Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
127 Cards in this Set
- Front
- Back
|
Describe the types of EPSP summation:
|
spatial- adding EPSPs generated similtaneously at different synapses on a dendrite
temporal- EPSPs generated at the same synapse in rapid succession |
|
|
list 4 dendrite properties
|
1. straight cable, electricall passive
2. membrane depolarization decreases with increasing distance 3. dendritic length constant- index of how far depolarization can spread down dendrite or axon 4. elaborate structures, contribute to complex integrative properties |
|
|
what affects length constant
|
internal resistence- depends on diameter and electrical props of cytoplasm
membrane resistence- depends on # of open ion channels |
|
|
what does Inhibition of potential do?
|
most inhibitory synapses are permeable only to Cl
bring equilibrium potential more negative, hyperpolarizing |
|
|
what are receptor antagonists?
|
inhibitors of NT receptors, bind and block receptor
|
|
|
what are receptor agonists?
|
bind to receptors and mimic actions of NT
|
|
|
describe the 3 criteria to be a NT:
|
1.synthesis and storage in presynaptic neuron
2.released by presynaptic axon terminal 3.produces response in postsynaptic cell |
|
|
What are the 3 classes of NTs?
|
amino acids
amines peptides |
|
|
name 3 techniques to localize a NT:
|
immunocytochemistry
In-situ hybridization microionophoresis |
|
|
explain immunocytochemistry
|
a NT candidate is inserted into the bloodstream, stimulating an immune response, antibodies are produced and bind to NT, antibodies are withdrawn and isolated and labeled with a colored marker, antibodies are applied to brain tissue, and you see which cells contain this NT
|
|
|
explain in-situ hybridization
|
chemically label a probe (cDNA for mRNA of NT), apply to brain tissue and search for labeled neurons
|
|
|
explain microionophoresis
|
studies postsynaptic actions by injecting small amount through current of NT soln before postsynaptic membrane and observing response with microelectrode
|
|
|
how can release of a NT be studied?
|
keep a brain slice alive in vitro, bath it in high [K], which will cause depolarization stimulating NT release, collect and measure all chemicals released; make sure release of NT happens only when Ca is present
|
|
|
what is synaptic mimicry?
|
dissolve NT in solution and place in a glass pipette, position near postsynaptic membrane and eject in small amounts using electrical current through pipette; measure the membrane potential of the postsynaptic membrane with microelectrode; see if change mimics NT release
(using microionophoresis) |
|
|
how can pharmacology be used to study receptors?
|
you can study drugs that act as agonists and antagonists and see how they affect receptors; whether they open, close or last longer...
|
|
|
Decribe NMDA receptors:
|
glutamate receptor type and agonist
allows Na and Ca in, K out voltage dependent, at normal resting potential a Mg blocks the pore, Mg moves when membrane is depolarized some by AMPA channels long term effects, memory |
|
|
describe AMPA receptors:
|
glutamate receptor and agonist
Na in and K out Na into cell depolarizes small response |
|
|
what are opiates?
|
medically important drugs, commonly abused- heroin, morphine
used to study receptors with ligand binding method receptors in some neurons of brain endorphins are naturally occuring NT that bind to opiate receptors |
|
|
what is ligand-binding?
|
a method to study receptors using radioactive labeled ligands (compound that binds to a specific site on a receptor)
if receptor exists ligand will bind and show up with radioactive label |
|
|
What are the receptor types for the NT Acetylcholine?
|
nicotinic
muscarinic |
|
|
How do Nicotinic receptors work?
|
nicotine is an agonist
curare is an antagonist ion channel: Na flows in, K flows out |
|
|
How do Muscarinic receptors work?
|
Muscarine is an agonist
Atropine is an antagonist has no pore but is a G-protein receptor |
|
|
Describe the life cycle of ACh:
|
enzyme ChAT combines acetyl CoA and Choline to make ACh
ACh transporters concentrate ACh into synaptic vesicles ACh is released into the cleft and attaches to postsynaptic receptors AChE breaks ACh down into acetic acid and choline transporter takes choline back into neuron (rate limiting step) |
|
|
how are catecholamines related in structure?
|
they come from the precursor tyrosine
contain catechol structure (benzene with 2 OHs) |
|
|
How do you get from tyrosine to epinephrine?
|
tyrosine--(TH)-->dopa--(dopa decarboxylase)-->dopamine--(DBH)-->norepinephrine--(PNMT)-->epinephrine
|
|
|
From what amino acid is GABA synthesized and how?
|
glutamate with GAD
role in synaptic inhibition |
|
|
What are the Glutamate Receptors?
|
AMPA
NMDA Kainate |
|
|
what are retrograde messengers?
|
released from postsynaptic neurons and act on presynaptic terminals
|
|
|
what is the essential link b/t neurons and effector cells?
|
neurotransmitters
|
|
|
What are the Norepinephrine receptors, agonists and antagonists?
|
α receptor - phenylephrine - phenoxybenzamine
β receptor - isoproterenol - propranolol |
|
|
What is Dale's Principle?
|
that one neuron has only one NT
(not true) |
|
|
what are cotransmitters?
|
when two or more NT are released from one nerve terminal
an amino acid or amine plus a peptide |
|
|
What are chatecholaminergic nerons and what are they involved with?
|
involved in movement, mood, attention, and visceral function
includes tyrosine and the NTs: dopamine, norepinephrin, and epinephrine |
|
|
What are serotinergic neurons and what do they regulate?
|
amine NT- seretonin which is derived from tryptophan (obtained in diet)
regulates mood, emotional behavior, and sleep |
|
|
What are the Amino Acidergic Neurons?
|
NTs: glutamate, glycine, and GABA
quantitative not qualitative differences |
|
|
What is one way to treat depression?
|
block reuptake of serotonin, so that it remains in synapse working longer
block with selective serotonin reuptake inhibitors(SSRIs)=antidepresssants |
|
|
What is Glutamic Acid Decarboxylase? (GAD)
|
key enzyme in GABA synthesis
good marker for GABAergic neurons main for synaptic inhibition |
|
|
What are endocannabinoids?
|
retrograde messengers
drugs that dull the senses and cause loss of cognitive ability there are natural receptors in the brain for marijuana series of AP causes an influx of Ca in postsynaptic cell, higher [Ca] causes enxzymes to make endocannabinoids that are recieved on presynaptic cell with CB1 receptors --g-protein reduces opening of presynaptic Ca channels which suppresses NT |
|
|
What are CB1 receptors?
|
G-protein receptors on presynaptic cells that recieve endocannabinoids and in turn reduce Ca channel opening suppressing NT release
|
|
|
What are 4 distinguishing properties of amino acid receptor channels?
|
kinetics of transmitter binding process
selectivity of ion channel conduction of open channels pharmacology of their binding sites |
|
|
what are some properties of transmitter-gated channels?
|
sensitive detectors of voltage and chemicals
fast synaptic transmission can regulate current flow differentiate b/t similar ions |
|
|
What is the basic structure of transmitter-gated channels?
|
pentamer: 5 protein subunits
|
|
|
How do Ach, GABA, Glycine, and Kainiate receptors differ in structure?
|
different transmitter binding sites
different amio acids around pore that allow only certain ions to pass |
|
|
what is required for nicotinic receptors to open?
|
ACh must bind to both α subunits simultaneously
|
|
|
when GABAa receptor is present what do benzodiazepines and barbiturates do?
|
increase inhibitory Cl current
slow down nervous system benzodiazepines- increase frequency of channel openings barbiturates- increase duration of channel openings |
|
|
What do GABA and Glycine gated receptors do?
|
synaptic inhibition (hyperpolarize)
gate a Cl channel- glycine and GABAa GABAb- g-protein linked to K channel- K leaves to hyperpolarize |
|
|
What are the different molecules that GABAa can bind?
|
ethanol
benzodiazepine GABA Barbiturate Neurosteroids |
|
|
what is the baisc structure of G-protein coupled receptors?
|
single polypeptide with seven membrane spanning α-helices
loops on outside of membrane bind NT loops on inside bind G-protein |
|
|
Describe the 5 steps of G-protein function:
|
1. 3 subunits of G-protein α,β, γ float right inside of membrane (α bound to GDP) -inactive
2. G-protein bumps into acitvated receptor w/ NT and GDP exhanges for GTP --active 3. Gα- GTP and Gβγ split and influence effector proteins 4. Gα inactivates by converting GTP to GDP 5. Gβγ recombines with Gα-GDP |
|
|
How can Ca be used as a secondary messenger?
|
Gα subunit triggers PLC, PLC acts on PIP2 splitting it into 2nd messengers: DAG and IP3
IP3 in cytosol binds to Ca channel receptors on smooth ER causing Ca to move into cytosol to act as secondary messenger- triggers long lasting effects, high [Ca] triggers NT release |
|
|
How is cAMP used as a second messenger?
|
NE binding to a β receptor activates G-protein, Gα unit stimulates adenylyl cyclase enzyme that converts ATP to cAMP
rise in cAMP activates protein kinase A |
|
|
divergence of neurotransmitter systems:
|
when one NT can activate more than one receptor and one receptor can have many effects
|
|
|
convergence of neurotransmitter systems:
|
when mulitple NT/receptors all act on one effector
|
|
|
what are the ways G-proteins can act:
|
on ion channels
on g-protein enzymes and effectors |
|
|
Explain the muscarinic receptor:
|
ACh binds and G protein becomes activated and Gα and Gβγ split
Gβγ effects a K channel opening pore this slows the heart rate (K flows out hyperpolarizing) |
|
|
what does protein kinase A do?
|
activated by cAMP, PKA phosphorylates Ca channels, increasing Ca flow
|
|
|
where is protein kinase C from?
|
its activated by secondary DAG messenger by PLC
|
|
|
what are protein phsphatases? Why are they important?
|
they remove phostphate groups from proteins
important to counter balance phosphorylation- changes biological conformation and activity |
|
|
what is the push and pull method?
|
when one NT receptor will activate an excitatory G-protein and another receptor for the same NT will activate an inhibitory G-protein
ex. NE- β receptor is stimulatory and α2 receptor uses inhibitory g-protein |
|
|
What is the importance of signal cascades?
|
they amplify the signal/ effect for greater response
signaling at a distance long lasting responses |
|
|
What happened to Bob Woodruff?
|
he had traumatic brain injury and lost his left cerebral hemisphere and speech production and comprehension
but somehow the circuits that were left were able to reconnect the right side complementary areas of warnikees and brocas took over for loss on left side |
|
|
What are the ATP NT receptor, agonists, and angtagonists?
|
P2x--ATP--Suramin
A type--Adenosine--caffine |
|
|
which molecules in cholinergic neurons are good for immunocytochemistry use?
|
ChAT(good b/c created only in these ACh neurons), but not AChE (bad b/c created in other neurons too)
|
|
|
How is TH (tyrosine hydroxylase) regulated?
|
by signals in the cytosol axon terminal
decreased catecholamine release causes increased [ ], inhibiting TH at high rate of catecholineamine release, elevated [Ca] that causes NT release, causes increase in TH activity |
|
|
What happens in Parkinson's disease and how can it be treated?
|
disrupts movement b/c dopanninergic neurons degenerate and die
treat by increasing DA synthesis in remaining living neurons |
|
|
what do the drugs cocaine and amphetamine do?
|
they bind to Na transporters which blocks the reuptake of NT and prolongs the action of NT in the cleft (Na transporter takes up NT=dopamine)
|
|
|
Explain the GABA receptors
|
GABA a- gates a Cl channel
GABA b- G-protein linked to K channel |
|
|
What are the 3 steps to neural structure development?
|
cell proliferation
cell migration cell differentiation |
|
|
how does position during cleavage affect cell fate?
|
with vertical cleavage- both cells have same fate, remain by ventricular surface and continue to divide
cells with horizontal cleavage- genetic markers are not cleaved evenly so, cell farthest from ventricular surface migrates away to cortex |
|
|
describe what notch-1 and numb do:
|
these are genetic markers that deal with migration; weehn a cell is cleaved horizontally, one cell has only notch-1 and one has only numb; the cell with numb remains at ventricular surface, while the notch-1 cell migrates to the cortex
in vertical cleavage, both cell have both markers and so both cells stay put |
|
|
describe cell migration:
|
cell migrate my moving up radial glial cells (fibers) that radiate from ventricular zone toward the pia
cortex assembles inside-out |
|
|
what role does semaphorin 3A play in neurite development?
|
it is a protein that is secreted in the marginal zone (close to pial surface)
it acts to repel axons and attract apical dendrites, controling pyramidal cell development |
|
|
what are the 5 positions of cell proliferation?
|
1. cell extends a process reaching toward pia
2. nucleus of cell migrates from ventricular surface toward pial surface (DNA copied) 3. nucleus move back to ventricular surface 4. cell retracts arm from pial surface 5. cell divides in 2 |
|
|
What is a reeler mouse?
|
mutant with wobbly appearance b/c neurons of cortical plate are unable to pass through the subplate, so they pile up below it
|
|
|
what is reelin?
|
protein that regulates the assembly of the cortex
disrupted in reeler mice |
|
|
what is a growth cone?
|
the growing tip of a neurite
the leading edge of the growth cone is the lamellipodia and the filopodia is spikes extending from the lamellipodia |
|
|
How does growth cone work?
|
growth will only occur if specific proteins are in the extracellular matrix
ex. laminin in the matrix binds to integrins in the growing axon |
|
|
how do axons in the spinal cord decide where to go?
|
interaction of molecules in axon and environment guide it
ex. netrin secreted in ventral midline of spinal cord, gradient of netrin attracts axons of dorsal horn neurons after crossing the midline, robo receptors increase in the axon and the protein slit binds to axon, repelling axon from the midline |
|
|
what is a chemoattractant?
|
diffusible molecule that acts over a distance to attract growing axons towards targets ex. netrin
|
|
|
what is a chemorepellent?
|
diffusable molecule that chases axons away
ex. slit; axons must express robo receptor for slit |
|
|
axons from the nasal retina go to...
|
contralateral optic tract
|
|
|
axons from temporal retina...
|
ipsilateral optic tract
|
|
|
what are ephrins and how do they work?
|
frog retinal axons connect to tectum
ephrins are proteins that act as repulsive signals for temporal retina contain eph receptor on axons and when ephrin bind it inhibits growth higher concentration of ephrin is in the posterior |
|
|
the nasal retina connects to the _________ tectum
|
posterior
|
|
|
the temporal retina innervates the ________ tectum
|
anterior
|
|
|
what are the phases of pathway formation?
|
pathway selection
target selection (structure to innervate) address selection (cells to synapse) |
|
|
how is information communicated in nervous system?
|
cell to cell contact
extracellular secretions diffusable chemicals electrically |
|
|
what is fasciculation?
|
mechanism that causes axons growing together to stick together
use cell-adhesion molecules (CAMs) |
|
|
what are pioneer axons?
|
they stretch as the nervous system expands
establish initial connections (connect the dots) trajectory of axon is broken into short segments guide neighbor axons to same targets |
|
|
what is special about CNS axons in amphibians?
|
they can regenerate
ex. you can rotate the eye 180 and the nerve will regenerate and connect, the axons will just be scrabled giving a mirror image to the brain |
|
|
describe synapse formation:
|
1. clustering of postsynaptic receptors under the site of nerve muscle contact triggered by interaction b/t protein secreted by growth cone and the target membrane
2. NT released is triggered by basil lamina factors that stimulate Ca entry into growth cone |
|
|
explain synapse formation in the NMJ:
|
agrin is released from the presynaptic axon terminal and the receptor MuSK is located in the muscle fiber membrane
MuSK communicates with rapsyn which gathers postsynaptic ACh receptors at the synapse # of receptors is regulated by neuregulin which stimulates receptor gene expression |
|
|
what are radial glial?
|
fibers that provide the scaffold on which the cortex is built, neurons migrate along radial glia toward the cortex
|
|
|
what is the cortical plate?
|
cell layer of immature cerebral cortex containing undifferentiated neurons
as neurons arrive at cortical plate they then differentiate into different cerebral layers |
|
|
what happens after adolescence to refine the neural connections?
|
large scale reduction in newly formed neurons and synapses
progressive decline in presynaptic axons and nuerons= cell death |
|
|
what are trophic factors?
|
they promote cell survival; life sustaining substances that are provided in limited quantities by target cells
|
|
|
how does selective cell death occur?
|
competition for trophic factors produces a proper match in the number of presynaptic and postsynaptic neurons
|
|
|
what is apoptosis?
|
expression of cell death genes causing neurons to die
|
|
|
what is necrosis?
|
accidental cell death due to injury to cells
|
|
|
what role does synaptic transmission play in synaptic elimination?
|
at first axons innervate multiple fibers, but upon maturation one axon goes to a single fiber
stimulation of axons leads to only one axon remaining on each fiber (maturation) insufficient receptor activation/stimulation causes receptors to internalize and axons to withdraw |
|
|
what is a Hebb Synapse?
|
when simultaneous activation of presynaptic and postsynaptic neurons causes an increase in effectiveness of a synapse
|
|
|
what is strabismus?
|
when the eyes are not perfectly aligned
can result in loss of stereoscopic vision |
|
|
what is the LGN?
|
lateral geniculate nucleus
thalamic nuclei that relays information from retina to primary visual cortex |
|
|
what is a nerve growth factor? NGF
|
first identified trophic factor
it is produced and released from a target tissue, taken up by sympathetic axons, transported retrogradely, and acts to promote neuronal survival |
|
|
what is ocular dominance?
|
when a region of the cortex recieves info primarily from one eye
|
|
|
what is synaptic capacity and how does it change?
|
def- the number of synapses a neuron can recieve on its dendrites and soma
before adolescence synaptic capacity is constant then during adolescence, you lose half of all synapses in 2 years at a rate of 5000 per sec lose polyneuronal innervation to just single neuron for fiber |
|
|
what is synaptic rearrangement and why does it occur?
|
the change of one pattern of neuronal connections to another
it occurs as a consequence of neural activity and synaptic transmission, molecular cues and activity dependent occurs during critical period |
|
|
what is synaptic segregation?
|
refinement of synaptic connections
experience dependent ex. retinal inputs ot the LGN, axons move into eye-specific domains fix monocular deprivation with reversed-occulsion |
|
|
what affects synaptic segregation in the retinal system?
|
TTX blocks APs and silences retinal activity, preventing segregation
|
|
|
how does segregation of retinal inputs to the LGN happen?
|
independent waves in each retina---spontaneously in the womb, b/c there is no light stimulation here
needs hebbian modification synaptic stabilization- only connections retained are --terminals active at same time as target neuron |
|
|
what does it mean that inputs compete on a winner takes all basis?
|
that one input will be retained and the other will be eliminated
|
|
|
inputs from LGN neurons serving the 2 eyes segregate into________
|
ocular dominance columns
|
|
|
what is monocular deprivation?
|
where one eyelid is sealed closed
|
|
|
what is the critical period?
|
period when modification can occur, after which you lose capacity for growth and retraction\
to 6-7 years old |
|
|
what is revered-occulsion?
|
when you stimulate the bad neural connections and stop the good ones to make the bad connections better
|
|
|
After subjecting a young macaque to monocular deprivation, you discover.....
|
the ocular dominance column for the normal eye widens as it is the only one recieving stimulation
|
|
|
what is the basis for binocular vision?
|
ocular dominance columns converge inputs from layer IV onto layer III
|
|
|
binocular fields depend on what?
|
correlated patterns of activity that arise from the two eyes as a consequence of vision
|
|
|
what is ocular dominance shift?
|
when there is a change in binocular organization of the cortex
this can occur beyond the critical period |
|
|
as you age what happens to plasticity?
|
it diminishes
|
|
|
what role do modulatory neural systems play in vision?
|
before birth spontaneous bursts of retinal activity can orchestrate aspects of address selection
after birth interaction with the visual environment is important pay attention to stimuli and use vision to guide behavior |
|
|
explain why NMDA receptor may not be the only receptor in a membrane
|
NMDA and AMPA are colocalized
NMDA is voltage dependent and requires initial depolarization of membrane to remove the Mg in the pore once Mg in the pore moves Ca and Na flow in and Ca can cause more long term synaptic transmission b/c it can signal for more AMPA receptors to move to the membrane |
|
|
what is Long-Term Potentiation?
|
the strengthening of synaptic transmission
consequence of strong NMDA receptor activation AMPA receptors being inserted into membrane b/c of Ca influx |
|
|
what is Long-Term Depression?
|
when active synapses decrease in effectiveness
lower levels of NMDA receptor activation and less Ca influs causes loss of AMPA receptors |
|
|
Why does the critical period end?
|
plasticity dimishes when:
-axon growth ceases -synaptic transmissino matures -cortical activation is constrained |
|
|
rules for cortical synaptic plasticity:
|
fire together wire together
fire out of sync lose the link |
|
|
what are noradrenergic neurons?
|
they produce and release norepinephrine NT
|
