Transcript How do neurons communicate?

What about communication between
neurons?
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presynaptic ending –
◦ portion of the axon conveying information to the
next neuron
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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
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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
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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
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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
synapse
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AP reaches presynaptic endingCa+2 channels in presynaptic ending open
and Ca+2 enters
Why are Ca+2 ions important?
Ca+2 entry into the presynaptic ending
critical for neurotransmitter release
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
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NT binds to postsynaptic receptors and causes
small local changes in electrical potential
(depolarizations or hyperpolarizations)◦ Called 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)
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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)
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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)
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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+
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EPSPs – excitatory postsynaptic potentials
 - increase the likelihood of an AP
 - opening of
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IPSPs – inhibitory postsynaptic potentials
 decrease the likelihood of an AP
 - opening of
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Axon hillock
◦ graded potentials are summed at axon
hillock and……if the sum is a great enough
depolarization….
action potential or
spike
Graded Potentials and AP differ in a number
of ways
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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
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Graded potentials can either increase or decrease
the likelihood of an action potential
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Postsynaptic receptor and NT – think about a
lock and key!
Neurotransmitter represents a key
Receptor represents the lock
directly opening the ion channel
1.
◦
occurs and terminates very quickly
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directly opening the ion channel
1.
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occurs and terminates very quickly
more indirect
2.
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ultimately opens ion channel via stimulating a
chemical reaction
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takes longer but lasts longer
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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
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)
enzyme degradation
2.
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enzyme - speeds up a reaction
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ex. acetylcholine (ACh)is a neurotransmitter is
broken down by acetylcholinesterase (AChE)
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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
acetylcholine (ACh) –
1.
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acetylcholine (ACh) – found in CNS and PNS
• receptor subtypes –
• nicotinic and muscarinic
acetylcholine (ACh) – found in CNS and PNS
• receptor subtypes –
• nicotinic and muscarinic
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nicotinic receptors – muscles
acetylcholine also important for various
behaviors including learning and memory
alzheimers disease, REM sleep, among other
things…
2.
Monoamines
1. dopamine (DA)
important for reward circuits
schizophrenia and Parkinsons disease
2.
Monoamines
1. dopamine (DA)
2. norepinephrine (NE)
important for arousal
altered activity implicated in depression
2.
Monoamines
1. dopamine (DA)
2. norepinephrine (NE)
3. serotonin (5HT)
aggression, anxiety, depression
3.
Peptides- really large neurotransmitters
3.
Peptides
1. substance P
important for pain
2. endorphins and enkephalins (endogenous
opiates)
pain relievers!
4. amino acids (tiny neurotransmitters)
1. glutamate
ALWAYS EXCITATORY (IE always causes EPSPs)
2. GABA –
always inhibitory ( always causes IPSPs)
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almost any aspect of the NT function can be
affected by drugs!
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synthesis of NT
storage of NT
release of NT
binding of NT
breakdown of NT
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agonist – mimics the neurotransmitter’s
effect
antagonist – blocks the neurotransmitter’s
effect
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acting like a receptor agonist
◦ nicotine
 ionotropic
 potent poison
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acting like a receptor antagonist
◦ curare
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alter breakdown of ACh
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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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alter breakdown of ACh
◦ blocks breakdown
 mustard gases, insecticides, physostigmine
 Gulf War Syndrome?
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alter release of ACh
◦ block release – botulism
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alter release of ACh
◦ block release – botulism
◦ botox
◦ stimulate release – black
widow spider venom