what about communication between neurons?. presynaptic ending – ◦ portion of the axon conveying...
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What about communication between neurons?
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presynaptic ending – ◦ portion of the axon conveying information to
the next neuron
Some terms…….
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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…….
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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…….
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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…….
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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
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Presynaptic ending
Postsynaptic ending
synapse
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AP reaches presynaptic ending-
Ca+2 channels in presynaptic ending open and Ca+2 enters
What happens at level of synapse?
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Ca+2 entry into the presynaptic ending critical for neurotransmitter release
Why are Ca+2 ions important?
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drugs that block Ca+2 channels…….
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protein embedded in membrane
mechanism for neurotransmitter to influence postsynaptic activity by binding to receptor
postsynaptic receptors
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NT binds to postsynaptic receptors and causes small local changes in electrical potential (depolarizations or hyperpolarizations)-
◦ Called graded potentials
Summary
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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
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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
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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?
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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?
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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
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http://www.blackwellpublishing.com/matthews/neurotrans.html
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Axon hillock
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◦ 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?
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action potential or
spike
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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
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Graded potentials can either increase or decrease the likelihood of an action potential
Graded vs Action Potentials
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Postsynaptic receptor and NT – think about a lock and key!
So what about these NT?
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Neurotransmitter represents a keyReceptor represents the lock
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1. directly opening the ion channel◦ occurs and terminates very quickly
2 ways that neurotransmitter exert these effects
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http://www.blackwellpublishing.com/matthews/nmj.html
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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
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http://www.blackwellpublishing.com/matthews/neurotrans.html
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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
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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
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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
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probably 100s of “putative” neurotransmitters – more being discovered all the time
role that the novel NTs play still being determined
Neurotransmitters
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1. acetylcholine (ACh) –•
Some classic NT
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acetylcholine (ACh) – found in CNS and PNS• receptor subtypes –
• nicotinic and muscarinic
Some classic NT
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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
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2. Monoamines
1. dopamine (DA)important for reward circuitsschizophrenia and Parkinsons disease
Neurotransmitters (cont)
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2. Monoamines
1. dopamine (DA)
2. norepinephrine (NE)important for arousalaltered activity implicated in depression
Neurotransmitters (cont)
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2. Monoamines
1. dopamine (DA)
2. norepinephrine (NE)
3. serotonin (5HT)aggression, anxiety, depression
Neurotransmitters (cont)
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3. Peptides- really large neurotransmitters
Neurotransmitters (cont)
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3. Peptides
1. substance Pimportant for pain
2. endorphins and enkephalins (endogenous opiates)
pain relievers!
Neurotransmitters (cont)
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4. amino acids (tiny neurotransmitters)
1. glutamateALWAYS EXCITATORY (IE always causes EPSPs)
2. GABA –always inhibitory ( always causes IPSPs)-
Neurotransmitters (cont)
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almost any aspect of the NT function can be affected by drugs!
How can drugs affect a neurotransmitter?
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synthesis of NT storage of NT release of NT binding of NT breakdown of NT
So….
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agonist – mimics the neurotransmitter’s effect
antagonist – blocks the neurotransmitter’s effect
What are possibilities?
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acting like a receptor agonist◦ nicotine
ionotropic potent poison
acting like a receptor antagonist◦ curare
ACh as an example
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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??
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con’t alter breakdown of ACh
◦ blocks breakdown mustard gases, insecticides, physostigmine Gulf War Syndrome?
alter release of ACh◦ block release – botulism
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con’t
alter release of ACh◦block release – botulism◦botox
◦stimulate release – black widow spider venom