TRAVERS 1 Flashcards
WHAT PART OF THE NEURON DOES GRADED POTENTIAL?
DENTDRITES
WHAT PART OF THE NEURON DOES ACTION POTENTIAL?
AXON
what is the exception to neurons being terminally differentiated?
hippocampus
how many percent of cns cells are neurons?
10%
what percent of cells in cns are glial cells?
90%
what is the myelinating glia in pns?
schwann cells
provides myelin to one axon
many schwann cells per axon
what is the myelinating glia in cns?
oligodendrocytes
contributes to many axons
what are microglia
macrophage like cell (phagocytic role)
what are astrocytes?
regulate extracellular fluid- remove k+ and neurotransmitter
provide neurons metabolically (eg glucose)
surround brain capillaries: form blood brain barriers
what is the structural component of axons?
microtubule
anterograde transport
from cell body towards terminal
motor proteins: kinesins
fast transport -organelles such as nt vesicles
slow transport- structural proteins
retrograde transport
dyneins
fast transport
from axon terminals toward cell bodies such as growth factors and viruses
why does damaged cns neurons no regenerate?
axons sprout but axons do not reach targets
scar formation prevents surviving axons from reaching targets
astrocytes make chondroitin sulfate proteoglycans that inhibit neuron growth
anterograde degeneration
distal to lesion
transganglionic degeneration
axon process heading toward cns degenerates
transynaptic degeneration
neuron contacted centrally by the axon dies
chromatolysis
associated with protein synthesis
cell body swells, eccentric nucleus
how does schwann cells contribute to regeneration?
schwann cells proliferate
produce laminin for substrate for regenerating axons
schwann cells secrete nerve growth factor
ngf transported to ganglion cell body
what does ngf do?
regulates gene expression and promotes sprouting
regulates: microtubules, microfilaments, nt production, ion channels, nt receptors
what is collateral sprouting?
most likely to occur when an axon fails to regenerate- surviving axon nearby may sprout new terminals into the area previously occupied by the other sensory cell
no evidence of collateral sprouting for teeth- soft tissue only
temporal summation
adding together of PSP from one synatic contact over time
spatial summation
adding together of PSP produced by diff synapses
action of drugs at synaptic junction
- increase leakage of nt from vesicle to cytoplasm, exposing it to enzyme breakdown
- inc transmitter release into cleft
- block transmitter release
- block transmitter reuptake
- block cleft enzymes that metabolize transmitter
- bind to receptor on postsynaptic membrane to block (antagonist) or mimic (agonist) transmitter action
- inhiibit or stimlate second messenger activity within post synaptic cell
actions of neuromodulators
may act postsynaptically to amplify or dampen on-going synaptic activity
may act on pre-synaptic cell to alter synthesis, release, uptake or metabolism of nt
actions involve changes in dna/protein synthesis or enzyme activity- slower in action
acetylcholine
synthesized from choline and acetyl coA by choline acetyltransferase in synaptic terminal
action stopped by diffusion and degradation by actylcholinesterase
choline reuptake by presynaptic neuron
neurons that release ach
motor neurons
neurons in nucleus basalis and pons
all pregang neurons sym and para sym
all post gang parasym neurons
basal forebrain and pontine nuclei
cognitive function
sleep regulation
diff acetylcholine receptors
muscarinic and nicotinic
muscarinic receptors
mainly found in cns except parasymp post gang synapse- salivary glands
binding of ach triggers g protein that open or close ion channels- depol or hyperpol
WHAT ARE MUSCARINIC RECEPTORS BLOCKED BY?
ATROPINE
nicotinic trceptors
relatively few in cns
ach binding opens ion channels within receptor- channel permeable to na and k
ex nmj
what are nicotinic receptors blocked by?
CURARE
myasthenia gravis
autoimmune disorder in which indibidual makes antibodies to nicotinic receptors
characterized by muscle weakness
treated with acetylcholnesterase inhibitors
alzheimers disease
most common form of dementia
etiology unknown
many neuronal pop involved
loss of neurons in nucelus basalis leading to decrease in cholinergic activity in cortex
what are biogenic amiens?
synthesized from amino acids
what are catecholamines?
dopamines, norepinepherine, epinephrine
synthesized from amino acid tyrosine
catecholamine life cycle
synthesis- presynaptic terminal- stored in vesicles
release- ca dependent
termination of action- presynaptic neuron reuptake and degradation
where are biogenic amines found?
neurons that synthesize the ligand in very limited locations
receptors for the ligands found extensively thruout cns
receptors are almost exclusively g-protein coupled receptors
what are biogenic amines involved in?
parkinsons, depression, schizophrenia
dopamine
found in areas of midbrain and brainstem
dopamine receptor subtypes
all g-protein coupled
two main groups: d1 and d2
d1- activate adenylate cyclase
d2- inhibit adenylate cyclase- hyperpolarization
what do drugs do to dopamine receptors?
block d2 receptors
ventral tegmental area and dopamine
associated with reward and addiction”
cocaine and amphetamine prolong dopamine action at synapse
substantia nigra and dopamine
associated with motor system
loss of dopamine assciated with parkinson’s disease
tardive dyskinesia
pt receive dopamine blocking drugs involuntary movements delayed onset inc incidence with advanced age rhythmic oral movements-involuntary, repetitive body movements d2 receptors
epinephrine
epinephrine requires presence of additional enzymes for synthesis from norepinephrine
norepinephrine neurons
sympathetic post ganglionc neurons and some cns
epinephrine
adrenal gland as circulating hormone- not much in cns
noradrenergic receptors
g-protein coupled
alpha receptors: a1- excittory- intracellular release of ca
a2- inhibitory via opening k channels or blocking ca
beta receptors- open ca channels
NE can have very diff effect on tissue depending on receptor
locus ceruleus and ne
attention/sleep
other brainstem and ne
autonomic and homeostatic functions
serotonin
synthesized from tryptophan
found in several discrete cns populations
involved in many functions ranging from sensorimotor systems to cognitive function
serotonin receptors
16 receptor subtypes
most are g-protein coupled
5-gt synapses target of mood altering drugs
rostral raphe nuclei and serotonin
sleep, mood, homeostatic function
caudal raphe nuclei and serotonin
sensori-motor function
amino acid neurotransmitters
excitatory aa such as glutamate and aspartate
binds to ionotropic and metabotropic receptors
ionotropic recept
ampa
kainate
nmda
receptors with channels permeable to na, k, ca
metabotropic receptors
g-protein receptor
nmda receptor
n-methyl-d-aspartate
involved in functions that last- memory formation, chronic pain
excitotoxicity- excessive excitation- cell death (epulepsy trauma, stroke)
neuron death from ca reaching toxic levels
synaptic mechanism of long term potentiation
gaba
major inhibitory nt in cns
modified form of glutamate
gaba receptors
gaba a- ionotropic receptor- opens cl- channel
gaba b- metabotropic receptor- opens k+ chammels
huntington chorea
form of motor spasticity
linked to gaba deficits
glycine
inhibitory nt (mostly spinal cord) receptor opens cl- channels blocked by strychnine
peptides
formed by peptide link between2 or more amino acids
over 90 id
often co-released with other nt- synthesized in soma and must be transported to be released
functions as neuromodulator
actions can last long time
action termiantaed by proteolysis and diffusiion
nitric oxide
gas
synthesis- l-arginine to no by nitric oxide synthase (nos)
not stored in vesicles
freely difusible across membrane (requires no synapse)
can modulate nt release
plays role in numerous brain functions
role in injuries: excitotoxicity
atp
usually excitatory
usually co-released with classical nt
