Ruth Epsom lectures Flashcards
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thalamus function
gateway to the cortex
reticular formation controls
level of consciousness
pre-frontal cortex controls
agression and emotion
hypothalamus is responsible for
hormonal integration
cerebellum controls
sensory feedback to the motor system
Brocas area
motor speech area
what is stored in the hippocampus
memory language and emotion
basal ganglia controls
voluntary and selection of movement
corpus callosum
joins both hemispheres of the brain
nervous tissue is made up of
neuron and glia cells
role of neurons
communication, carry electrical signal from brain to spinal cord or from spinal cord to effectors
example of a neuron
synapses
role of glia cells in nervous tissue
support
example of glia cells
myelin and CSF
another name for glia
neuroglia
four zones of an axon
input zone, summation zone, conduction zone and output zone
are neurons or glia excitable
neurons
glia are
non excitable but do still have a resting membrane potential
name the five steps involved in electrical excitability
1- stimulus gated sodium channels open which causes the MP to reach threshold
2- voltage gated sodium channels open and the stimulus gated channels close an AP is being fired
3-voltage gated sodium channels close at the peak of the AP
4- voltage gated potassium channels open causing the AP to be repolarised
5- voltage gated channels close causing hyperpolarisation and the MP is now restored.
what are two way conduction velocity can be increased in an axon
myelin sheath and increasing axon diameter
What junction on an electrical synapse allow the flow of current
gap junctions as they act as a pore to join two cells
how can synapse strength be modified in chemical synapses
changing the amount of receptors on the post synaptic membrane and the change in amount of neurotransmitter released from the pre synaptic vesicles.
are chemical or electrical synapses faster
electrical because chemical synapses rely on a series of events to occur
pre-synaptic specialisation
vesicles containing neurotransmitter
post-synaptic specialisation
neurotransmitter receptors
how is a membrane potential created
by the difference in ion distribution
chemical gradient
energy provided by the difference in concentration across the plasma membrane
write down the chemical energy equation
triangleu= RT In(inconc)/(outsideconc)
electrical gradient
energy associated with moving charged molecules across the membrane
write down the electrical energy equation
triangleu=RT In(inconc)/(outconc) +1(F) (-60mV)
what are the only two excitable cells in the body
nerve and muscle cells as they generate APs
define equilibrium potential
the energy in mV of a concentration gradient of an ion
equilibrium potential/ electrical potential
the electrical potential that exactly balances the concentration gradient of an ion
Nernst equation
Eion= 60/Z log (concout/concin)
RMP for a muscle compared to a nerve cell
RMP muscle -70mV and nerve -90mV
why do resting membrane potentials exist
the neuronal membrane at rest is slightly permeable to sodium ions
describe the RMP
large potassium ion out flow with a modified by a smaller sodium ion inflow
decrement of local potential depends on
length constant of the nerve
local potentials are
small ion fluxes across the membrane means that the RMP fluctuates these fluctuations are local potentials
local potentials/action potentials
local potentials influence the firing of an action potential
describe a local potential in five points
decremental in size graded in size summate temporally and spatially depolarise/hyperpolarise influence the generation of an action potential
describe an action potential in three points
all or nothing
self generating- propagate without decrementing
has to reach threshold 15mV
why is Ena often not reached
because the potassium channels open before its reached causing a decrease
what drives the AP
voltage gated sodium channels
what allows the sodium channels to shut fast
the inactivation gate
what substance can block and inhibit the sodium channels
tetrodotoxin
what allows the voltage gated sodium channels to turn on
the voltage sensor
where is the voltage sensor of the sodium channel located
in the 4th transmembrane domain of the protein
ball and chain model
inactivation gate
voltage gate and what are interchangeable
activation gate
do potassium channels have an inactivation gate
yes but this is slower than the sodium inactivation gate
relative refractory period
when another action potential is possible, however must work against potassium gradient as the potassium channels are open, therefore this is difficult and rare because the membrane potential is driving in a different direction.
refractory period
when the AP is repolarising or hyperpolarising
how does increasing axon diameter increase conduction velocity in an axon
decreases internal resistance
how does insulation/ myelination increase conduction speed
prevents leakage of the electrical current
how does insulation/ myelination increase conduction speed
prevents leakage of the electrical current increases the membrane resistance
three ways of enhancing conduction speed
increase axon insulation and diameter to reduce internal resistance but increase membrane resistance, also saltatory conduction
how does botox work
prevents the fusion of vesicles and blocks the synapse
proximal vs distal synapses
the closer the synapse is to the soma the bigger the AP
spatial summation of local potentials causes
takes the neuron above threshold and causes an AP
temporal summation causes
two APs in quick succession
what is subliner summation
also known as shunting
the more proximal to the soma the local potential is the
greater the AP
subliner summation/shunting
the first AP causes the membrane to be depolarised before the second AP reaches it, this makes it harder for the second AP to reach the cell body causing a summation of the APs smaller than what they would be if added together
facilitation
occurs in the pre synaptic terminal, EPSP gets bigger due to repetitive inputs of APs and a build up of calcium in the terminal meaning more vesicles get released at each AP
LTP and LTD
post-synapse change in size of local potential
name the six types of neurotransmitters
ach, biogenic amines, amino acids, purines, gas and peptides
where are the sites of action for Ach
NMJ, autonomic endings, basal ganglia and GI tract
what are the types of biogenic amines
adrenaline, nor adrenaline, serotonin and histamine
where are the three sites that biogenic amines act
brain, spinal cord and sympathetic ends
what are the types of amino acids in the body
glutamate, GABA, aspartate and Gly
where in the body do amino acid neurotransmitters act
brain, spinal cord and retina
what are the types of purines
adenosine and ATP
where in the body do purines act
brain and autonomic ganglia
what is the main gas neurotransmitter in the body and where does it act
nitric oxide and brain, spinal cord, GI tract
what are the main peptides in the body and where do they act
oxytocin and somatostatin they act in the brain, spinal cord and pituitary gland
what is the Ach receptor permeable to
sodium ions
what does P do to the body and why is it bad
increases levels of noradrenaline dopamine and serotonin and is neurotoxic
what does the GPCR Gs do
stimulates adenylyl cyclase
in nicotinic Ach receptors what binds to where to open the pore
Ach binds to the alpha subunit to open the pore
what blocks the nicotinic Ach receptor
bungarotoxin
three types of glutamate receptors
AMPA, NMDA and Kainate
what ion blocks the NMDA receptor
magnesium
which glutamate receptor is critical for LTP
NMDA
what type of potentials do glutamate receptors produce
EPSPs
what does PCP/angel dust do
blocks the NMDA receptor leading to induced psychosis
what effects do metabotropic glutamate receptors have
downstream changes in calcium and phosporylation
how do metaboptropic glutamate receptors cause an increase in calcium ions
when glutamate is released into the synaptic cleft it binds to both the AMPA receptor and the glutamate receptor which drives a signalling change leading to more calcium release
how does a LTD occur
coincidence of both temporal and spatial summation causes a rise in calcium release this causes a long lasting strong synapse
what kind of response does a GABA-A receptor trigger
IPSP , hyperpolarisation
what ion is GABA-A permeable to
chloride
what can block the GABA-A receptor
picrotoxin
