Chapter 4 - Electrical & Chemical Signalling Between Neurons Flashcards
epilepsy
accounts of epileptice seizures throughout human history - often attributed to mystical or demonic forces now attributed to misfiring of electrical signals
galviani - 18th century - view on electrical stimulation and behaviour
reflexive responses of disscted frog legs to electrical impulses - figured that must have an impulse at some point
hans berger
inventor of the first EEG
waves differ through stages of sleep
electrical activity in the brain forms different wave patterns
confirmation of evolvement of electricity
microelectrodes
- measure a neuron’s electrical activity
- deliver an electrical current to a single neuron
how can it be easier to measure neuronal activity
since human neurons are very small - it is easier to look at bigger neurons - the giant axon of the squid which is visible to the human eye
cations
positively charged ions - sodium and potassium
anions
negatively charged ions - chloride, A- (negatively charged proteins)
two gradients that control the movement of ions
concentration gradient
voltage gradient
concentration gradient
movement of ions to a space where there are fewer of them
voltage gradient
opposites attract - movement of ions to a space where they are attracted to based on there charge
movement of chloride ions being impacted by both gradients
chloride in one side of the cup
concentration gradient causes it to move to the other side but voltage gradient does not allow a lot to go outside but outside is more negative and inside is more positive
resting potential
-70mV
rmp
a store of negative energy inside the neuron membrane relative to the outside
internal potential at rmp
lots of negative proteins
lots of pottasium
K+ characterstics
eflux of this controls hyperpolarization
easy to get in and out
external potential at RMP
lots of sodium
lots of calcium
Cl- ion characteristics
harder to move in and out
influx of these might cause hyperpolarization
sodium potassium pump
3 NA out
2 K in
Na+ characteristics
causes depolarization by influx
controlled by voltage gated channels
inhibitory signals
hyperpolarization - reduce the chance that an action potential will be created
excitory signals
depolarizatin - increase the chance of the action potential
how an action potential is created
when the membrane recieves enough stimulation - voltage gated sodium channels and sidum flows in (depolarization)
pottasium gates open adn potassium goes out (repolarization)
sodium channels inactivate pottasium keeps flowing out (hyperpolarization)
rules of action potential
- one direction
- length of axon
- all or none law
relative refratory period
During relative refractory, voltage-gated potassium channels are open, allowing positively charged potassium ions to leave the cell. Some voltage-gated sodium channels begin to recover from inactivation and may be opened again.
absolute refractory vs relative refractory
During absolute refractory, the neuron cannot fire another action potential. Relative refractory occurs after absolute refractory. During relative refractory, it is possible for the neuron to produce another action potential, but it requires a much greater stimulus to reach the threshold.
myelin in CNS
oligodendrocyte
myelin in the PNS
shwaan cells
myelin colour
white - white matter
nodes of ranvier
gaps in myelin - where the sodium and potassium channels are
purpose of myelin
signal goes faster - does not recieve resistance at every point - more efficent
saltatory conduction
signal doesn’t react at every point
which disease attacks myelin
MS
2 types of interneuron signals
EPSP + IPSP - inhibitory and excitory
temporal summation
Temporal summation involves a single presynaptic neuron rapid-firing signals to a single postsynaptic neuron’s synapse. Because the signals are received in rapid succession, they compound into a greater signal.
spatial summation
Spatial summation involves multiple presynaptic neurons simultaneously sending signals to a single neuron.
where are signals summed
axon hillock
postsynaptic potentials can be…
graded - vary in strength
what affects the influence of the dendrites
it’s location in relation to the axon hillock - closer = more influence
hair cells + AP
displacement of hair cells opens up mechanically gated sodium channels in the sensory neuron
which causes action potential and causes voltage sensitive pottasiuma dn sodium channels to open
anisthetic
prevent’s action potentials
which cells have a lot of dendrites
cerebellum - purkinje cells
deep brain simulation
electrodes implanted deep in the brain stimulate a targeted area with a low voltage electrical current to facilitate behaviour
- parkinsons, epilepsy, and other brain disorders
deep brain stimulation in parkinson’s
cell die in substantia nigra - in the mid brain - stimulation in this area
hypothesis of the otto loewi
stimulated the vagus nerve of a frog heart in water - slow beating
connected fluid transfer also slowed the heartbeat - evidence of chemical neurotransmitter
1st neurotransmitter
acetylecholine
criteria for identifying neurotransmitters
- chemical must be synthesized or present in neuron - created inside or produced onsite
- when released chemical must produce response in target cell
- same receptor action must be obtained when chemical is experimentally placed on target
4.there must be a mechanism for removal after chemical’s work is done
microtubule
transport structure that acrries substances to the axon terminal
mitchondrion
organelle that provides the cell with energy
synaptic vesicle
round granule that contains neurotransmitter
storage granule
large compartment that holds synaptic vesicles
synaptic cleft
small space seprating presynapti c termicnal and postsynaptic dendritic spine
presynaptic membrane
encloses membrane that transmit chemical messages
postsynaptic membrane
contains receptor molecules that recieve chemical messages
postsynaptic receptor
site to which a neurotransmitter molecule binds
electrical synapses are
gap junctions - fast but inflexible
can’t amplify or diminish signal
neurotransmitter release
action potential reaches terminal
opens calcium channels
calcium binds to protein forming a complex
complex binds to vesicles - releasing some from filaments or exocytosis
steps of neurotransmission
synthesis
release
receptor action
inactivation
synthesis
some neurotransmitters are trandported from the cell nucelus and others are made from building blocks imported into the terminal and are packaged into vesicles
release
in response to an action potential the transmitter is released across the membrane by exocytosis
receptor action
the transmitter crosses the synaptic cleft and binds to a receptor
inactivation
the transmitter is either taken back into the terminal or inactivated in the synaptic cleft
5 types of inactivation
diffusion
enzyme degradation
reuptake
astrocyte uptake
autoreception
diffusion - inactivation
float away - maybe picked up by other cells
enzyme degradation
neurotransmitter will be broken down by enzymes
reuptake
taken back up into presynaptic cell
astrocyte uptake
taken back up by astrocyte and used again at some point
autoreception
might engage the neurotransmitter on presynaptic cell - used as feedback mechanism
neurotransmitter activated receptors
act as binding sites for specific neurotransmitters
two types of receptors
ionotropic + metbotropic
ionotropic receptor
simple
fast
lets ions in
depolarixe or hyperpolarize
metabotropic receptor
involved and delayed
g protein + 2nd messenger
first messenger is metabotropic receptor
second messenger is g protein which sends enzyme to nucleus to change DNA
dna change by metatropic receptor
results in structural changes in neurons
examples of plastic changes in neuron
- increased axonal transport
- increase in number of synaptic vesicles
- changes in size of synaptic cleft
- change in stem length and width
- increase in protein transport for spine construction
- increase in size or area of spine
- increase in density of contact zones
- increase in size or area of terminal
- more dendrites
goes both ways - increase/decrease
changes dont stay
neurotransmitter activating systems
a series of connected neural pathways in which one specific neurotransmitter dominates
main neurotransmitters
acetylecholine
dopamine
norepinphrine
serotonin
acetylcholine function
in cholinergic system - midbrain and basal forebrain
learning, memory
with attention and waking us up
primary NT of the PNS
goes to muscle fibers and depolarizes
norepinephrine function
in the noradrenergic system
provides energy to sympathetoc nervous system to kickstart with acetylcholine
two main pathways of dopamine
nigrostriatal and mesolimbic pathway
nigrostriatal pathway for dopamine
repetitive and moderated movements in the substantia nigra
mesolimbic pathway for dopamine
in the basal ganglia - nucleus accumbens - reward center
overactivity of dopamine leads
schizophrenia
seratonin function
in brainstem and digestin
- mood and emotion
schizophrenia + lsd - HALLUCINATONS
controls appetitive since its lined with seratonin neurons
major NT in sleep cycles
glutamate
excitory in the CNS
most numerous
GABA
inhibitory in the CNS
neuroinflammatory response
defense mechanisms that intially protect the brain against pathogens
carried out by microglia and assisted by atsrocytes
glutamate and GAB modulate
too much glutamate
excitoprosisity - overexitability - overinflammation - damage aka stroke
astrocytes supposed to help with reuptake of glutamate
role of microglia and astrocytes in neurodegenerative diseases
both can switch from neuroptoective role to neurotoxic one - may differ with the severity and stage of disease
neuropeptide NTs
opiods and endorphins
natural painkillers - drugs
agonist
substance that enhances the function of neurtransmitters at a synapse
antagonist
substance that inhibits the function of neurotransmitters at a synapse
Ach agonist - diet
choline rish diet increases acetylcholine - not produced naturally in CNS
agonist ACh - black widow
starts as agonist - increases acetylcholine - muscle switches - exahusts - rigid muscle - stop breathing - not usually in humans
botulin antagonist Ach
boutlin toxin blocks release - type of food poisioning
agonist Ach nicotine
nicotine stimulates Ach with sensitivyt increase for nicotine - increases focus
anatognist in Ach - curare
blocks and crowds receptors
agonsit - Ach enzymes
physostigmine and organophosphates block enzyme degradation
agonist MAO inhibior seratonin
inhibits breakdown of seratonin so there is more for release
selective seratonin reuptake - agonist
block transporter protein for serotonin reuptake so that serotonin stays in the syanpse longer
