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What about communication between neurons?
presynaptic ending – ◦ portion of the axon conveying information to
the next neuron
Some terms…….
presynaptic ending – ◦ the portion of the axon that is conveying
information to the next neuron
synapse or synaptic cleft◦ the space between neurons where
communication occurs
Some terms…….
presynaptic ending – ◦ the portion of the axon that is conveying
information to the next neuron
synapse or synaptic cleft◦ the space between neurons where
communication occurs postsynaptic membrane
◦ the portion of the neuron (usually dendrite) that receives information
Some terms…….
presynaptic ending – ◦ the portion of the axon that is conveying information to the
next neuron
synapse or synaptic cleft◦ the space between neurons where communication occurs
postsynaptic membrane
◦ the portion of the neuron (usually dendrite) that receives information
pre and postsynaptic receptors
◦ proteins in both the presynaptic and postsynaptic ending that allow for information to be transferred
Some terms…….
synaptic vesicles --small enclosed membranes that contain neurotransmitter - found in presynaptic ending
neurotransmitter – substance in vesicles that are released in synapse and convey info to the next neuron
Presynaptic ending
Postsynaptic ending
synapse
AP reaches presynaptic ending-
Ca+2 channels in presynaptic ending open and Ca+2 enters
What happens at level of synapse?
Ca+2 entry into the presynaptic ending critical for neurotransmitter release
Why are Ca+2 ions important?
drugs that block Ca+2 channels…….
protein embedded in membrane
mechanism for neurotransmitter to influence postsynaptic activity by binding to receptor
postsynaptic receptors
NT binds to postsynaptic receptors and causes small local changes in electrical potential (depolarizations or hyperpolarizations)-
◦ Called graded potentials
Summary
increase or decrease the likelihood of the neuron receiving info to generate an action potential◦ graded potentials that increase the likelihood of an action
potential are called EPSPs (excitatory postsynaptic potentials)
Graded Potentials
increase or decrease the likelihood of the neuron receiving info to generate an action potential◦ graded potentials that increase the likelihood of an action
potential are called EPSPs (excitatory postsynaptic potentials)
◦ graded potentials that decrease the likelihood of an action potential are called IPSPs (inhibitory postsynaptic potentials)
Graded Potentials
NT binding to postsynaptic receptors cause local ion channels to open
chemically dependent ion channels ◦ (in contrast with electrically dependent ion
channels in the axon)
How does the neurotransmitter cause EPSPs and IPSPs?
postsynaptic receptors open ion channels – ◦ ion channels in postsynaptic membrane (that we
need to worry about) include Na+, Cl- and K+
How does the neurotransmitter cause EPSPs and IPSPs?
EPSPs – excitatory postsynaptic potentials
- increase the likelihood of an AP
- opening of
IPSPs – inhibitory postsynaptic potentials
decrease the likelihood of an AP
- opening of
Two kinds of Graded Potentials
http://www.blackwellpublishing.com/matthews/neurotrans.html
Axon hillock
◦ graded potentials are summed at axon hillock and……if the sum is a great enough depolarization….
How do graded potentials result in an action potential?
action potential or
spike
Graded Potentials and AP differ in a number of ways
◦ AP – occurs at the axon◦ GP – occurs anywhere the neuron receives info
from another neuron (usually dendrite although NOT ALWAYS)
◦ action potentials are “all or none”graded potentials decrease over space and
time◦ Graded potentials are localized – has
impact in limited region; AP travels down the axon
Graded potentials vs action potentials
Graded potentials can either increase or decrease the likelihood of an action potential
Graded vs Action Potentials
Postsynaptic receptor and NT – think about a lock and key!
So what about these NT?
Neurotransmitter represents a keyReceptor represents the lock
1. directly opening the ion channel◦ occurs and terminates very quickly
2 ways that neurotransmitter exert these effects
http://www.blackwellpublishing.com/matthews/nmj.html
1. directly opening the ion channel◦ occurs and terminates very quickly
2. more indirect ◦ ultimately opens ion channel via stimulating a
chemical reaction takes longer but lasts longer
2 ways that neurotransmitter exert these effects
http://www.blackwellpublishing.com/matthews/neurotrans.html
1. reuptake - most common ◦ protein on presynaptic ending transports it back
into the neuron that released it◦ Means of recycling NT
saving energy (neurons have to synthesize or produce their own NT)
◦ a common way for drugs to alter normal communication
2 main ways for getting the neurotransmitter out of the synapse
cocaine, amphetamine, methylphenidate (Ritalin) – block reuptake of a number of NT – particularly dopamine (reward)
many of the newer antidepressants are SSRIs (selective serotonin reuptake inhibitors)
Examples of reuptake inhibitors
2. enzyme degradation ◦ enzyme - speeds up a reaction
◦ ex. acetylcholine (ACh)is a neurotransmitter is broken down by acetylcholinesterase (AChE) For ACh – this is done in the synapse
probably 100s of “putative” neurotransmitters – more being discovered all the time
role that the novel NTs play still being determined
Neurotransmitters
1. acetylcholine (ACh) –•
Some classic NT
acetylcholine (ACh) – found in CNS and PNS• receptor subtypes –
• nicotinic and muscarinic
Some classic NT
acetylcholine (ACh) – found in CNS and PNS• receptor subtypes –
• nicotinic and muscarinic
• nicotinic receptors – muscles
• acetylcholine also important for various behaviors including learning and memory alzheimers disease, REM sleep, among other things…
Some classic NTs
2. Monoamines
1. dopamine (DA)important for reward circuitsschizophrenia and Parkinsons disease
Neurotransmitters (cont)
2. Monoamines
1. dopamine (DA)
2. norepinephrine (NE)important for arousalaltered activity implicated in depression
Neurotransmitters (cont)
2. Monoamines
1. dopamine (DA)
2. norepinephrine (NE)
3. serotonin (5HT)aggression, anxiety, depression
Neurotransmitters (cont)
3. Peptides- really large neurotransmitters
Neurotransmitters (cont)
3. Peptides
1. substance Pimportant for pain
2. endorphins and enkephalins (endogenous opiates)
pain relievers!
Neurotransmitters (cont)
4. amino acids (tiny neurotransmitters)
1. glutamateALWAYS EXCITATORY (IE always causes EPSPs)
2. GABA –always inhibitory ( always causes IPSPs)-
Neurotransmitters (cont)
almost any aspect of the NT function can be affected by drugs!
How can drugs affect a neurotransmitter?
synthesis of NT storage of NT release of NT binding of NT breakdown of NT
So….
agonist – mimics the neurotransmitter’s effect
antagonist – blocks the neurotransmitter’s effect
What are possibilities?
acting like a receptor agonist◦ nicotine
ionotropic potent poison
acting like a receptor antagonist◦ curare
ACh as an example
con’t alter breakdown of ACh
blocks breakdown◦ mustard gases, insecticides, ◦ nerve gases
Sarin - estimated to be over 500 times more toxic than cyanide
◦ Gulf War Syndrome?◦ other current syndromes??
con’t alter breakdown of ACh
◦ blocks breakdown mustard gases, insecticides, physostigmine Gulf War Syndrome?
alter release of ACh◦ block release – botulism
con’t
alter release of ACh◦block release – botulism◦botox
◦stimulate release – black widow spider venom