What about communication between neurons?

presynaptic ending – ◦ portion of the axon conveying information to

the next neuron

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

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

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

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

AP reaches presynaptic ending-

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

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

NT binds to postsynaptic receptors and causes small local changes in electrical potential (depolarizations or hyperpolarizations)-

◦ Called 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)

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)

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)

postsynaptic receptors open ion channels – ◦ ion channels in postsynaptic membrane (that we

need to worry about) include Na+, Cl- and K+

EPSPs – excitatory postsynaptic potentials

- increase the likelihood of an AP

- opening of

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

◦ 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 can either increase or decrease the likelihood of an action potential

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

Neurotransmitter represents a keyReceptor represents the lock

1. directly opening the ion channel◦ occurs and terminates very quickly

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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

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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)

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

1. acetylcholine (ACh) –•

acetylcholine (ACh) – found in CNS and PNS• receptor subtypes –

• nicotinic and muscarinic

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…

2. Monoamines

1. dopamine (DA)important for reward circuitsschizophrenia and Parkinsons disease

2. Monoamines

1. dopamine (DA)

2. norepinephrine (NE)important for arousalaltered 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 Pimportant for pain

2. endorphins and enkephalins (endogenous opiates)

pain relievers!

4. amino acids (tiny neurotransmitters)

1. glutamateALWAYS EXCITATORY (IE always causes EPSPs)

2. GABA –always inhibitory ( always causes IPSPs)-

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

synthesis of NT storage of NT release of NT binding of NT breakdown of NT

agonist – mimics the neurotransmitter’s effect

antagonist – blocks the neurotransmitter’s effect

acting like a receptor agonist◦ nicotine

ionotropic potent poison

acting like a receptor antagonist◦ curare

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??

alter breakdown of ACh◦ blocks breakdown

mustard gases, insecticides, physostigmine Gulf War Syndrome?

alter release of ACh◦ block release – botulism

alter release of ACh◦block release – botulism◦botox

◦stimulate release – black widow spider venom