14) Synapses Flashcards
IPSP
Inhibitory postsynaptic potential
EPSP - abbreviation
Excitatory postsynaptic potential
EPSP - definition
depolarization of the neuron
IPSP - definition
hyperpolarization of the postsynaptic neuron
What pattern do neurons fire in?
They fire spontaneously at regular rates
What effect does ipsp have on the rate of APs in the post synaptic neuron
decrease
for epsps to increase the rate of APs in the post synaptic neuron what needs to happen
the firing needs to be above the threshold
AP
Action potential
Synapse
Gap between neurons where chemical information is transmitted
where is action potential
presynaptic neuron
where is postsynaptic neuron
post synaptic neuron
Neurotransmitters
chemical particles used to transmit the information through the synapse are called neurotransmitters
tell me about the stability of the amount of neurotransmitters
unstable
explain synaptic process
AP in presynaptic neuron - changes at end of presynaptic neurons membrane - into ‘holes’ in the membrane
- neurotransmitters released into the gap and diffuse across to the postsynaptic neuron
- where they bind to receptors - opening holes in the postsynaptic neuron’s membrane
- this movement of ions in/out of the gap causes post synaptic potential in the postsynaptic neuron
detailed explanation of presynaptic synaptic process
action potential reaches end of axon
depolarization opens calcium gates in the pre synaptic membrane
this provokes the sudden release of neurotransmitters into a synaptic cleft.
what effect do synapses have on the speed of transmission
slow transmission
transmission takes 2ms (0.0000001cm/ms)
how long does synaptic transmission take
transmission takes 2ms (0.0000001cm/ms)
what is the speed of conduction along an axon
4cm/ms
outline a neurotransmitters journey
diffuses across the synaptic gap to reach post synaptic membrane where it is attached to the receptors
then neurotransmitter binds to the receptor gates open in the postsynaptic membrane
what effect does the quantity of NTs have
the quantity of NTs released impacts the robustness of changes in the post synaptic membrane
what is a synapses function
to send chemical information through the gap and open ions’ gates in the post synaptic neuron
How does sodium move through an excitatory synapse
sodium gates open - sodium ions enter the postsynaptic neuron - EPSP
how do chloride and potassium move through the inhibitory synapse
chloride gates open - chloride ions enter postsynaptic neuron - IPSP
potassium gates open - potassium ions leave the post synaptic neuron - IPSP
What element is associated with excitatory synapse
Sodium - Na+
What elements are associated with inhibitory synapses
Potassium and Chloride
Three examples of excitatory neurotransmitters
glutamate
epinephrine
norepinephryne
glutamate
excitatory NT
epinephrine
excitatory NT
norepinephryne
excitatory NT
two examples of inhibitory NTs
GABA
glycine
GABA
Gamma aminobutyric acid
inhibitory NT
glycine
inhibitory NT
three examples of NTs that can be both inhib and excit
acetylcholine
dopamine
serotonin
acetylcholine
inhib and excit NT
dopamine
inhib and excit NT
serotonin
inhib and excit NT
receptors
chemicals specific to a given type of neurotransmitter - each type of NT interact with multiple different types of receptors
what are the two types of receptors
ionotropic and metabotropic
ionotropic receptors
open fast gatest
excit and inhib examples of ionotropic receptor
glutamate - excitatory
GABA - inhibitory
Metabotropic
open slow gates
ionotropic effects on postsynaptic membrane
as soon as NT binds to a receptor on the membrane - the ion gates open
what is the speed of the ionotropic effect
the process starts in 1ms and lasts for 20ms
metabotropic effects on postsynaptic membranes
a sequence of metabolic changes in a larger area of the cell
speed of metabotropic effects
the process starts in 30ms and lasts for seconds, minutes or longer
what two processes use ionotropic synapses
vision
hearing
what three processes use metabotropic synapses
taste
hunger
fear
neuromodulators
chemicals affecting metabotropic receptors
- distinguishes them from the fast effects of the NTs at ionotropic synapses
what chemicals may activate metabotropic receptors
dopamine
norepinephrine
serotonin
neuropeptides
glutamate
GABA
how many NTs do the majority of neurons release?
two or more
each neuron may respond to all types of NTs received at postsynaptic membrane of different synapses
synaptic strength
plasticity
the strength of a synapse is defined by the size of the postsynaptic potential
how may synaptic strength vary?
varies over time
short term changes - seconds minutes
long term changes - memory, learning effects, brain plasticity
long term potentiation
intensive use of a synapse may lead to its potentiation - and therefore stronger effects on postsynaptic membrane
the mechanism behind memory and learning
name two ways that plasticity effects brain development
synaptogenesis (formation of synapses)
synaptic pruning (elimination of unnecessary synapses - age 2 to 16)
what happens to used NTs
three options
action must be terminated to stop effect on the receptor and to allow frequent responding
reuptake
broken down
diffuse
reuptake (NTs)
brings NTs back to the presynaptic neuron (by transporters)
recycling process concerns serotonin and catecholamines
catecholamines
dopamine
norepinephrine
epinephrine
break down of NTs
eg acetylcholine
broken down to remove used NTs
diffusion of used NTs
big NTs (peptides) simply diffuse away
enzymatic degradation
broken down by acetylcholinesterase into acetate and choline
acetylcholine breakdown official name
enzymatic degradation
what cells reabsorb NTs at some synapses
glial cells
how does reabsorption affect synaptic activity
grants of withholds absorption of NTs
astrocyte
an astrocyte encloses the synapse where it absorbs the neurotransmitter glutamate (Glu) from the cleft and recycles glutamate into its precursor glutamine (Gln). Glutamine returns to the presynaptic terminal for re-use.
what are the two types of pharmaceutics that affect synaptic transmission
agonist and antagonist
agonist pharmeceutic
facilitate transmission at synapses
antagonist pharmaceutic
inhibit transmission at synapses
what do agonist/ antagonist pharmaceutics affect
the amount of neurotransmitter in the cleft
risks related to synapses
(8)
amphetamine
cocaine
methylphenidate (Ritalin)
MDMA/ Ecstasy
Nicotine
Opiates (heroin/ morphine)
Cannabinoids (marijuana)
Hallucinogens (LSD)
Amphetamine
Blocks reuptake of dopamine and several others transmitters
Cocaine
Blocks reuptake of dopamine and several others transmitters
Methylphenidate (Ritalin)
Blocks reuptake of dopamine and others , but gradually
MDMA (Ecstasy)
Releases dopamine, serotonin, and norepinephrine
Nicotine
Stimulates nicotinic-feedback receptors on presynaptic cells
Opiates (heroin/ morphine)
stimulates endorphin receptors
cannabinoids (marijuana)
excites negative-feedback receptors on presynaptic cells
hallucinogens (LSD)
stimulates serotonin type 2A receptors ((5-HT)2a)
SSRIs
selective serotonin reuptake inhibitors
ssris process
reuptake of serotonin from the synaptic cleft is reduced - serotonin may bind to receptors several times
drug addiction
brain disease that produces profound modifications in human behaviour
alcohol effects in normal people
increases dopamine release
alcohol effects on alcoholics
reduced number of dopamine receptors
reduced dopamine release
meaning craving
characteristics of risk of addiction
not everyone runs the same risk
dopamine uses several different receptor types
people at risk of addiction are characterised by specific balance of different types of receptors (research in progress)
