What about communication between neurons? - PowerPoint Presentation

Slide1

What about communication between neurons?Slide2
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presynaptic ending –

portion of the

axon

conveying information to the next neuron

Some terms…….Slide4
Slide5

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…….Slide6
Slide7

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…….Slide8
Slide9

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…….Slide10
Slide11

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 neuronSlide12

Presynaptic

ending

Postsynaptic ending

synapseSlide13

AP reaches presynaptic ending-

Ca+2 channels in presynaptic ending open and Ca+2 enters

What happens at level of synapse?Slide14

Ca

+2

entry into the presynaptic ending

critical for neurotransmitter release

Why are Ca

+2

ions important?Slide15
Slide16

drugs that block Ca

+2

channels…….Slide17

protein embedded in membrane

mechanism for neurotransmitter to influence postsynaptic activity by binding to receptor

postsynaptic receptorsSlide18

NT binds to postsynaptic receptors and causes

small local changes

in electrical potential (

depolarizations or hyperpolarizations)-

Called graded potentials

SummarySlide19

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 PotentialsSlide20
Slide21

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 PotentialsSlide22
Slide23

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?

Slide24

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?

Slide25

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

Slide26

http://www.blackwellpublishing.com/matthews/neurotrans.htmlSlide27

Axon hillockSlide28

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? Slide29
Slide30

action potential or

spikeSlide31

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 Slide32

Graded potentials can either increase or decrease the likelihood of an action potential

Graded vs Action PotentialsSlide33
Slide34

Postsynaptic receptor and NT – think about a lock and key!

So what about these NT? Slide35

Neurotransmitter represents a key

Receptor represents the lockSlide36

directly opening the ion channel

occurs and terminates very quickly

2 ways that neurotransmitter exert these effects Slide37
Slide38

http://www.blackwellpublishing.com/matthews/nmj.htmlSlide39

directly opening the ion channel

occurs and terminates very quickly

more indirect

ultimately opens ion channel via stimulating a chemical reaction

takes longer but lasts longer

2 ways that neurotransmitter exert these effects Slide40
Slide41

http://www.blackwellpublishing.com/matthews/neurotrans.htmlSlide42

1. reuptake - most common

protein on

presynaptic

ending transports it back into the neuron that released itMeans of recycling NTsaving 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 synapseSlide43

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 inhibitorsSlide44

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 synapseSlide45

probably 100s of “putative” neurotransmitters – more being discovered all the time

role that the novel NTs play still being determined

Neurotransmitters Slide46

acetylcholine (ACh) –

Some classic NTSlide47

acetylcholine (

ACh) – found in CNS and PNS

receptor subtypes –

nicotinic and muscarinic

Some classic NTSlide48

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 NTsSlide49

Monoamines

dopamine (DA)

important for reward circuits

schizophrenia and Parkinsons disease

Neurotransmitters (cont)Slide50

Monoamines

dopamine (DA)

norepinephrine (NE)

important for arousal

altered activity implicated in depression

Neurotransmitters (cont)Slide51

Monoamines

dopamine (DA)

norepinephrine (NE)

serotonin (5HT)

aggression, anxiety, depression

Neurotransmitters (cont)Slide52

Peptides- really large neurotransmitters

Neurotransmitters (cont)Slide53

Peptides

substance P

important for pain

2. endorphins and enkephalins (endogenous opiates)

pain relievers!

Neurotransmitters (cont)Slide54

4. amino acids (tiny neurotransmitters)

glutamate

ALWAYS EXCITATORY (IE always causes EPSPs

)

2. GABA

–

always

inhibitory ( always causes IPSPs)

-

Neurotransmitters (cont)Slide55

almost any aspect of the NT function can be affected by drugs!

How

can drugs affect a neurotransmitter? Slide56

synthesis of NT

storage of NT release of NTbinding of NT

breakdown of NT

So….Slide57

agonist – mimics the neurotransmitter’s effect

antagonist – blocks the neurotransmitter’s effect

What are possibilities?Slide58
Slide59

acting like a receptor agonist

nicotine

ionotropic

potent poisonacting like a receptor antagonistcurare

ACh as an example Slide60

con’t

alter breakdown of

ACh

blocks breakdown

mustard gases, insecticides,

nerve gases

Sarin

- estimated to be over 500 times more toxic than cyanideGulf War Syndrome?other current syndromes??Slide61

con’t

alter breakdown of ACh

blocks breakdown

mustard gases, insecticides, physostigmine

Gulf War Syndrome?

alter release of ACh

block release – botulismSlide62
Slide63

con’t

alter release of

ACh

block release –

botulism

botox

stimulate release – black widow spider venom