Neurophysiology exam Flashcards
what does the CNS consist of?
brainstem, spinal cord, cerebellum, subcortical nuclei, cerebral cortex
soma
cell body, contains nucleus and nucleolus, and cytoplasm around nucleus
processes on neurons
axons and dendrites
dendrite
net electrical impulse travels TO cell body
axon
net electrical impulse is AWAY from cell body. Often myelinated.
fiber
process plus sheath (axon and myelin)
synaptic terminal
where presynaptic neuron connects with postsynaptic one
what determines the postsynaptic neuron response
citation or inhibition depends on the chemical released at the synaptic terminal
what must the post synaptic cell express in order for “communication” at the synaptic terminal to be successful
receptors
What does the PNS consist of?
dendrites and cell bodies of primary sensory neurons, axons of motor neurons from spinal cord & brain stem that terminate on muscle cells, and major parts of autonomic nervous system
autonomic nervous system
part of CNS and PNS, responsible for unconscious regulation of body functions, divided into sympathetic and parasympathetic
what do the sympathetic and parasympathetic nervous systems have in common?
both have a 2-neuron connection (pre-ganglionic and post-ganglionic neurons) from the CNS to the target tissue
where do most organs and glands receive fibers from?
both the sympathetic and parasympathetic nervous system (except adrenal medulla, some sweat glands, and arrector pili muscles)
does the ANS receive sensory input?
yes, influenced by higher brain centers- hypothalamus
Can CNS neurons regenerate?
NO in mammals
- no mitotic organelles
Can PNS neurons regenerate?
YES
under certain circumstances
1st layer of protection for brain and spinal cord
skull and vertebrae
3 layers that cover the CNS
known collectively as meninges
1. dura mater - external most & toughest
2. arachnoid membrane - more delicate
3. pia mater - more delicate
glial cells
supporting cells within nervous system
four classes of glia in the CNS
microglia, ependymal cells, astrocytes, oligodendrocytes
glial cells in PNS
satellite cells and neurolemmocytes (Schwann cells)
Schwann cells
IN PNS, wrap nerve processes with myelin
oligodendrocytes
IN CNS, produces myelin for several nerve processes. also surround neurons in CNS
astrocytes
in CNS, cover surface of CNS capillaries to form blood-brain barrier
also protect connections zone between neurons referred to as synapses
in the PNS, what is analogous to astrocytes?
satellite cells, they surround cell bodies of sensory neurons
microglia
macrophages of CNS
ependymal cells
line CSF filled passageways and form barrier between CSF and ventricles and the neuronal/glial layers of CNS
what “environment” do neurons operate in?
an aqueous medium that is part of extracellular space within the brain, spinal cord, and PNS
- “salt-water bath”
filled with + charged ions Na, K and CA & negatively charged ions Cl
what influences charged particles like ions
concentration gradients and electrical gradients
these two things generate an electrochemical homeostasis
ion channels
complexes of proteins that have 2+ structurally similar subunits that form a channel by lining
- can be opened of closed, controlling the flow of specific ions in/out of cell along their concentration gradient
- also act as receptors for various ligands such as NT’s
ion channel features
can be selective or non-selective as determined by the molecular structure of the channel
- pore size
- ion filters (highly selective for binding of distinct ions)
- channel gates: gated channels require opening of a gate for ions to go through while closed gates prevents ion passage
(non-gated channels are generally open whereby diffusion of ions though the channels is mostly determined by concentration gradient (& pore size))
What are the characteristics of gated channels that allow changes between open and closed states?
- kinetics of voltage-dependent (voltage gated) channels is determined by how fast or how slow the gate portion of the channel opens and closes
- concentration gradient for an ion
- current running through a channel can dictate how rapidly ions move through (current is influenced by membrane voltage)
- concentration of a ligand for a gated channel can influence how rapidly the channel is activated or inactivated/ how long it remains open or closed
How are gated ion channels activated?
- changes in membrane potential
- chemical, extracellular, and intracellular ligand
- mechanical deformation of their structure (mechanoreceptors)
resting membrane potential
-70 mV
electrical potential at which activity within a neuron is at equilibrium
- concentration of ions inside/outside of cell are key determinants
what is open/closed at resting membrane potential
K and Cl are OPEN
Na and Ca are CLOSED
what equation allows for calculation of the charge differences established between inside and outside of neurons across membrane
nernst equation
- * the larger the gradient = the larger the equilibrium potential
what is the problem with membranes during RMP?
To keep equilibrium at RMP, channels must be closed to Na, BUT membranes are leaky to Na. As Na slowly leaks in, it changes electrical potential for K and K is pushed out. So therefore slightly less negative RMP than K+ potential (-70 vs -96)
Due to leakiness & buildup Na IN and K OUT what happens?
must be balanced out, Na/K pump maintains Na and K gradients for RMP by actively pumping 3 Na OUT and 2 K IN
- constantly active
- is an ATPase- hydrolyzes ATP to ADP for energy
depolarization
membrane potential becomes more positive (relative to -70 mV)
hyperpolarization
membrane potential moves from -70 to more negative (closer to K @ 96)
repolarization
movement of membrane potential from either depolarized or hyperpolarized back to RMP
what defines a graded potential
when the membrane is depolarized up to -40, or more negative than -70
(if depolarized more + than -40 = AP)
small potentials and subthreshold
what are the characteristics of graded potentials
- generated by sub-threshold stimuli and small potentials that result in depolarization of the membrane up to -40 mv (hyper-polarizing currents)
- can be caused by a small local change in membrane permeability to ions
- either depolarizing or hyper polarizing depending on charge of the ions being moved in and out of the affected neuron
How would the following affect a graded potential:
opening of Na channels
results in movement of Na into cell and down its concentration gradient and electrical gradient resulting in DEPOLARIZING graded potential
How would the following affect a graded potential:
opening of K channels
results in movement of K OUT of cell and down its concentration gradient (towards equilibrium) resulting in HYPERPOLARIZING graded potential
An important characteristics of graded potentials are ability to be added together, what are these 2 types?
temporally = 2 + of the same stimuli at slightly different times
spatially = 2 + of different stimuli at different location but applied at same times
both instances result in a larger potential
- receive signal from pre-synaptic neuron, summate, AP if great enough
what does decremental mean in terms of graded potentials?
graded potentials decrease in size a short distance from the site of the stimulus
therefore graded potentials are generally used for local signaling within small regions of a neurons membrane
how does a graded potential propagate down a membrane?
so any change in membrane permeability will result in ion flow in/out of cell, which will cause a change in membrane potential. the potential difference causes local current flow (direction of movement of positive charges). the influx of positive charge (Na= depolarizing potential), repels positive charges and attracts negative charges. this causes positive charged to move in both directions away from the point of ion entry
graded potentials
- local currents
- die out quickly
- within short distance from point of stimulus
- ions diffuse passively and re-equibrilate across membrane
what type of receptor neurons can only produce graded potentials
rods and cones in retina
T/F: most neurons use graded potentials for generating action potentials
true
ligand gated channels
channel where activation is mediated through binding of chemical, extracellular, and intracellular ligands
- cation permeable Ach receptor
how are graded potentials generated?
By means of ion channels opening and closing
are propagated by means of ion channels opening and closing due to changes in electrical potential in adjacent areas of the membrane
how can a graded potential lead to action potentials
summation of subthreshhold graded potentials (largely due to Na) leads to the all or none activation of an AP
what are some key characteristics of action potentials?
AP don’t diminish
rapid/shortlived - msecs
all or none
magnitude always the same
cannot be summated
frequency can be increased or decreased to reflect magnitude of signal
what determines where in neuron and how AP are generated?
differential sub cellular concentration and distribution of voltage-gated Na channels
where are the most voltage gated Na channels in a neuron
axon hillocks
result in area being very sensitive to summated graded potentials and the generation of action potentials
where in the neuron does summation occur
dendrite
sub threshold graded potentials
stimuli underlying an action potential
usually due to opening of ligand-gates or non-gated Na channels
what does summation on graded potentials in the dendrite lead to
all or none activation of AP at axon hillock via activation of Na channels
at what mV does the neuronal membrane reach for an action potential to be generated
-40 mV
what determine/ influence the threshold for an action potential
- increase N and outward K currents before reaching threshold, results in increase in membrane potential away from rest. Na conductance is unstable when nearing AP threshold and so a minor increase in Na ions causes AN EXPLOSION of inward Na current which causes an AP (evolution)
- changes in RMP can increase or decrease the threshold, hyper polarization will require more Na ions to reach threshold. depolarization will require less Na ions
- Ca++ outside cell can influence because of its effects on charged particles on cell surface . Can also BLOCK Na and K channels thereby making changes in membrane potential more difficult. Increase extracellular Ca++ will increase threshold and decreases in Ca++ extracellularly will decrease threshold
what is responsible for the RISING PHASE of the action potential
Na channels are activated rapidly and the sudden flow of Na inward
- open Na channels
- increased permeability of Na
- increased Na flow
- depolarization
falling phase of action potential
relative slow responsiveness of K channels to impulses is the underlying mechanism for the outward flow of + charge and the depolarization of the membrane
action potential sequence of events
- summated graded potentials move the membrane potential towards -40 mV
- large number of voltage gated Na channels are active rapidly and sudden inward flow of Na is responsible for rising phase (AP)
- at peak (+59) voltage gated K are activated very slowly and flow of Na slows down and the outward efflux of K results in outward flow of + charge and repolarization of membrane potential
- special gating by Na channels inhibits consecutive initiation of AP, this secondary-gating blocks Na influx by keeping Na channels in an inactive state for a latent period. this is basis of refractory period and uni-directional propagation of AP
Na equilibrium potential
+59
what is the basis of unidirectional propagation of AP
special gating by Na channel inhibits consecutive initiation of AP. keeps Na channels in an inactive state for a latent period
myelin
80% lipid and 20% protein substance that insulated axons
- in CNS oligodendrocytes myelinate axons
- in PNS Schwann cells myelinate axons; also more elegant and allows for rapid propagation
lipid component of myelin
mostly a glycolipid called galactocerbroside
protein component of myelin
myelin basic protein (MBP)
myelin oligodendrocyte glycoprotein (MOG)
proteolipid protein (PLP)
how does conduction velocity relate to diameter of axonal fiber
conduction velocity increases with increasing diameter of axonal fiber
- fastest = larger diameter & myelinated
- slowest = smallest diameter & unmyelinated
how does an action potential work in unmyelinated nerves?
AP at site of stimulus sets up local current flow to adjacent parts of the cell membrane, this causes depolarization of the adjacent membrane to threshold, giving rise to AP at adjacent site. inward Na and outward K keeps occurring at adjacent parts of membrane and thus AP propagates through ionic conductance
even if local current flow is in reverse direction, AP cannot be conducted in reverse direction because the membrane is in refractory period
all or none
microscopic unmyelinated regions between successive myelin wrappings of the axon
interfiber nodes
“nodes of ranvier”
What is the function of myelin
forms an insulating layer around the axon which prevents leakage or diffusion at all points.
why do action potentials travel much faster in myelinated neurons vs unmyelinated neurons
within interferer nodes (where no myelin), there is a high concentration of Na channels which allow for generation of AP’s. Charge rapidly distributes to next interferer node and so AP travel down myelinated axon very rapidly (in comparison to unmyelinated of same diameter and length)
when does myelination occur?
perinatal period
axon diameter and myelin sheaths grow during first 2 years of life
may not even be fully mature before adolescence
How does diet relate to the myelination process?
Myelination is a metabolically demanding process and therefore young animals need high fat diets
What can disruption of myelin lead to>
disorders regarding motor control, hyper excitability, uncontrolled shivering
Multiple sclerosis
autoimmune disorder resulting in degeneration of myelin on nerve fibers
results in progressive nerve paralysis
canine shaking pups disease
genetic myeline disease
results in decreased weight and size during first 10 days of life, most pups overcome
visna & k9 distemper
inflammatory diseases in dogs that affect myelination and nerve conductance
viral infection affects myelin indirectly
ataxia, hyperesthesia (+ sensitive), myoclonus (twitching), paresis (weak), depression
What type of drugs are Na channel blockers?
- local anesthetics
- proCAINE, tetraCAINE, lidoCAINE, cocAINE
act on unmyelinated pain fibers
blocks AP of free nerve endings so pain is not communicated to CNS - Tetrodotoxin- from puffer fish and some bacteria, block Na too (block multiple NA channels, result in paralysis)
- Saxitoxin- in butter clam, produced by cyanobacteria (block multiple NA channels, result in paralysis)
how can calcium levels cause seizures?
Ca is a stabilizer of membranes, keeps Na channels closed, so when Ca levels are too low, membrane have a high permeability to Na and nerves can become spontaneously excitable, can leads to muscle spasms and rigidity
synapse
specialized junction between 2 neurons by which electrical activity in one neuron influences the other through the secretion of NT at presynaptic axonal terminals and activation of of NT receptors at postsynaptic neurons
electrical signal in presynaptic neuron is converted into a chemical message
what are the most common type of synapses?
chemical
also rare examples of electrical synapses for extremely fast communication - cardiac muscle
How do chemical signals translate to electrical signals, and vice versa?
E signal @ Pre-syn neuron is converted into chemical message
chemical message affects postsynaptic membrane receptors
chemical message is converted to E signal in post synaptic neuron
what dictates if the outcome of a neurotransmission is excitatory or inhibitory?
depends on on NT and type of receptor activated
what does it mean for inputs to converge?
at the cellular level, synaptic inputs from multiple axons may converge on one dendrite
neuron may receive info from up to thousands of other neurons
what does it mean for synaptic input to diverge?
input can diverge from one neuron via branching of its axons and formation of synapses on multiple dendrites of many recipient neurons
synaptic cleft
small space that separates the pre-synaptic axon terminal from the membrane of the post-synaptic neurons (dendrites or cell body)
what does the entire process of neurotransmission depend on?
the specialized vesicles that are packaged with, carry, and secrete NT from presynaptic neuron at synaptic cleft
where are NT synthesized?
depending on the size, either the soma (LARGE) or within the axonal terminals (SMALL)
example of large NT
protein/ peptide NT
example of small NT
glutamate, GABA, Ach, norepi
enzymes responsible for production are in nerve terminal
vesicular life cycle
- NT synthesis & packaging
- Vesicular transport to packaging sites
- Packaging of NT vesicles - “maturation of vesicle”
- Formation of reserve pool of vesicles
- Ca++ entry in response to AP
- Vesicular mobilization to active site on terminal
- Docking on membrane, fusion, exocytosis of NT into synaptic cleft
- Endocytosis of vesicles and their recycling
how is ATP involved in mobilization of vesicles
ATP is required for enzymatic activity of protein kinase Ca/calmodulin kinase II (CaMKII) & the myosin light chain kinase (MLCK). these 2 kinases will phophorylate the proteins that function as substrates for mobilization of synapses I and myosin II which prime the vesicle for correct transport in the active zone of the terminal membrane
proteins required for fusion and exocytosis of vesicles at the synaptic terminal
SNARE proteins
- vesicles and membrane associated protein required for fusion of vesicles to the active zone of the terminal membrane
Ca++ dependent process!!!!
Snare protein
vesicles and membrane associated protein required for fusion of vesicles to the active zone of the terminal membrane
synaptic delay
time between the pre-synaptic release of NT and postsynaptic response
includes time taken for NT discharge from vesicles, NT diffusion across synaptic cleft, binding of NT to receptor, and rate of ion diffusion in response to nT
Botulism toxin
cleaves SNARE proteins
therefore unable to fuse and secrete NT
neuromuscular junction
specialized synaptic junction between a nerve and a muscle fiber
where the nerve axon terminal (non-myelinated) fits into a groove in the membrane of the muscle fiber forming MOTOR END PLATES, which is invaginated into the synaptic cleft
motor neurons
large, myelinated neurons, with their cell bodies located in the spinal cord
motor end plate
where the nerve axon terminal fits into groove in membrane of the muscle fiber, which is invaginated in the synaptic cleft
what is the Nt always at the NMJ
acetylcholine (Ach)
Describe an AP at the NMJ
- AP arrives at axon terminal causes voltage sensitive Ca channels to open and Ca enters axon terminal
- Ca causes Ach release from vesicles into synaptic cleft
- Ach binds to receptors on muscle and causes Ach gated Na/K channels to open
- Na causes depolarization & generation of end-plate potential (graded)
- local current flow generates AP in both directions along muscle membrane
- Ach diffuses into cleft and it metabolized by Acetylcholinesterase (AchE) (limits action of Ach in NMJ)
Every action potential in a motor neuron will result in what?
An AP in a muscle cell
What type of input is to the NMJ?
all excitatory
curare
- Ach Antagonist
- poison on arrow tips by S. Americans
- binds strongly to receptors and does not allow ion channels to open thereby preventing Ach from binding
- not metabolized by AchE
- leads to muscle paralysis, and death by asphyxiation
muscle relaxant at low doses
snake venom
from plants
organophosphates- pesticides
AchE inhibitors
- excessive Ach therefore HYPER stimulates its receptors due to inability to breakdown Ach
- results in spasms and can result in laryngeal spasms and therefore suffocation
botulism
prevents docking and secretion of Ach from nerve terminals at NMJ, can cause death by paralysis of breathing muscles
targets snare
0.0001 mg can kill a pig
myasthenia gravis
muscle weakness, caused by decreased numbers of Ach receptors at NMJ, so therefore Ach is released but is ineffective b/c not binding. causes muscle paralysis
TX= blockers of acetylcholinesterase to provide relief of symptoms
milk fever
low blood calcium after onset of lactation
muscle weakness is caused by failure to transmit nerve signals across NMJ
skeletal muscle features
long & cylindrical
multinucleated
striated
voluntary
cardiac muscle features
short & branched
uninucleate
striated
involuntary
intercalated disks
smooth muscle features
spindle shaped
uninucleated
non-striated
involuntary
What doe all skeletal movements rely on?
tension generated by muscle cells which ATP is required for (from aerobic and anaerobic metabolism)
Major function of skeletal muscle
contraction and relaxation controls the movement of joints
major function of smooth muscles
contraction and relaxation controls the constriction and dilation of numerous tubular organ systems
major function of cardiac muscle
contraction and relaxation controls the rhythmic beating of the heart and consequently blood flow in the CV system
what is skeletal muscle innervated by?
the somatic nervous system
voluntary & contractible
high force
easily fatigued
Describe the structure of a skeletal muscle from largest to smallest
whole muscle
muscle facile
myofibrils in sarcoplasm (cytoplasm of a muscle cell)
myofilaments
sarcomere
structures between 2 Z discs
H zone in between
sarcoplasmic reticulum
surrounds myofibrils
tubules
longitudinal to myofibrils
terminal cisternae
transverse muscle fibers, STORE CA
what are the characteristics of white muscles
little myoglobin
mostly ANAEROBIC glycolysis
fast & forceful contraction
rapidly tiring
what are the characteristic of red muscle
lots of myoglobin
AEROBIC glycolysis
slow, less forceful shortening of the muscle
high endurance
white and red skeletal muscle cells can be further classified base don what?
their functional characteristics
S fibers
SLOW
(group I, similar to red)
FR fibers
FAST, FATIGUE-RESISTANT
group IIA, between red and white (medium exertion, aerobic & anaerobic)
FF fibers
FAST, easily FATIGUABLE
IIB, like white
Type I fibers
slow twitch
known as red or also slow
Type II fibers
fast
IIA= red, fast oxidative, medium resistance to fatigue
IIB= white, fast glycolytic, least resistance to fatigue
what controls smooth muscles
autonomic
involuntary contractile control
BP, GI contraction,
Desnse bodies of smooth muscle
equivalent to Z plate of skeletal muscle
contain the actin filaments connected to the sarcolemma
intermediate filaments
transfer force from myosin filaments to sarcolemma
endoplasmic reticulum
Ca++ store in skeletal muscles and smooth muscles
Ca binding protein = troponin/tropomyosin in skeletal
Ca binding protein= calmodulin in smooth
intercalated discs
cardiac muscle feature
stair-step fashion to connect muscle cells to each other
gpa junctions in cardiac muscle
where transmission of cardiac muscle stimuli occur
what is mechanical stability facilitated by in cardiac muscle?
maculae adherent and fasciae adherens
striated muscle contraction at NMJ
ACh binds postsynaptic N2 receptors (Na/K channels), depolarization of muscle cell membrane is conducted inward via T tubules and initiates Ca++ release from sarcoplasmic reticulum
what is the initial signal to the target muscle for contraction?
transmission of an AP from the CNS via motor neurons to the motor endplate
once ACh is released by motor or autonomic neurons, what happens?
binds to nicotinic ACh recpeptors on postsynaptic muscle fibers
result sin NA influx via depolarization of sarcolemma = ENDPLATE POTENTIAL
what happens after endplate potential triggers AP
diffusion to the entire sarcolemma as well as transverse tubules
Voltage gated and tension sensitive Ca channels activated
increase in release of Ca ions, and increase in Ca concentration around myofibrils
contraction trigger
where does a VOLUNTARY triggered contraction stem from
cerebral motor cortex whose long axon transmits the electrical impulse to motor neurons in anterior horn of spinal cord
Common neuromuscular blocking drugs
Atacurium and vecuronium
used to paralyze patients during surgery via blocking nicotinic ACh receptor
drug used to TX myasthenia gravis
Pyridostigmine
cholinerase inhibitor so increased ACh in NMJ
sarcoplasmic reticulum
specialized smooth ER
encircles myofibirls
always in pairs
T tubules
invaginations of sarcolemma into cell interior
between paired terminal cisternae to from a triad
lumen is continuous with extracellular space within myofibrils , conduct AP into every sarcomere
ensures each sarcomere contracts simultaneously in response to depolarization of sarcolemma
what happens when impulses are conducted via T tubules?
signal the opening of voltage gated Ca channels in membranes of terminal cisternae and Ca is released from adjacent paired terminal cisternae to the adjacent sarcomere
T/F: sarcoplasmic reticulum regulated the intracellular sarcoplasmic Ca++ concentration, which rises and falls during contraction and relaxation of myofibrils
true
motor unit
structure containing muscle fibers of a common branch, which are innervated by a single alpha-motor neuron (from anterior horn of spinal cord). the AP of a single alpha-motor neuron is responsible for simultaneous contraction of all muscle cells of a motor unit
electrochemical coupling
the process of transforming an electrical impulse into a muscle contraction
Z disc of sarcomere
proteins perpendicular to axis of myofibril, the lateral bounds of a sarcomere
thin filaments of actin are anchored to the z bands
actin filaments extend inwards from each z disc to the middle of the sarcomere
actin filaments partially overlap the thick myosin filaments
I band of sarcomere
thin actin filaments ONLY, encompass Z disc
A band of sarcomere
overlapping thin actin and myosin heads and thick filaments
encompass the H zone and the M line
H zone of sarcomere
thick MYSOSIN HEADS ONLY
M line of sarcomere
thick filaments linked to myosin which hold the myosin in place
sliding filament theory
describes the interaction of the actin filaments with the myosin filaments, leading to muscle contraction
no change in length of myofilaments during a contraction but rather only shortening of the sarcomere through the sliding of the myofilaments
how is the myosin head activated?
It has ATPase activity and can split TAP and store the energy
cross-bridge
short-term chemical bond between actin and myosin molecules occurs when troponin/tropomyosin complex binds CA ions released by the intracellular stores
how does the sarcomere shorten
myosin head tilts 45 degrees which pulls the bound actin filament to the middle of the sarcomere
what happens to allows the myosin head to disconnect from the actin filaments
a new ATP can be bound following the positional change of the myosin head, a new cross bridge cycle can begin
how does a muscle contraction end
by lowering the intracellular Ca++ level in response to cessation of AP in motor unit
where is energy derived from during short, intensive efforts, like sprinting?
ATP synthesis from existing creatinine phosphate and anaerobic glycolysis of glucose from muscle glycogen with lactate release
where is energy derived from during long, lasting efforts?
glucose breakdown from muscle glycogen through aerobic glycolysis and ATP recovery through oxidative phosphorylation
where is energy derived from during bodily exertion for hours?
glucose breakdown from muscle and liver glycogen and triaglycerol
isotonic contraction
tension overcomes load
all jumping and throwing activities involved both type of isotonic
help stabilize joints and maintain posture while other joints move
muscle shortens, and tension remains constant
TWO TYPES
1. concentric
2. eccentric
concentric contraction (isotonic)
tension develops as there muscle shortens
eccentric contraction (isotonic)
tension develops while the muscle lengthens
(quads stretch and develop tension eccentrically to counteract gravity and control descent)
isometric contraction
load exceeds muscle peak tension developing capability
muscle develops maximum tension and does nit shorten
is work performed during an isometric contraction?
no
work is computed by considering product of muscle shortening and load
invested energy for isometric is transformed into heat
how do red muscle fibers increase muscle performance
increase myoglobin content, number of mitochondria. and capillary formation
how do white muscle fibers increase muscle performance
increase number of myofibrils and glycogen storage to increase muscle diameter — muscle hypertrophy
length tension curve
the longer a muscle is in a state of strain the more force has to be exerted
clinically: in cases of excessive strain. muscle fibers are damaged, known as a muscle tear
what determines the classification of smooth muscles
different contraction behaviors
single unit smooth muscles
coupled by gap junctions therefore work as one coherent functional unit - muscles contract together
found predominantly along organ walls and blood vessels
multi unit smooth muscles
capable of contracting independently of one another due to the predominantly autonomic innervation
few gap junctions
electric coupling occurs via basal-membrane like layer
NT are distributed by varicosities
in iris and in the arrector pili muscles
special features of smooth muscle contraction
spontaneous autonomous contraction
affected by NT: ACh AND norepinephrine (on adrenergic receptors)
predominant share of Ca is from extracellular space
SR much less developed
no T tubules
no troponin site for Ca
MLCK activates myosin ATPase
cross bridging occurs very easily since myosin binding sites are always exposed
smooth muscle contraction steps:
- Ca binds to calmodulin
- MLCK activate through CA- calmodulin complex
- phosphorylation of the light chain of the myosin head through MLCK, using TAO
- contraction via cross-bridge formation
- separation of remaining phosphate from the light chain of the myosin head through myosin light chain phosphatase (MLCP) causes dissolution of the actin myosin bond
How can selective control of smooth muscle contraction be obtained?
the use of adrenergic drugs
albuterol is a brochodilater
acts on beta-2 adrenergic receptors to relax the bronchial smooth muscles and dilate them
how are electrical impulses transmitted through the heart
transmitted via gap junctions to the cardiac muscle and later to the working myocardium
divisions of specialized cardiac muscle cells
electrical impulse formation and conduction systems
features of the systems of specialized cardiac muscle cells (electrical impulse formation and conduction system)
- SA and AV nodes
- Bundles of His
- Bundle branches
- purkinje fibers
- working myocardium, (ventricular and atria cardiac muscles)= cells connected by gap junctions to from a syncytium- where conduction of impulses can occur rapidly
what isolated syncytia
through annulus fibrous (valve connective tissue)
what is responsible for mechanical work in the heart
working myocardium
How does stimulation cause cardiac contraction
stimulation transmitted from SA node (impulse formation system) to syncytium to AV node
to bundle of HIs
to branches of Purkinje fibers (rapidly spread impulse to apex of heart and papillary muscles of heart valves)
reflex arc
populations of ins neurons that respond to specific chemical or physical stimuli via the sensory components of the somatic and visceral sensory fibers that enter the CNS. sensory info is integrated in CNS where appropriate actions are recruited to address a homeostatic issue. Action is relayed via somatic and/or visceral motor fibers out of CNS, to target muscle and organ systems altering the physiology to resolve the homeostatic issue
Is the following a feature of the parasympathetic or sympathetic nervous system?
preganglionic neuronal cell bodies are in cranial nuclei of brain stem and motor fibers exist at the level of the brainstem or sacral spinal cord
parasympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
preganglionic neuronal cell bodies are in the thoracolumbar spinal cord
sympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
peripheral ganglia are near to target organ
parasympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
peripheral ganglia are distant to target organ, in chain ganglia outside spinal cord
sympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
small ratio of postganglionic to preganglionic neurons
parasympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
large ratio of postganglionic to preganglionic neurons
sympathetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
the preganglionic NT = ACh
the postganglionic NT= ACh
parasympthetic
Is the following a feature of the parasympathetic or sympathetic nervous system?
the preganglionic NT = ACh
the postganglionic NT= NE
sympathetic
How does a somatic reflex arc difference from autonomic reflex arcs?
all of the generic components of somatic are also in autonomic
but somatic efferents are myelinated motor axons that synapse on skeletal muscle- conduct AP directly and rapidly to their target skeletal muscle
whereas
autonomic motor fibers (efferent) always consist of at least 2 neurons separated by peripheral ganglion
peripheral ganglion contents
axon terminals of preganglionic neurons that synapse onto dendrites of postganglionic neurons in the autonomic motor pathway
where are the cell bodies of preganglionic neurons
CNS within various nuclei or the brainstem and lateral horns or the T, L, and, S spinal cord segments
where are the cell bodies of postganglionic neurons
in the autonomic ganglia and their axons will innervate the target organs
where do parasympathetic branches come from
from the brainstem and caudal aspects of the spinal cord (lower lumbar and sacral levels)
where do sympathetic branches come form
exit the spinal cord at the thoracic an lumbar levels
cholinergic neurons
ACh producing
PARASYMPATHETIC
noradrenergic neurons
NOR–EPI producing
SYMPATHETIC
what features can distinguish the parasympathetic from the sympathetic nervous system
location of cell bodies of preganglionic neurons
distance between ganglion and effector organ
ratio of post ganglionic neurons to preganglionic neurons in the efferent pathway
how does the relationship of having a SMALL number of POSTganglionic neurons for each preganglionic neurons effect the response?
parasympathetic
discrete control
not highly distributed responses
how does the relationship of having a LARGE number of POSTganglionic neurons for each preganglionic neurons effect the response?
sympathetic
widely distributed responses
parasympathetic
rest and digest
conservation of metabolic energy
sympathetic system
during exercise or physical or emotional stress
flight or flight
energy consuming
ANS innervation
synaptic vesicles containing NT are contained in numerous varicosities along terminal portion of the nerve fiber
so occurs throughout muscle vs at distinct location
somatic innervation
precise innervation of individual striated muscles by individual motor axons
baroreceptor reflex
baroreceptors in carotid sinus and aortic arch are stretch by high B, so sensory neurons in these regions are activated resulting in a signal that is transducer to the brainstem
brainstem cardiac centers are recruited, leads to reduction of sympathetic feedback and lowering HR aswell as dilation of blood vessels- which will decrease BP
catecholamines
epinephrine and norepinephrine
directly releases as hormones into blood stream for broad physiologic effects
secreted by mature adrenal medullary cells
what initiates the release of adrenal medullary hormones
cholinergic neurotransmission
what are the type of receptors for ACh
cholinergic
what are the type of receptors for NE and epi
adrenergic
what type of receptors are cholinergic neurotransmission in all autonomic ganglia and at the adrenal medulla through?
nicotinic (N) cholinergic receptors
what type of receptors are the cholinergic receptors at all parasympathetic final effector sites
muscarinic
divisions of adrenergic receptors present in cell membranes of tissues innervated by postganglionic sympathetic neurons
alpha and beta
further subdivided into a1, a2, b1, b2, b3
alpha adrenergic receptors
a1 and a2
g-protein coupled receptors
muscarininc in autonomic
effector target stimulated by postganglionicn neuron in sympathetic division
a1= smooth muscle contraction
a2= inhibition of transmitter release
beta adrenergic receptors
effector targets are stimulated bay postganglionic neuron in sympathetic division
B1 and B2
coupled receptor
B1= heart muscle contraction
B2= smooth muscle relaxation
muscarinic receptors
M1
M2
M3
M4
M5
