Neurophysiology Flashcards
excitable cells
- have the ability to generate electrical signals
- control transmission of information
- an effector response
examples of excitable cells
nerves, muscle cells, receptor cells, and some secretory cells
excitable membrane
- one that changes its conductance in response to a stimuli
cell functions primarily…
electrically
- signal in neuron travels electrically to target cell
synapse functions primarily…
chemically
- action potential arrives at presynaptic terminal-> releases neurotransmitter
synapse
- site of communication between neuron and target cell
(between presynaptic cell and postsynaptic cell) - site of control for transmission or information
- points where learning can occur
presynaptic terminals
where neuronal output occurs
neuron
a cell that is adapted to generate an electrical signal (usually as an action potential)
dendrites
- receptors on cell
- receptive region
- picks up electrical charge from presynaptic cell
- convey info to soma
soma
- cell body
- contains nucleus and cytoplasm
- site of information processing (integration)
axon
- specialized for conduction (when signal arrives at axon, neurotransmitter is released
- AP spread down electrically, triggers neurotransmitter to be released into synapse
- most vertebrate axons are myelinated
Nodes of Ranvier
break between Schwann cells
more elaborate dendritic fields=
more inputs
Schwann cells
type of glial cell that wraps itself around the axon (shows no excitability)
Myelin sheath
multiple wrappings of insulating glial cell membranes that increase the speed of action potential transmission
4 types of glial cells
- Schwann cells (envelop axons)
- oligodendrites (envelop axons)
- astrocytes (interact with neurons, blood vessels, and other cells)
- microglial cells
glial cells
surround neurons; important to nervous system function
why are astrocytes important at synapses
they modulate neurotransmission by taking up neurotransmitters from extracellular space and regulating extracellular ion concentrations
resting potential
- separation of positive and negative electrical charges
- potential difference between internal and external charges of cell (potential difference across the membrane)
- measured with electrodes
- takes into consideration relative permeability of each substance and concentration of each
- value of membrane potential predicted by unequal contribution of 1 or more ions
nonexcitable cell resting potential
-30 mV
excitable cell resting potential
more negative than nonexcitable cells
resting potential stems from
1) ionic concentration inside vs outside cell
2) electrical gradient (variations in concentration of ions generate this–> has no effect if membrane is impermeable)
3) Permeability of membrane to ions (varies with ions, K+ is more permeable than Na+–> neg potential inside; the ease with which ions can cross the membrane determines charge distribution)
cell membrane permeability
- cell membranes are much more permeable to K+ than to that of Na+ or Cl-
- greater flux of K+ out of cell, than Na+ or Cl in–> negative resting potential
Nernst equation
- relation between concentration difference of a permeating ion across a membrane and the membrane potential at equilibrium
- looks at potential difference generated by 1 specific ion
important factor in generating a resting potential:
you have potential difference generated by K+ ion
- more K+ goes out than Na+ goes in
what happens during the firing of a neuron?
- Action potential (only in excitable cells)
- with addition of positive charge (Na+ entry0 it reduces the potential difference–> makes membrane difference more positive
- when an action potential travels in neurons, the amplitude always stays the same
Na+/K- pump
actively transports Na+ out of cell and K+ into it (3 Na+ out and 2 K+ in)–> generates net current across membrane= generates potential
action potential
momentary reversal of membrane potential from -65 mV to +40 mV, then returning to original membrane potential
depolarization
- entry of positive charge
- membrane potential becomes less negative (inside positivity of cell membrane increases)
when is AP generated
- once cell is depolarized enough (up to threshold)
- results from intense localized increase in permeability to specific ions
during action potential
- the polarity of the cell is reversed
- inside is now positive, and outside is negative
hyperpolarization
cell membrane becomes more inside negative
graded potential
magnitude of response is dictated by size of the stimulus
3 components of action potential
rise, fall, stabilization
time of AP
1/3 time in rise; 2/3 time in fall
- total ~1 msec
threshold
smallest amount of potential current necessary to generate an AP (to depolarize a cell completely)
- if threshold is achieved AP is all or nothing
refractory periods
- during certain stages of action potential, the nerve won’t fire
- length of refractory period determines AP frequency
absolute refractory
- nerve won’t fire (action potential can’t be generated)
relative refractory
- with a lot of stimulus, the nerve might fire (harder to generate action potential)
- if so, AP is smaller and threshold is higher than normal
strength duration curve
- necessary to achieve AP
- at sufficiently low current: no AP is generated regardless of duration
- at greater strengths, there is still and initial time required
rheobase
minimum amount of current needed to get an AP
permeability of membrane to Na+ and K+
- dependent on the voltage across the membrane
conductance of Na+ and K+ throughout AP
- Na+ permeability accounts for rising phase
- K+ permeability accounts for falling phase
- K+ remains high after Na+ is back (absolute refractory)
- when K+ permeability goes back to normal, you’re at steady state
spread of excitation in non-myelinated nerves
- spread of AP is determined by the diameter
- increase velocity by increasing dimeter
- this causes limitations
spread of excitation in myelinated nerves
- faster velocity
- lower thresholds
- bigger AP
spread of excitation via cable conduction, electronic currents, local currents
all mean the same, and are the mechanisms by which AP travels in nonmyelinated and myelinated axons
local currents: electrotonic conduction
- local currents depolarize the membrane next to the spot of the original stimulus (Na+ entry depolarizes the membrane and opens additional Na+ channels)
- this can cause more local currents which spread out again
- spot of original stimulus sets up a local current; so positive charge flows to adjacent sections of axon
- won’t go backward because first AP cells are refractory
- AP generates current that produces electrotonic depolarization of membrane ahead of AP (AP propagates as a result of ionic current flowing ahead of impulse)
propagation of AP in myelinated nerves
- local currents are much bigger which run through the cell to the node and this depolarizes next
saltatory conduction
jumps from node to node
- Schwann cell provides great resistance, but at nides this insulation is less, so current jumps from node to node
- local currents are still there, the conduction velocity increases because AP jumps along nerve
- AP at one node electronically depolarize the membrane of next node
AP occurs ONLY at nodes of Ranvier
transmission occurs…
at the synapse
synapse
primarily chemical transmission of info
- electric current from one cell flows directly into next cell, changing its membrane potential
- chemical (neurotransmitter) released by the presynaptic cell
- diffuses across cleft and affects post synaptic cell-> some depolarization
- if enough neurotransmitter is released-> AP is post-synaptic cell
terminal buttons or presynaptic cell
store neurotransmitter in secretory vesicles
Ca++ needed for release of neurotransmitter
- AP impulse results in opening of Ca++ channels at the pre-synaptic terminal
- Increase Ca++ permeability causes increased influx of Ca++ at nerve terminal
- Ca++ triggers exocytosis
exocytosis
fusion of vesicle membrane to surface membrane and expulsion of the contents into cells exterior (ex: synaptic cleft)
neurotransmitters work in 2 ways
1) produce fast change in membrane potential by directly increasing permeability to ions
2) triggering a signaling cascade of second messengers in postsynaptic cell (have slow, modulatory, long-lasting effects)
Acetylcholine
- cholinergic neurons release Ach
- Found in CNS (sympathetic cholinergic), myoneural junctions, also parasympathetic neurons)
- need to be able to quickly inactivate Ach
Ach release->
binds surface receptor-> opens water channels, increases permeability to all ions-> Na+ influx
- binding to receptors may result in increase in cAMP which turns on permeability of cell (may also increase cGMP)
parasympathetic
outside spinal cord
inactivate Ach
1) primary with enzyme acetylcholinesterase (produced by post-synaptic cell, breaks down Ach via hydrolyzation)
Ach + water + cholinesterase -> acetic acid + choline (which can repenetrate presynaptic cell and resynthesize with acetyl-coenzyme A
2) diffusion into neighboring areas
3) resynthesis or back transport of Ach into membrane
- all 3 things can occur
AChE
terminates postsynaptic effects of ACh and provides choline (rate limiting substrate) for resynthesis of ACh in presynaptic terminal
nicotinic
- acetylcholine receptor
-stimulated by nicotine (blocked by curare) - neuromuscular junctions
- Autonomic ganglia (rare in CNS)
Muscarinic
- acetylcholine receptor
- stimulated by muscarine (blocked by atropine)
- parasympathetic post-ganglionic
- CNS, autonomic ganglia
butulinum toxin
prevents release of Ach by presynaptic cell
- affects myoneural junctions (synapse between motor neuron and muscles)
succinyl choline
agonist to Ach (binds to receptors and causes changes in Na+ permeability)
Curare
affects Ach at myoneural junctions
- nicotinic receptors: Ach antagonist (blocks)
- an alkaloid from plants, D-tubocurarine
- reduces amplitude of end plate potential
- blocks muscle contraction by restricting depolarization
atropine
toxin of night shade mushrooms Atrops belladorna
- Muscarinic: interferes with Ach receptors (antagonist)
- blocks muscarinic receptors (ex: at SA node)
- atropine blocks-> HR goes up
bungarotoxin
snake venom
- nicotinic
- binds irreversibly to receptors of Ach on skeletal muscles (alpha-bung)
- also inhibits neurotransmitter release from pre-synaptic cell (beta bung)
carbachol
Ach agonist (nicotinic)
eserine
prevents Ach breakdown by inactivating Ach-esterase
organophosphates
(insecticides)
- inhibits Ach-esterase; binds to its active site
epinephrine
- catecholamine
- adrenaline
- primarily chromaffin cells from adrenal medulla
norepinephrine
- catecholamine
- noradrenaline
- postganglionic sympathetic nerve cells
adrenergic neurons release…
either epi or norepi
sympathetic adrenergic neurons release
primarily norepi
synthesis pathway
phenyl alanine-> tyrosine-> Dopa-> dopamine (by enzyme DDC)-> norepi-> epinephrine
at synapse
what is released
with increase Ca++ influx (due to AP) norepi is released and diffuses to post-synaptic cell
Norepi is gotten rid of by
1) pre-synaptic cell reabsorbing it (primary route)
- COMP enzyme, catechol-o-methyltransferase breaks down norepi and is produced by post-synaptic cell
3) MAO: monoaminexoxidase: dec release of NE (produced by presynaptic cell, degrades NE in presynaptic cell)
2 types of post-synaptic cells
(or sympathetic adrenergic fibers)
- i.e. 2 types of binding sites (described by their reaction to certain drugs)
-alpha receptors and beta receptors
alpha receptros
dec cAMP, bind mostly NE, may also use PI as second messenger
beta receptors
increase cAMP, binds mostly epinephrine
norepi
- neurotransmitter which could be the cause of many mental disorders
- hallucinogenic drugs (ex: mescaline, amphetamines are all structurally similar to NE)
- act on the receptros
- they keep the neuron firing and depolarized
- are broken down as readily as NE
- changes in concentration and amount of NE release has certain effects on schizophrenia
other drugs
- can act at the synapses
1) prevent the reabsorption of NE by presynaptic cell (ex: cocaine)
2) prevent breakdown of NE
3) stimulate release of NE (ex: amphetamines stimulate secretion of NE-> hallucinations)
resepine
antihypertension drug
- interferes with NE storage: this depresses NE actively
- Affects: decrease in NE reactions by decreasing incorporation of NE into vesicles
- depression my be caused by dec NE release by presynaptic cells
dopamine
- catecholamine: mostly in brain
- effects on receptors: mostly increase cAMP
- broken down like NE
- may contribute to schizophrenia, like NW
amphetamines->
increased NE and dopamine-> psychosis, hallucinogens
serotonin
5-hydroxytryptamine (5-HT)
- in CNS, GI tract, retina
- In Pineal and retina: serotonin-> melatonin
- formed from hydroxylation and decarboxylation of trypophan
- 2nd messenger: cAMP and PI
LSD
(lysergic acid diethylamine) is structurally similar to serotonin and occupies binding sites
Glycine
- amino acid
- direct inhibition in spinal cord
- IPSPs
- Increased Cl- permeability for hyperpolarization
GABA
gamma-aminobutyric acid
- transmitter at the inhibitory neuromuscular junctions]
- also in brain and CNS
- Increased conductance Cl- -> hyperpolarize
- facilitated by drugs: benzodiazepines (valium, diazepam)
- anti-anxiety activity, muscle relaxions, sedatives
glutamic acid
- glutamate
- excitatory transmitter at the myoneural junctions in insects
Neuropeptides
- Enkephalins: pentapeptides
- Endorphins: 16AA peptides
- found in regions of pain reception and hypothalamus
- both endogenous morphine-like substances, binding receptors for opiates
- aubstance P: neurotransmitter for pain signals (inhibited by endogenous opiates)
- ADH (vasopressin)
- hypothalamic releasing hormones
- gastric hormones
opiate receptors
opium, heroin, morphine
naloxone
opiate antagonist
other neurotransmitters
- Nitrogen oxide (NO), synaptic modulation
- ATP: both fast and slow synaptic transmission
- Histamine: slow modulation
electrical synapse
- fusion of membrane of pre and post synaptic cell
- so the current (electrical) passes onto the post-synaptic cell (no chemical transmission involved in depolarizing post-synaptic cell)
- faster than chemical synapse
nervous system make up
neuron - gap - neuron - gap
- this gap (synapse) allows action potential to be stopped at certain points
- this provides 1) conduction of wanted current, 2) inhibition of unwanted current–> transmission of information which is modified at synapse
neuron-neuronal synapses
- presynaptic cell has an effect on the post synaptic cell
- 1 synapse won’t cause the post-synaptic cell to fire
post synaptic potential
transitory, graded change in resting membrane potential in postsynaptic cell
EPSP
(Excitatory Post Synaptic Potential)
- excitatory= depolarize cell membrane
- 1 synapse-> 1 EPSE
- causes slight depolarization of post-synaptic cell
- Greater # EPSPs-> AP
- change in permeability (caused by transmitter release and binding)
- inc in Na+ and K+ permeability (opens all ions to 0mv)–> flow of ions through all channels that open in response to release of neurotransmitter constitute a synaptic current that produces the depolarization that is the rising phase of an EPSP
- More Na+ goes in than K+ out-> slight depolarization, not enough to fire
- multiple EPSPs in post-synaptic cell are generated (electrotonic spread) tot eh axon hillock (AH)
- EPSPs are gathered and funnels to AH and if its enough, than an AP occurs at AH
# and size of EPSPs depend on the type and amount of neurotransmitter released from the terminal buttons
IPSIs
(Inhibitory Post-synaptic Potential)
- hyperpolarization of post synaptic cell
- increase in K+ and Cl- permeability-> mroe negative inside (hyperpolarization)
- if interior is more negative then the impact of presynaptic cell must be stronger to overcome this
graded response
- of EPSPs or IPSP
- some info is transferred (electrotonic)–> not all or none
- info is modified at synapse
pattern making of behavior
- graded response at some (ex: EPSPs)-> AP at axon (frequency controlled)-> Graded response… etc.
- Involves: AP in axon, EPSP, IPSP, EPP (neuro-muscular)
- a graded response produces a certain pattern
- pattern is very important in information processing
microcircuitry
axon branches
divergence of AP
of presynaptic cell to a # of postsynaptic cells
convergence
of presynaptic input into 1 part of post synaptic cell
feedback
+ or -
spatial summation
EPSP from 2 inputs being summed
Temporal Summation
- peripheral nerve is stimulated repeatedly and rapidly, the resultant EPSPs combine
- ex: “A” fire in rapid succession
- depends on the refractory period of pre-synaptic cell
facilitation
- multiplicative effect
- interaction of overlapping synaptic potentials from different sources (spatial) or same source (temporal) can depart from a simple sum
- ex: presynaptic cell fires once and then again in rapid succession
- 1st EPSP arrives at post synaptic cell and 2nd one is fired before 1st reaches the post synaptic cell or before the 1st EPSP has subsided-> summation of 2nd is bigger than you would expect (based on 1st one)
- increase in efficiency of the synapse as a result of a preceding activation of that synapse
- key to learning!
ionic basis for facilitation
- due to increase in Ca++ in pre synaptic cell
- 1st impulse-> increase Ca++ for neurotransmitter release
- 2nd impulse comes before 1st Ca++ is gotten rid of so more neural transmitter is released
- or maybe 2nd AP causes a greater influx of Ca++ than the 1st
post-tetanic potentiation
- long period of high frequency stimulation
- tetanizing stimulus-> # of stimuli/unit time-> enhancement
1) dec in activity of post synaptic cell (small EPSPs); amount of neural transmitter doesn’t have time to build up in presynaptic cell, its released faster than its replaced
2) after a rest, with more stimulus (not tetanic)-> inc in potential over normal - synapse has gotten better in generation of an AP in post-synaptic cell
- involves Ca++ thought to still be around from the tetanizing stimulus
- another stimulus-> more Ca++-> increased neurotransmitter released-> potential in post synaptic cell
- this lasts for quite a period of time, involved in simple learning (ie: neural muscular, since it increases neurotransmitter release and you need this for learning)
myoneural junction
neuromuscular junction
motor neuron
bifurcates (forks/branches) with non-myelinated endings
- at synapic cleft, muscle cell folds some around the motor neuron, which fits into fold
motor end plate
thickest portion of the muscle membrane
with vertebrates
- there’s only 1 pre synaptic input
- i.e. only 1 nerve fiber ends on each end plate (no convergence of multiple inputs, as with insects)
muscle cells are excitable tissues
- electrical events and ionic fluxes similar to nerves but with quantitative differences in timing and magnitude
- resting potential of muscle = -90 mV
at myoneural junctions
impulses of presynaptic (motor neuron) produces end plate potentials (EPP) in post synaptic membrane (muscle)
- if EPPs are sufficient, then an action potential is generated
- EPP depolarizes post synaptic membrane
chemical transmission acetylcholine with verts
- muscle membrane has receptors for Ach
- Increased Ca+ in motor neuron-> neurotransmitter released
- depolarizing mechanism-> open water channels by Ach, so all ions can get through
- each tries to reach its equilibrium potential
- Na+ moves 1st then K+ moves-> EPPs
summation of EPPs->
an action potential
- once generated, AP is transmitted along the muscle fiber and initiates a contractile response
**muscles have both electrical and mechanical events taking place, and you must distinguish between these
skeletal muscle
- attached to bone
- well developed cross striations (transverse bands)
- won’t contract without stimuli
- lacks connections between individual muscle fibers
- produce smooth, fluid movements that are generated by continuous and finely controlled neural input (only contract when stimulated by motor neurons)
cardiac muscle
- has cross-striations
- has involuntary inherent rhythmicity
- has connections between fibers
smooth muscle
- not organized into cross striations
- has inherent rhythmicity (irregular)
- found primarily in hollow/tubular organs (intestine, uterus, blood vessels)
muscle
tissue that consists of contractile cells
myosin
molecular motor
actin
works with myosin to generate force
striated muscle cells
have transverse bands, giving them a striped appearance
- bands show myosin/actin organization into regularly repeating units called sarcomeres
composition of skeletal muscle
- composed of long, cylindrical cells called muscle fibers
- each muscle fiber is a single cell, long and multinucleated
- each muscle fiber (myofibril) made up of filaments (actin/myosin)
- muscle fibers are surrounded by a cell membrane called the “sarcolemma”
muslce fiber
make up skeletal muscle; composed of long, cylindrical cells
myofibril
regularly repeating transverse bands
sarcotubular system
sarcolemma surrounding the muscle fibers made up of:
1) “T” system
2) Sarcoplasmic reticulum
“t” system
tubules used for rapid transmission of action potential
- formed from invaginations of plasma membrane
sarcoplasmic reticulum
- membrane system, analogous to ER
- source for Ca++ for muscle movement
sarcomere
portion of a myofibril between 2 Z disks
- functional units of striated muscle
cross striations of myofibrils, explained by arrangements of thick and thin filaments
how is striated appearance made
Z discs of adjacent myofibrils are lined up in register with each other-> pattern of alternating A and I bands is continuous for all myofibrils of a muscle fiber
thick filaments
mostly myosin, confined to A band of sarcomere
thin filament
- make up I band
- mostly actin, anchored to proteins in Z disk
- also tropomyosin and troponin proteins
contraction
involves shortening of the sarcomeres (ie: distance between “z” lines is shortened)
relaxed state
“Z” lines far apart
contracted state
-“Z” lines are pulled closer together as thick and thin filaments overlap
- there is binding between the thin and thick filaments that pull and contract the muscle
H zone
central region of A band that only has thick filaments, appears lighter than rest of A band
M line
narrow, dense region, bisects H zone
sliding-filament theory of muscle contraction
- filaments of constant length slide past each other (breaking and reforming cross bridges)
- with contraction, myosin cross bridges alternately attach to actin and detach, pulling the actin filaments toward the center of the sarcomere
- during contraction, the thick and thin filaments do not shorter, instead, slide by each other
myosin
- filament with double globular head at “C” terminal (globular heads joined to long rod/tail-> heads = cross-bridges)
- ATPase molecule is located in the heads of the myosin (this will cleave ATPP)
- in relaxed state these heads are in the “cocked” position
- tail contributes to backbone of thick filament
- during polymerization the myosin molecules orient themselves with their tails pointing toward center of thick filaments and head toward ends
actin
- small spheroid in double helix
- globular proteins joined with 2 double helix of actin
tropomyosin and troponin complex
-tropomyosin: long and thin
-troponin complex: includes the globular troponin
- regulate contraction by controlling whether or not myosin cross-bridges can interact with the thin filaments
cross-bridging
- cross-linkages form between heads of the myosin and actin molecules (ie: myosin heads extend outward and contact with actin during contraction)
- in relaxes state, the tropomyosin/troponin complex bloxks this cross-linkage
- when muscle is stimulated to contract, myosin cross-bridges interact transiently with overlapping actin thin filaments-> generates force for muscle contraction
stimulation of myoneural junction
- 1st AP in motor neuron
- Ca+ dependent release of Ach at synaptic cleft of motor end plate
- depolarization causing “End plate potentials” (EPP)
- summation of EPP-> AP which is transmitted into muscle cell via tubule system
- results in Ca++ release from the sarcoplasmic reticulum
- Ca++ is needed before cross-bridge formation can occur
Ca++ important for muscle contraction
- the terminal cisternae of the SR stored Ca++
- upon depolarization Ca++ is released
- Ca++ then binds to troponin which then undergoes a change in configuration and this results in a movement of tropomyosin/troponin complex (moves tropomyosin out of the way so actin can bind to myosin
- for contraction to occur, Ca++ must bind to troponin which triggers conformational changes that remove tropomyosin steric blocking of myosin-binding sites on actin
mechanisms of myofilament contraction
- Ca++ allows cross-bridge attachment
- power stroke: myosin head bends as it pulls the actin filament
- cross bridge detachment occurs as a new ATP attaches to the myosin head (breaking rigor)
- cocking of the myosin head occurs as ATP is split into ADP na dPi
rigor
muscles are stiff because they lack ATP
swiveling energy for muscle contraction
- ATP is not needed for crossbridge formation (Ca++ is needed to form actomyosin complex)
- also swiveling energy for contraction comes from the sequential binding on several sites on the myosin head to sites on actin filaments Differential binding sites, each with different affinity for binding and this causes the swivel)
function of ATP
1) breaking rigor after the swivel: ATP attaches to myosin head, causing release of myosin from the actin filament (relaxation with ATP binding to myosin)
2) “bound ATP” hydrolysis to ADP and Pi returns myosin head to original configuration (recocking of myosin head)–> the energy stores of bound ADP and Pi is later used at the time of the power stroke, when ADP and Pi is released from head)
3) necessary to get Ca++ back into the sarcoplasmic reticulum (active transport)-> this crossbridge is then free to repeat the cycle, a little further along the actin filament
electrical and mechanical events of a muscle twitch and contraction
- Motor neuron-> Ach-> sum EPPs-> AP-> tubule system-> Ca++ release from SR-> crossbridge formation
- latent time period between stimulus and muscle contraction is due to Ca++ release
twitch
mechanical response of muscle to a single AP
- during single twitch caused by single AP, Ca++ ions released from SR into cytoplasm then quickly pumped back into SR
- result: short burst of cross-bridge binding and unbinding
building up of tension
- with continued stimulation, there is a building up of tension in the muscle
- electrically, amplitude of depolarizations are still the same
- mechanically, greater tension occurs (greater active state, time of attachment of myosin to actin)
- 2nd impulse comes before the muscle can relax, so Ca++ is still present and this causes the development of greater tension
** during most of rise and portion of fall, the muscle is electrically refractory but not mechanically refractory–> incapable of contractions**
tetanus
summation of contraction for a muscle can lead to tetanus
- gradual increase in tension until leveling off point
- propagation of activated state by repeated APs
- results in smooth sustained muscle contractions
- Ca++ released and not taken back up since its too short of a time period
- NO RELAXATION
- when rate of stimulation is inc, twitches blur into single-fused tetanus-> Ca++ reaches steady state
- add up through summation
ATP generated by
- Glycolysis (anaerobic metbolic)
- TCA cycle
- Glycogen
- Free fatty acids
- faster way to get it is through regeneration by dephosphorylation of ADP by energy rich Phosphocreatine (verts) or Phosphoarginine (inverts)
ATP
immediate source of energy for powering muscle contraction
- muscle contains only enough ATP to sustain contraction for a few seconds–> muscle work requires production of ATP while muscle is active
NeuroControl of muscular contraction
2 processes control tension
- 2 processes control tension
1) recruitment of motor units
2) summation of contractions (by varying frequency on any one motor neuron)
motor unit
motor neuron and all muscle fibers innervated by it
- control of tension by recruitment of motor units allows for gradation of contraction (recruitment of greater number of motor units-> inc strength of contraction)
since tension is modulated by all or none effects of the motor unit, the problem of increasing overall muscle tension in a graded fashion is solved by recruitment
- control of tension involves varying # of motor units recruited and/or the frequency of contraction of any 1 motor neuron
invertebrate control of tension
- problem with recruitment is that they have smaller muscle cells, not a lot to recruit
1) arrangement of motor neuron and muscle fibers (arthropods: multi-terminal input)
2) neuronal input (arthropods: multi-neuronal input, more than 1 motor neuron inputting on any 1 muscle fiber, fast and slow excitatory neurons) - sum of IPSPs and EPSPs in muscle fibers determines amount of tension
greater depolarization=
greater Ca++ released from SR = greater tension
fast neurons
involves almost all muscle fibers
- 1 AP-> contraction
- all or none reaction above threshold
- no summation
slow neurons
- involves ~ 30% of fibers
- with 1 AP doesn’t lead to contraction
- requires temporal summation-> contraction
- summation can be graded for more control of muscle action
sensory physiology
- ability to pick up a particular type of input (ex: chemical, light, pressure)
- ie: take energy from external environment and generate an action potential
sensitivity
ability to distinguish among stimuli of different types
sensory receptor cell
cell that is specialized to transform the energy of a stimulus into an electrical signal (chemical, mechanical, electromagnetic)
sensory stimulus
form of external energy that a sensory receptor cell can respond to
mechanical receptors
respond to mechanical stimuli
- ex: hearing, sonar, lateral line, touch, pressure, equilibrium, hearing, some osmotic stimulation
- sensitive to pressure and tough
- baroreceptors
proprioceptors
monitors the status of the animal itself, located in joints
- internal mechanoreceptor associated with musculoskeletal system-> provide into to brain about muscle contraction, position, and movement of parts of the body
- provide animal with info about where the parts of its body are in space
chemical receptors
ex: taste, smell
- sensitive to a particular type of chemical
- pheromone
light receptors
vision
pain receptors
sensitive to all types of energy
receptors
receptors can also be responsive to these other inputs as well, but the threshold is much higher
(ie: one type of receptor is most sensitive to 1 particular type of sensory input
- adequate stimulus: particular form of energy to which a receptor is most sensitive
how is environmental energy converted to an action potential
- there is a change in membrane permeability as stimulus binds (or impacts) to a binding site-> depolarization
Pacinian corpuscles
- pressure receptors in fingers
- single cells
- Touch-> increase Na+ entry-> depolarization-> generating “generator potentials” (receptor potential)-> graded response-> action potential
- phasic receptor
- adapt so quickly that normally give only single AP at onset/offset of prolonged stimulus
- sensitive only to sudden indentation/vibration of skin
generator potentials
- receptors produce generator potentials (in dendrites)
- also referred to as receptor potentials (analogous to EPSPs, EPPs)
- generator potentials lead to APs
- generator potential increases with inc intensity
1) amplitude of prepotential is proportional to stimulus intensity
2) once you reach a certain depolarization-> AP - with strong stimulus-> AP with a higher frequency
- significantly large generator potentials accompanied by 1 or more AP
3) AP frequency is proportional to stimulus frequency
primary sensory system
sensory portion of cell is the ending of the afferent neuron which carries into to the brain
secondary system
sensory cell transmits into to afferent neuron which carries it to the brain
2 principles are used to ensure the animal has a wide range of perception
1) receptors cover a wide range of intensity
- intensity coded in frequency of 1 neuron or a # of neurons which fire at the same time
2) discharge frequency of receptors are classified into 2 types (tonic and phasic)
tonic receptors
- slowly adapting
- are spontaneously active at rest (have a resting frequency of APs)
- with stimulus-> change in resting frequency (+ or -)
- tonic receptors fire for length of stimulus
- receptors in beginning fire with a higher discharge rate, and then settle to a lower rate which reflects intensity of stimulus
- dec slowly in frequency and generally continue for as long as the stimulus is present
adaptation (habituation)
- arousal then settles lower to reflect intensity of stimulus (decline in frequency of AP)
- when frequency of AP in response to continuous and constant stimulation dec over time
phasic receptors
- only fires when stimulus is applied
- no AP at rest
- high discharge receptors on a change of stimulus intensity, then they stop firing
- phasic receptors initial burst reflects the intensity of stimulus (ie: its amplitude)
- shows great amount of adaptation (firing subsides after the onset of a steady stimulus)
- phasic responses generally signal changes in touch/pressure
doctrine of specific nerve energies
- each systems has specific tract it follows to certain regions of the brain
- the sensations evoked by impulses generated in a receptor depends upon the specific part of the brain they activate
- you can stimulate this system anywhere along the line and results in the brain coding it such that the stimulus is the same (conscious sensations, phantom limbs)
2 ways brain monitors intensity of stimulus
1) variation in the frequency of AP generated by the activity in a given receptor
- inc stimulus intensity-> depol (inc generator potentials)-> graded response-> AP
- # of AP depends on the strength of the stimulus
- temporal distribution of impulses
2) recruitment of sensory units
recruitment of sensory units
- single sensory axon and all its peripheral branches
- threshold levels of these receptors may be different
- weak stimuli only activate those receptors with lowest threshold
- strong stimuli activate both low and high threshold receptors
- some receptors activated are part of same sensory unit and the impulse frequency in the unit increases
efferent control adjusts receptor sensitivity
- CNS can modulate the sensory information it receives
- via excitatory efferent innervation and inhibitory efferent innervation
efferent neurons
relay control signals (instructions from CNS to target cells that are under nervous control)
lateral line of fish
- mechanical receptors
- neuromasts: basic unit of LL
- Hair cell= sensory unit
- tonic receptors
hair cell
sensory mechanoreceptor cells in vertebrate acousitco-lateralis (includes vestibular organs-> for balance/ detection of acceleration, and lateral line system in fish/amphibians-> detects water flow and other stimuli, and mammalian cochlea-> auditory organ)
- do not have axons= do not generates APs-> release neurotransmitter onto afferent neurons that conduct APs into CNS
stereocilium
microvilli that make up hair bundle
- arranged by increasing height
- actin in stereocilia make them rigid-> when pushed to side, they pivot their base-> produce shearing force between neighboring stereocilia-> transduced into a change in hair cell’s membrane potential
- displacement toward tallest= depolarization= inc neurotransmitter released-> inc AP produced
- displacement toward shorter side-> hyperpolarizes-> dec neurotransmitter released
spinal reflexes
- mediated by neural circuits of vertebrate spinal cord
- sensory input to spinal cord is provided by the axons of sensory neurons that enter spinal cord through dorsal roots
stretch reflex
oppose stretch of a muscle
- essential to maintenance of posture and coordination of movements
- involves skeletal muscle
- done by muscle spindle (proprioceptor)-> monitors length of skeletal muscle
reflex
an involuntary, graded behavioral response to a specific stimulus
