heart Rate:
SNS (NE or EPI)- increase pacemaker rate, increase heart rate PNS (ACh)- decrease pacemaker rate, decrease heart rate Contractility: SNS (NE or EPI)- increase force of ventricular contraction |
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Lungs - reciprocal effects of PNS/SNS
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bronchiolar smooth muscle:
SNS (NE)- relax PNS (ACh)- constrict and increase glandular secretions |
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Salivary gland- cooperative effects of PNS/SNS
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SNS-viscous secretion
PNS- watery secretion |
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Lacrimal glands- cooperative effects of PNS/SNS
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SNS/PNS both cause secretion
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Sexual response- cooperative effects of PNS/SNS
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PNS-erection
SNS-ejactulation "point and shoot" |
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Autonomic centers in hypothalamus and brainstem- function
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visceral reflex control
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Smooth muscle contraction functions
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propel contents through hollow organ or tube
maintain pressure against contents within hollow organ regulate internal flow of contents by changing tube diameter |
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Smooth muscle cell description
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spindle-shaped cells with single nucleus, usually arranged in sheets within muscle, dense bodies containing same protein found in Z-lines, single-unit/multi-unit. less developed sarcoplasmic reticulum but it is in contact with plsma membrane. caveolae-membrane lipid rafts for extracellular communication.
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Single-unit (visceral) smooth muscle
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gap junctions conduct Na+ and Ca2+. cells funcation as syncytium.
myogenic (self-excitable) fibers contract as single unit. contraction slow and energy efficient |
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Filaments in smooth muscle
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thick myosin-longer than in skeletal
thin actin- no troponin intermediate size-form part of cytoskeletal framework that supports cell shape and hold dense bodies in place. diamond shaped lattice. 15:1 ratio resting length is shorter than skeletal muscle |
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Smooth muscle innervation
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variscosities
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Multi-unit smooth muscle-description
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neurogenic (nerve-produced)
discrete units that function independently of eachother units must be separately stimulated to contract |
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Multi-unit smooth muscle- where
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walls of large blood vessels
small airways to lungs muscle of eye that adjusts lens iris base of hair follicles (goose bumps) |
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Single-unit smooth muscle- where
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GI
bladder small blood vessels uterus ureter |
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Electrophysiology of smooth muscle cells
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RMP- variable -65mV to -45mV
AP- Ca2+ dependent most multi-unit do not fire APs spontaneous depolarization of single unit: pacemaker potential, slowwave potential |
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Pacemaker potential of single-unit smooth muscle cells
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membrane potential gradually depolarizes until it reaches threshold for firing single AP
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Slow wave potential of single-unit smooth muscle cells
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membrane potential alternately depolarizes and hyperpolarizes. when threshhold is reached, cell fires a burst of APs
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Smooth muscle contraction regulation
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regulation of crossbridge cycling occurs on myosin filament.
light chain proteins attach to heads of myosin |
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Smooth muscle excitation-contraction coupling
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increase in cytosolic Ca2+
Ca2+ binds to calmodulin in cytosol Ca2+-calmodulin complex binds to and activates enzyme myosin light-chain kinase (MLCK) MLCK uses ATP to phosphorylate myosin cross bridges Phosphorylated myosin cross-bridges bind to actin Cycling produces tension and shortening Power stroke- release of ADP-Pi from myosin head cross-bridge detachment requires ATP |
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Smooth muscle contraction when P is removed when actin/myosin are bound
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myosin remains bound to actin
latch-bridge forms and detaches very slowly or not at all tonic level of tension with little ATP consumption |
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Smooth muscle contraction gradation
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increased Ca2+ causes increase in cross-bridges and therefore greater tension
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Mechanisms for increasing intracellular [Ca2+] in smooth muscle (4)
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voltage-gated Ca2+ channel (single-unit only)
ligand-gates Ca2+ channel SERCA Ip3 gated Ca2+ channel |
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Types of smooth muscle contraction (3)
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basal tone
phasic contraction tonic contraction |
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Basal tone in smooth muscle
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low level of force in absence of extrinsic factors.
intrinsic property of smooth muscle. cytosolic [Ca2+] sufficient to maintain low level of crossbridge cycling |
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Phasic smooth muscle contraction- characteristic and where
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rapid production of force and subsequent rapid relaxation as [Ca2+] returns to basal levels
*GI tract and GU organs |
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Tonic smooth muscle contraction- characteristic and where
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continuous production of force in presence of falling [Ca2+] that remain above basal levels. crossbridge cycling continues at low level.
*airways, blood vessels, GI |
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Relaxation of smooth muscle
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decrease in cytosolic [Ca2+]
MLCK returns to inactive form enzyme myosin phosphate removes phosphate from myosin cross-bridge reattachment inhibited |
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Mechanisms for decreasing intracellular [Ca2+] in smooth muscle (3)
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SR Ca2+ ATPase (SERCA)
Sarcolemmal Na+/Ca2+ exchanger Sarcolemmal Ca2+ ATPase |
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Main structural differences in cardiac muscle
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Many mitrochondria
Capillary Increased % of connective tissue Gap junctions Intercolated disk |
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Major types of cardiac cells (3)
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Contractile
Conductile Pacemaker/Nodal |
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Contractile cardiac cells
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ventricular and atrial.
contraction (pumping) fast APs |
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Conductile cardiac cells
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Purkinje.
rapid spread of electrical signal fast APs |
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Pacemaker (Nodal) cardiac cells
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SA and AV node
pacemaker activity slow APs |
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Phases of fast action potential in contractile and conductile/purkinje cells
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Phase 0: upstroke of AP, due to fast inward iNa+
Phase 1: early repolarization due to activation of some transient K+ channels (iKto) Phase 2: plateau phase due to balance between iCa2+L and iK Phase 3: repolarization due to iCa2+L turned off and increase in iK Phase 4: resting potential, due to large iK1 |
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Absolute refractory period in cardiac muscle
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Na+ channels inactivated
extends from onset of Phase 0 to half-way through Phase 3 when membrane potential has reached ~-50mV |
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Relative refractory period in cardiac muscle
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Na+ channels becoming activated again
halfway through Phase 3 to end of Phase 3 repolarization |
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Action potentials of nodal cells
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maximum diastolic potential~-65mV to -55mV
Ca2+ dependent upstroke |
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Pacemaker currents
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iF-funny current-inward mixed cation (Na+ and K+)
iCa2+T- transient inward iCa2+L- long-lasting inward iK+-delayed rectifier outward |
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Excitation-contraction coupling in cardiac cells events
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1. Excitation-AP cause depolarizaton of membrane
2. Ca2+ channels open (L-type) 3. Ca2+ enters cell 4. Ca2+induced Ca2+ release (CICR) from SR 5. cytosolic Ca2+ levels increase 6. Ca2+ binds to troponin 7. crossbridge cycling 8. contraction |
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Regulation of cardiac contraction
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alterations in fiber length
changes in contractility |
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Length-tension relationship in cardiac muscle
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stretching cardiac muscle fibers (to a point) increases strength of contraction because it is though it isn't overlap of myosin/actin but the distance between them that affects force by affecting sensitivity to Ca2+
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Ca2+ and cardiac contractility
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modulation of L-type Ca2+ channels and the SR
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