Midterm Flashcards
animal physiology
study of how animal function at all levels of organization to accomplish something by considering physiology, biochemistry, morphology, and biomechanics
comparative animal physiology
in light of evolution, compare species, and bodily systems to understand the diversity of physiological systems
August Krogh Principle
there are optimally-suited animals study study most biological problems, which provide insight into principles that are highly applicable because traits are often conserved
2 types of physiological regulation
conformers and regulators
conformers
internal fluctuation matches external fluctuation as in a line of conformity
regulators
internal fluctuation is minimal with respect to external fluctuation within the zone of stability, internal fluctuation is greater with respect to external fluctuation outside the zone of stability
zone of stability
indicates physiological conditions that an animal’s physiological systems are best adapted to and work best under
homeostasis
the tendency to maintained relative internal stability in the face of external fluctuations, maintained by regulatory systems
homeostasis nor regulatory systems equate to
constancy
parameter specific regulation
whether an animal uses conformity or regulation is parameter specific – lizard conforms to external temperature but regulate water chloride concentrations
negative feedback
control system regulates a variable by opposing it deviation from a set point therefore keeping the variable within its homeostatic range
positive feedback
control system regulates a variable by rapidly deviating from a set point therefore promoting a unidirectional response that is a non-homeostatic change
acclimation
process of change in response to an isolated environmental variable in the lab, within an organism’s lifespan, largely reversible
acclimatization
process of change in response to a natural environmental variation including multiple variables, within an organism’s lifespan, largely reversible
adaptation
process of change through natural selection leading to an organism whose physiology, anatomy, and behaviour are suited to the demands of its environment by changes to the DNA, over multiple generations, largely irreversible
lipid bilayers separate
the intracellular fluid from the extracellular fluid
lipid bilayers composition
peripheral membrane proteins, integral membrane proteins, and phospholipid molecules
fluid mosaic
the lipid bilayer composition is constantly changing and is composed of multiple subunits
permeability of epithelial cells
high permeability, thin epithelium and high SA, passive diffusion of O2 and CO2 down the concentration gradient
permeability of integument cells
low permeability, thick epithelium impenetrable to water to regulate internal environment
integument low permeability depends on 3 possible substances
keratins, lipids, waxes
2 paths materials follow across an epithelium
transcellular path and paracellular path
transcellular path
larger and/or charged molecules require 2 sets of membrane transporters to cross the (1) apical and (2) basolateral membranes
paracellular path
small and/or polar molecules must be able to move the the band of tight junctions
heterogenous composition of lipid membranes
inner and outer membrane layers are distinct, lipid rafts are regions that accumulate cholesterol and glycolipids
lipid rafts
regions that accumulate cholesterol and glycolipids, they are more rigid, highly mobile, and recruit specific proteins involved in signalling pathways
membrane fluidity alters between 2 states
liquid crystalline (oil) and gel (butter)
general changes that allow membranes to retain their fluidity
homeostatic changes, changes in phospholipid composition
membrane fluidity state at the norm
liquid crystalline, allows for functional proteins
4 changes that can occur to alter membrane fluidity for acclimation or acclimatization
fatty acid chain length
saturation
polar head groups
cholesterol
fatty acid chain length and membrane fluidity
inversely related to membrane fluidity
saturation and membrane fluidity
inversely related to membrane fluidity
polar head groups and membrane fluidity
phosphatidylcholine (PC) cylinder like so more compact, phosphatidylethanolamine (PE) cone like so less compact
cholesterol and membrane fluidity
directly related to membrane fluidity
cholesterol has complex membrane properties for 2 reasons
(1) cholesterol disrupts interaction between fatty acid tails, increasing membrane fluidity and (2) cholesterol fills gaps between polar heads, decreasing membrane fluidity to small molecules
homeoviscous adaptation
under physiological conditions, animals have similar membrane fluidity, maintained by changes in phospholipid composition
it is of physiological important that concentrations of inorganic solutes are regulated between
intracellular and extracellular compartments
muscle cell interior of [Na+], [K+], [Ca2+], [Cl-], [A-]
[Na+] 10 mM [K+] 140 mM [Ca2+] <10-3 mM [Cl-] 3-4 mM [A-] 140 mM
[A-]
molar equivalent of negative charges carried by molecules and ions, primarily large proteins
simple diffusion
overall movement down the concentration gradient, more molecules pass through the membrane from high to low concentration by a chance process
Fick’s law of diffusion calculates
net rate of diffusion os a solute across a membrane
Fick’s law of diffusion variables J, D, P, MW, C1, C2, X
J rate of diffusion, quantity of solute diffusing per unit time
D diffusion coefficient
P permeability (pore size)
MW molecular weight
C1 value of high concentration
C2 value of low concentration
X distance separating C1 from C2 (thickness of membrane)
5 factors influence J, rate of diffusion
concentration gradient (direct), permeability (direct), molecular weight (inverse), distance (inverse), temperature (direct)
electrochemical gradient
movement of solutes across a permeable membrane determined by the electrical (charge) gradient and the chemical (concentration) gradient
ionic charge separation occurs where with respect to the membrane, why
within nanometers of the membrane (net positive and net negative charges concentrate) because the lipid bilayers can maintain separation of oppositely charged ions
reinforcing with respect to the electrochemical gradient
concentration and electrical effects support fast diffusion
opposing with respect to the electrochemical gradient
concentration and electrical effects contrasting, slow diffusion
osmosis
diffusion of water through a semipermeable membrane from a region of low solute concentration to a region of high solute concentration
is osmosis, water stops moving when
hydrostatic pressure (weight of water) equals osmotic pressure (force associated with movement of water)
osmolarity
accounts for the total concentration of penetrating and non-penetrating solutes
tonicity
accounts for the total concentration of non-penetrating solute only
the effect of tonicity depends on difference in 2 things
osmolarity and the permeability of the membrane
Donnan equilibrium
predicts the distribution of ions across a membrane will be unequal is the membrane is impermeable to one or more types of charged particles
3 rules dictate the distribution of ions across a membrane that is impermeable to one or more types of charged particles
chronological order only: (1) principle of electroneutrality, (2) product of the concentration of permeant ions inside = the concentration of permeant ions outside, (3) osmolarity in = osmolarity out
2 types of membrane transport
passive and active
passive transport
requires no energy, solute moves from high to low concentrations
active transport
requires energy, solute moves from low to high concentrations
2 types of passive transport
simple diffusion and facilitated diffusion
simple diffusion membrane transport
gases, no transporter required
facilitated diffusion membrane transport
requires either (a) channel proteins (open/close) or (b) carrier proteins (change in conformation via non-covalent bonds)
equations that illustrates the saturation kinetics of facilitated transport
Michaelis-Menton equation
describe facilitated diffusion curve
hyperbolic curve with plateau at the point of transporter saturation
saturation point of facilitated diffusion versus simple diffusion
simple diffusion does not have a saturation point
the substrate concentration [S] that gives 1/2 Vmax
Km Michaelis constant
3 types of transporters
uniporter, antiporter, symporter (co-transporter)
substrate transport is determined by
channel composition
transporters are driven by either
a concentration gradient or ATP
uniporter
glucose, Na+, unidirectional transport of 1 substrate
antiporter
Na+/K+ ATPase, Cl-/HCO3- exchanger, counter-directional transporter of 2 different subtrates
symporter (co-transporter)
KNCC (Na+, K+, 2Cl- co-transporter), K+/Cl- co-transporter, unidirectional transporter of 2 or more different substrates at the same time
3 types of ion channels involved in facilitated diffusion
voltage-gated channels, ligand-gated channels, mechanically-gated channels
voltage-gated channels
Na+ and heart contraction, open/close in response to changes in membrane potential
ligand-gated channels
acetylcholine and neurotransmission, open/close in response to presence/absence of ligand
mechanically-gated channels
pushing on skin and firing of AP to nerve for sense of touch, open/close in response to changes in cell shape
2 types of active transport
primary active transport and secondary active transport
primary active transport
energy released by ATP hydrolysis drives solute (X) movement against an electrochemical gradient
secondary active transport
energy from electrochemical gradient (X) drives co-transport of a second solute (S) against its electrochemical gradient
2 types of primary active transport pumps
electrogenic and electroneutral
electrogenic primary active transport pump
sets of a difference of electrical charge, Na+/K+ ATPase maintains electrical potential, maintains high [K+]in and [Na+]out for use in secondary transport (3Na+ for 2K+)
electroneutral primary active transport pump
does not set up a difference in electrical charge, H+/K+ ATPase responsible for secretion of stomach acid in vertebrate stomach lining, protein expressed along the canaliculi (invaginations to increase SA) of parietal cells that line stomach cavity wall (2H+ for 2K+)
aquaporin
uniporter channel protein discovered by Peter Agre who determined the DNA and amino acid sequences of the water channel AQP1 using Xenopus (frog) oocytes (eggs) to demonstrate that AQP1 is responsible for osmosis
Xenopus oocyte experiment
Xenopus oocyte is naturally water resistant. Xenopus oocyte microinjected with RNA coding for AQP1 (mammalian protein) expresses protein, tritiated water (radioactive) in hypotonic solution indicates increased permeability (cell ruptures). Xenopus oocyte microinjected with RNA coding for AQP1 (mammalian protein) and RNA inhibitor (mercury) does not express protein, absence of movement of tritiated water (radioactive) in hypotonic solution indicates no change in permeability.
aquaporins are abundant in
the kidney and RBCs
aquaporins in the kidney
Arginine vasopressin (AVP) hormone regulates kidney water permeability. The pituitary gland releases AVP in response to thirst when blood concentration in increased. AVP binds to vasopressin receptor, triggering the signalling molecule cAMP to activate protein kinase A. Protein kinase A phosphorylates storage vesicles with aquaporins, which move water from collecting duct of kidney back to blood
prior to Cajal’s microscopy work and drawing of
cells of the chick cerebellum the nervous system was though to be one elongate body
application of August Krogh principle and neurons
giant axon of the squid was the source of fundamental knowledge of the nervous system
fraction of neural cells that generate action potential
1/10, neurons
4 functional zones of neurons
dendrites, axon hillock, axon, axon terminals
function of dendrites
signal reception, input
function of axon hillock
signal integration
function of axon
signal conduction
function of axon terminals
signal transmission, output
synapse
connection between 2 nerves, or 1 nerve and 1 muscle cell (myocyte)
myelin sheath
insulation for effective transmission of AP, prevents unintended transmission between nerves
loss of myelin sheath associated with
multiple sclerosis
soma of the neuron
cell body
glial cells
majority of neural cells, do not generate AP, support neurons
4 types of glial cells
Schwann cells, oligodendrocytes, astrocytes, microglia
Schwann cells
form myelin in the PNS
oligodendrocytes
form myelin in the CNS
astrocytes
transport nutrients, regulate synaptic neurotransmitter levels (clean up released neurotransmitters to maintain rapid response), remove dead cell in CNS
microglia
remove debris in CNS, remove dead cells in CNS
neural signals are
unidirectional: cell body to axon terminals
CNS
brain and nerves with cell body in brain case or spinal cord
PNS
nerves with cell body outside of brain case or spinal cord
PNS function
sends output from sensory pathways to CNS and carries out motor pathways as directed by the CNS
3 types of motor pathways
(1) autonomic (involuntary: sympathetic (stress/adrenaline) and parasympathetic (relax / acetylcholine)) and (2) somatic (voluntary)
neuromuscular junction stage 1
electrical potential: AP arrives to pre-synaptic cell, triggering voltage-gated Ca2+ channel to open, Ca2+ enters the pre-synaptic cell
neuromuscular junction stage 2
chemical potential: Ca2+ signals vesicle filled with neurotransmitters to release ACh into synaptic cleft
neuromuscular junction stage 3
chemical potential: ACh triggers ligand-gated channels to open in the post-synaptic cell, Na+ enters the post-synaptic cell which generates post-synaptic AP
neuromuscular junction stage 4
electrical potential: propagation of electrical potential in the post-synaptic cell activate the myocyte to contract
resting membrane potential
difference in charge across the membrane caused by differences in ion concentration across the membrane
neurons are excitable
(can rapidly change their membrane potential) due to the activation of channel and carrier proteins which rapidly move ions
changes in membrane potential act as
electrical signals
the distribution of an ion across a semi-permeable membrane depends on
the electromotive force
electromotive force
force generates by electrical gradient and chemical gradient
potential difference across a membrane when the forces generated by the electrical and chemical gradient are in equilibrium
equilibrium potential
equilibrium potential, resting Vm
-70 mV
depolarization, how to return to resting potential
more positive than resting potential, undergo repolarization to return to resting potential
hyperpolarization, how to return to resting potential
more negative than resting potential, undergo repolarization to return to resting potential
Nernst equation
calculates the equilibrium potential for single ions, proportional to the ratio of the concentration of an ion X across the membrane (greater ion ratio, greater equilibrium potential), Ex
Nernst equation variables R, T, s, F
R gas constant
T absolute temperature
z valence on ion (+/-)
F Faraday constant
Nernst equation is standardized at
18˚C
Goldmann equation
calculates the final membrane potential Vm for all contributing ions, proportional to the ratio of the concentrations of ions across the membrane and the permeability (depending on presence / number of ion channels) of the membrane to the ions (greater ion ratio, greater equilibrium potential)
Goldmann variables R, T, F, P
R gas constant
T absolute temperature
F Faraday constant
P permeability
Goldmann equation is standardized at
18˚C, use proportionality of permeability: low permeability to Cl- and Ca2+, permeability of Na+ is 1/100 of K+
Vm (-92 mV) of a cell is relatively close to Ek (-101 mV)
(1) cell membranes have a higher permeability to K+ than to other ions, (2) the Na+/K+ ATPase pump indirectly contributes to the Vm by maintaining high internal [K+] (move negative inside cell than outside because 3Na+ out for every 2K+ in)
neurons have massive amount of 2 things
mitochondria and ribosomes to produce neurotransmitters
ligands are released from neurons in proportion to
AP
neurons are organized into
functional circuits
functional circuits
rapidly conduct information to a target
information through neuronal circuits alternate between 2 signal types
graded signals (dendrites, soma) and all-or-none- signals (axon hillock, axon, axon terminals)
information is carried through neuronal circuits via
alternating electrical signals (AP) and chemical signals (neurotransmitters)
sensory neurons
afferent fibres, carry information inward toward interneurons
motor neurons
efferent fibres, carry information outward toward effectors (ie. muscle)
grade potential
electrical signals generated by ligand-gated channels in the dendrites and soma, the ion carries the charge down the electrochemical gradients, net movement stops when equilibrium potential is reached
ligand-gated ion channels convert chemical signals in electrical signals
by changing membrane potential
the magnitude of grade potentials is proportional to
stimulus strength (ie. concentration of the neurotransmitter)
graded potential can either
depolarize the cell (less negative via Na+ and Ca2+ channels) or hyperpolarize the cell (more negative via K+ and Cl- channels)
3 reasons graded potential travel short distances
membrane permeability, cytoplasmic resistance, decremental spread (electrotonic conduction)
membrane permeability impacts graded potential
leakage of charge ions across the membrane
cytoplasmic resistance impacts graded potential
inherent resistance to current flow, ion entry difficulty, friction of medium
decremental spread (electrotonic conduction) impacts graded potential
net charge decreases further away from ion entry
local charge does not equal
axon hillock charge
in order for the exon to fire an AP, graded potentials in the axon hillock need to depolarize the membrane beyond
threshold potential
spatial summation
graded potentials from different locations can interact to influence the net change in membrane potential at the axon hillock (consider inhibition and activation signals)
temporal summation
graded potentials occurring at slightly different times can interact to influence the net graded potential at the axon hillock (sub-threshold potentials that do not overlap in time do not summate, sub-threshold potentials that overlap in time summate and may trigger an AP – even though same number of ions involved in each scenario)
sub-threshold stimulus induce
proportional response in voltage threshold
supra-threshold stimulus induce
uniform action potential
instead of increasing AP, multiple action potentials are fired in series in response to
chronic stimulation
AP triggered
when membrane potential at axon hillock reach threshold (~55 mv)
AP are charcertistically
large (~△100 mV), brief (2-3 msec), and carry an all-or-none response
current is carried by
ions
ion concentration is restored by
Na+/K+ ATPase pump
Na+/K+ ATPase pump versus AP formation and ATP
Na+/K+ ATPase pump requires ATP, AP formation does not require ATP
structure and function of the startle response in cockroaches
mechanically-gated channels in the filiform hair receptors are stimulated by wind and initiate AP across the giant interneuron, leg motor neurons fire a series of AP to effectors in response to chronic stimulus, muscle tension is controlled in 1/10 sec
single cell patch clamp rig
isolated neurons bathed in mimic extracellular solution, glass micro-pipette electrode containing mimic extracellular solution uses suction to remove membrane patch containing singular channel and surrounding membrane, bathed in mimic intracellular solution, path-clamp recording of a single-channel currents using amplified to detect fine change in voltage by using electrons to quantify sodium current
use the single cell path clamp rig to
map the relative timing or opening and closing of voltage-gated channels to the characteristic phases of the AP
in the single cell patch clamp rig, conductance equates to
membrane permeability
Na+ and K+ channels are activated by the same AP but
exhibit different timings of response
following initial depolarization, inward current of Na+ is
‘instant’ and short-lived, depolarization involves 30x increase in Na+ conductance (gNa)
following initial depolarization, outward current of K+ is
delayed and longer-lived, repolarization involves a decrease in gNa and a delayed increase in K+ conductance (gK)
hyperpolarization follows AP initial repolarization
because gK remains elevated for some time after the AP
2 gates in voltage-gated Na+ channels
voltage-dependent activation gate (open/close) and voltage-dependent time-delayed inactivation gate (open/close)
conformation states in voltage-gated Na+ channels
(1) activation gate closed (capable of opening), (2) open (activated), (3) inactivation gate closed (inactivates, not capable of opening)
Na+ channel gates
activation gate (fast, ‘stick’) and inactivation gate (slow, ‘ball’)
1 gate in voltage-gated K+ channels
voltage-dependent time-delayed gate (open/close)
conformation states in voltage-dependent K+ channels
(1) closed, (2) open
refractory period
prevents back flow of sodium channel activation
absolute refractory period
the inactivation gate of the Na+ channel closes to prevent backward signalling, no AP can be triggered
relative refractory period
K+ channel opens to return membrane to rest, difficult for AP to be triggered because charge is hyperpolarized
propagation of AP
Na+ local currents spread longitudinally via electrotonic conduction depolarizing adjacent patches
AP at nodes of Ranvier via
voltage-gated channels
electronic conduction along internode via
diffusion of ions carrying charge
AP is triggered at
axon hillock
why does axonal conduction use a combination of electrotonic current flow and APs
electrotonic flow is faster but graded and can only travel short distances, AP increase efficiency but is slow
saltatory conduction
the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials: combination of electronic (passive diffusion) and action potential
2 factors affecting conduction speed
length constant and time constant
length constant λ
length taken for Vm to reach 63% of its maximal value, but electrotonic conduction enhanced by high membrane resistance Rm and low longitudinal (axoplasmic) resistance Rl
time constant τ
times taken for V, to reach 63% of its maximal value, but membrane voltage changes are reduced by high membrane resistance Rm and high membrane capacitance (ability to absorb / store electric charge) Cm
axon myelination increases
speed of propagation of an AP because myelination increase the length constant because insulation inhibits loss of charge (Rm increases)
increasing axonal diameter increases
speed of propagation of an AP because increasing axonal diameter increases the length constant because with increased diameter there is less interaction between the ions and cell walls which reduced resistance and flow distance increases (Rl increases)
myelination increases rate of conduction velocity in lieu of
a larger axon diameter, smaller axon diameter allow for more nerves per cubic area allowing for more complex neuronal processing
2 types of signals across the synapse
electrical and chemical
electrical synapse
transfer information between cells directly via ionic coupling via gap junctions: connexon proteins
how to connexon proteins of gap junctions help transfer information between cells directly via ionic coupling
by narrowing the gap between cells and lowering the resistance between cells
advantage of electrical synapse
faster response than chemical synapse because of discrete bridges between cells
disadvantage of electrical synapse
current decays between neurons exist, decremental charge spread across cells leads to reduced voltage in postsynaptic cells
crayfish escape circuit
electrical synapses first demonstrated between ventral nerve cord giant axons and motor neurons responsible for tail-flip reponse
chemical synapse
transfer information between cells indirectly via neurotransmitters, involves a signal transmission zone consisting of a presynaptic cleft, a synaptic cleft, and a post-synaptic cell (either neuron, muscle, or endocrine glands)
advantage of chemical synapse
induce APs so long as the threshold potential is reached, efficient transduction
disadvantage of chemical synapse
slower response than electrical synapse because of indirect bridging between cells, energetically expensive to (1) make dendritic spines, (2) prepare ACh in vacuoles – high demand for mitochondria
fast and slow chemical synapses are defined by and not by
their post-synaptic mechanisms and not their neurotransmitters
fast chemical synapses
act through ionotropic receptors on the post-synaptic membrane
slow chemical synapses
act through metabotropic receptors on the post-synaptic membrane
ionotropic receptors
ligand-gated ion channels, fast change in charge because voltage-gated channels are near ligand-gated channels on postsynaptic cell
metabotropic receptors
neurotransmitter binds to either a channel or not a channel (eg. ligand binds to G Protein Coupled Receptor (GCPR), activates G Protein, activates Effectors – memory, gene expression, growth (hormones))
primary neurotransmitter at the vertebrate neuromuscular junction
ACh
signal strength across the neuromuscular junction influenced by 2 things
neurotransmitter amount and receptor activity
neurotransmitter amount
rate of release (primarily) vs rate of removal (by enzyme)
receptor activity
density of receptors on postsynaptic cell
site of synthesis and recycling of ACh for the neuromuscular junction
synapse
post-synaptic cell manipulation and the neuromuscular junction
manipulates the response of the post-synaptic cell and creates a highly controlled system response
pre and post synaptic specializations and the neuromuscular junction
pre-synaptic terminal boutons, Schwann cell sheath. basement membrane, junctional folds, mitochondria, synaptic vesicles, high concentration of ACh receptors activate adjacent voltage-gated channels
pre-synaptic terminal boutons and the neuromuscular junction
branching termini to simultaneously innervate multiple muscle cells to activate contraction, insulated by Schwann cells
basement membrane and the neuromuscular junction
invaginations into muscle cells
junctional folds and the neuromuscular junction
invaginations into muscle cells
synaptic vesicles and the neuromuscular junction
pre-packaged ACh available for instant release
7 neuromuscular junction events
- presynaptic cell voltage-gated Ca2+ channels are opened by AP
- Ca2+ concentration increases, signals synaptic vesicles to bind to docking protein
- vesicles release neurotransmitter: ACh exocytosis
- neurotransmitter binds to ligand-gated channel on post-synaptic cell
- current is induced, produces end plate potential
- induction of postsynaptic AP
- acetylcholine esterase catalyze the breakdown of acetylcholine, delivers choline back to pre-synaptic cell
excitatory and inhibitory postsynaptic potentials are based on
manipulation of the stimulus and manipulation of pre and post synaptic cells
ESPS
excitatory postsynaptic potentials move the membrane potential toward the threshold potential (hypopolarize)
ISPS
inhibitory postsynaptic potentials move the membrane potential away from the threshold potential (hyperpolarize)
EPSPs and IPSPs can
summate
ESPS and ISPS impact depends on relative closeness to
stoma and axon hillock
whether a neurotransmitter is excitatory and inhibitory depends on
properties of its receptor
eg. ionotropic ACh nicotinic receptors – impacts channel protein, eg. metabotropic ACh muscarinic receptors – impacts channel protein or some other cellular process pathway
plasticity is rooted in the diversity at
the chemical synapse
plastcity
ability to change synaptic strength over time via synaptic connections and functional properties of neurons: ↑plasticity, ↑complexity, ↑specificity, ↑response
example of plasticity of chemical synapse
use and production of neurotransmitters and receptors
neurons can synthesize more than one kind of neurotransmitter and receptor, including
biogenic amines, amino acids, neuropeptides, others…
learning and memory are based on
modification of neuropathways based on experience
learning
process of acquiring new information
memory
retention and retrieval of information
synaptic transfer of information depends on
its history
facilitation
strength of response increases despite signal remaining the same, unknown mechanism, opposite of habituation
habituation
strength of response decreases despite signal remaining the same, unknown mechanism, opposite of facilitation
sensitization
strength of response increases in response to a novel stimulus, ‘restores’ habituation effects
potentiation
strength of response increased in response to a strong chronic stimulus
2 types of short-term neuromodulation
habituation (post-synaptic) and sensitization (post-synaptic)
Eric Kendel and the sea slug
August Krogh principle example, insight into the brain and learning: stimulation of the mantle or siphon leads to gill withdrawal, this reflex habituates with repeated stimulation (to mantle), this reflex is sensitized (enhanced) with novel stimulation (to head) – observe relatively increased gill withdrawal following novel stimulus, and subsequent habituation
reduction and enhancement of motor-neuron EPSP mirror the behaviour of
habituation and sensitization, respectively
sensitization involves
as secondary facilitating interneuron (head sensory neuron: indirect (secondary) contact with motor neuron, axon termini in contact with axon termini of skin sensory neuron)
in short-term habituation, there is a reduction in
neurotransmitter release by the skin sensory neuron: Ca2+ voltage-gated channel opens less with each tap, less Ca2+ enters the cell, less protein kinase is activated, fewer neurotransmitters vesicles are phosphorylated, fewer ligands are available to bind to ligand-gated channels on the postsynaptic cell, lesser response
in short-term sensitization, there is an increase in
neurotransmitter release by the skin sensory neuron as a result of presynaptic facilitation from the head sensory neuron: serotonin binds to serotonin receptors in the axon termini, activating a metabotropic pathway which activates cAMP synthesis and increases [cAMP] in the cell, which activates cAMP dependent protein kinase, which phosphorylates channel proteins: Ca2+ channel stays open longer and more Ca2+ is transported into the cell, K+ channel stays closed longer and less K+ is transported into the cell to broaden action potential
1 type of long-term neuromodulation
potentiation (or long-term potentiation) (post-synaptic)
tetanic stimulation simulates
strong emotion, repetition of events
tetanic stimulation of neurons in the hippocampus leads to
increased EPSPs
normal synaptic transmission: 1 pule per second
Ca2+ is unable to enter the cell via NMDA receptor channel because NMDA Glu receptors are blocked at resting potential by Mg2+ ions even if bound to the ligand Glu, AMOA Glu channel receptors are open at resting potential to produce fast ESPS
long-term potentiation induction: 100 pulse per second
tetanic stimulation results in strong depolarization of the postsynaptic cell, NMDA Glu receptors release bound Mg2+ so Ca2+ enters the NMDA Glu receptor channel – Ca2+ influx activates Ca2+ dependent protein kinase C which phosphorylates AMPA Na+ channel receptors stored in vesicles stimulating the fusion of the vesicles to the cell membrane, new AMPA Glu channel receptors results in increased capacity to respond to the neurotransmitter Glu
long-term sensitization is characterized by
increase in neuroreceptors (protein synthesis), as a result of chronic kinase activity: with a strong chronic stimulus, protein kinase C chronically (‘permanently’) phosphorylates AMPA Glu receptors to deliver receptors to the cell membrane, and can activate ↑ gene expression for such receptors at the level of the nucleus
what is responsible for the effects of LTP
differential gating properties of NDMA and AMPA glutamate receptors and the events regulated by Ca2+ in the postsynaptic neuron
glutamate uncaging on a single dendritic spine
glutamate is packaged, uncaged by UV light, causes significant depolarization of dendrite, activates protein kinase, which phosphorylates vesicles, which are incorporated into the membrane, resulting in a larger dendritic spine and greater possible response because more ligand-gated channels are available
stress hormones encode
neurotransmitters, stimulating system consolidation (ie. long term potentiation)
