Chapter 3 Synapses Flashcards
What is a reflex?(3.1)
Automatic muscular response to stimuli
What experimental evidence did Sherrington have for synaptic delay? For temporal summation? (3.1)
Pinched a dogs foot…pinched foot flexed after a short delay.
Temporal summation rpt’d stimuli within a brief time have a cumulative effect.
Rpt’d light pinches of a dogs foot=> a response.
What evidence did he have for spatial summation? For coordinated excitation and inhibition? (3.1)
Summation over space- synaptic input form separate locations combine their effects on a neuron eg pinched two points at once on a dog.
Sensory input that arrives at the brain individually produces weak effects but if each neuron receives many incoming axons ensures the response is activated.
Describe John Eccles’s experimental support for Sherrington’s inferences. (3.1)
Eccles measured the post synaptic neuron during synaptic activation. After he had briefly stimulated an axon, Eccles recorded a slight depolarization of the membrane of the postsynaptic cell. Note: this is a partial depolarization also known as a graded potential. A graded potential is know as an excitatory postsynaptic potential. When Eccles stimulated an axon twice, he recorded two EPSPs. If the delay between EPSPs was short enough, the second EPSP added to what was left of the first one, producing temporal summation. A quick sequence of EPSPs combines to exceed the threshold and produce an action potential.
EPSPs (3.1)
Excitatory postsynaptic potential
Which is a graded potential or partial depolarization. Note: graded potentials can either be excitatory or inhibatory.
Spatial Summation (31)
Summation over space.
Synaptic inputs for separate locations combine their effects on a neuron.
What is an EPSP, and what ionic flow is largely responsible for it? (3.1)
Excitatory post synaptic potential aka graded depolarization.
This results from a flow of Na2+ ions into the neuron.
IPSPs (3.1)
Inhibitory postsynaptic potential which is temporary hyperpolarization.
What is an IPSP, and what ionic flows can produce it? (3.1)
Inhibitory postsynaptic potential-temporary hyperpolarization.
Open gate- K leaves cell or Cl enters the cell carrying neg charge.
Re: the relationship among EPSP, IPSP, and action potential. Why may some synapses have a greater influence than other? (3.1)
Different wiring–some need one synapse to excite it, others need 2 and others cause inhibition.
Re: the relationship among EPSP, IPSP and action potential. What influence do EPSPs and IPSPs have on neurons with a spontaneous rate of firing? (3.1)
Spontaneous rate of firing: periodic production of action potentials even without synaptic input.
EPSPs increase the frequency of action potentials
IPSPs decrease the frequency of action potentials
Re; The neuron as a decision maker.
What factors influence a cells “decision” whether or not to produce an action potential? (3.1)
The summation of EPSPs and IPSPs as a decision because it determines whether or not the postsynaptic cell fires and action potential.
What did T. R. Elliott propose? (3.2)
In 1905 he suggested that the sympathetic nerves stimulate muscles by releasing adrenaline or similar chemicals
Describe Loewi’s experiment with the two frogs’ hearts (3.2)
He repeatedly stimulated a frogs vagus nerve, thereby decreasing the heart rate. He then collected fluid from that heart transferred it to a second frogs heart, found that the second heart also decreased its rate of beating. Also did the same with the accelerator nerve => transfer of chemicals and not electricity.
What are the major events, in sequence, at a synapse? (3.2)
- Neuron synthesizes chemicals that serve as neuotransmitters.
- Action potentials travel down the axon at presynaptic terminals. An action potentila enables Ca2+ to enter the cell. Ca2+ releases neurotransmitters from terminals into the synaptic cleft
- Released molecules diffuse aacross the cleft attach to the receptors and alter activity of post synaptic neuron
- Neurotransmitters separate from their receptors
- Neurotransmitters either recycled back into presynaptic neuron or diffuse away
- Some post synaptic cells send reverse messages to control further release of neurotransmitters.
List major neurotransmitters (3.2)
Amino acids containing an amine group (NH2) Monoamines Acetylcholine Neuropeptides Purines Gases (nitric oxide)
How is nitric oxide unlike most other neurotransmitters? (3.2)
(NB this is not laughing gas)
Many neurons release nitric oxide when they are stimulated
Dilates nearby blood vessels=> increased blood flow to brain
When brain area becomes highly active => increased blood flow
How is the synthesis of peptide neurotransmitters different from that of most other neurotransmitters? (3.2)
Synthesis of peptides is from food aa’s
List the three catecholamines in the order of their synthesis. What is their amino acid precursor (3.2)
- dopamine (precursor is phenylalanine)
- Norepinephrine
- Epinephrine
Precursor is phenylalanine (from diet)
=> tyrosine
=> Dopa
=> Dopamine
=> norepinephrine
=> epinephrine
How might one increase the amount of acetylcholine in the brain? Serotonin? (3.2)
Increased choline in the diet (eg milk, eggs, peanuts) => increased acetylcholine
To increase serotonin- tryptophan such as soy and american corn (but decreases consumption of phenylalanine because it competes with binding sites.
How quickly can peptide neurotransmitters be transported to the terminal? Why is this not a problem for smaller neurotransmitter? (3.2)
1-2 miliseconds after calcium enters the presynaptic terminal it causes exocytosis (release of neurotransmitters in bursts form the presynaptic neurons into the synaptic cleft that separates one neuron form another.
Describe the process of exocytosis. (3.2)
Release of neurotransmitters in bursts form presynaptic neuron into the synaptic cleft.
What generalization ca be drawn regarding the release of neurotransmitters at the terminals of given neuron? (3.2)
The brain as a whole uses many neurotransmitters, no single neuron releases them all. Most neurons release a combination of two or more transmitters.
Eg: Motor neurons in the spinal cord have one branch to the muscles, where they release acetycholine and another branch to other spinal cord neurons, where they release both acetylcholine and glutamate.
A neuron releases a combination of transmitters to make the message more complex.
Contrast ionotropic and metabotropic synaptic mechanisms. List three ionotropic neurotransmitters receptors. (3.2)
3.2
Ionotropic receptors form an ion channel pore. Brief on off action
Metabotropic receptors are indirectly linked with ion channels on the plasma membrane of the cell through signal transduction mechanisms often G proteins. Slower but longer lasting effect
Both receptor types are activated by specific neurotransmitters.
Three ionotropic neurotransmitters: Nicotinic acetylcholine (excitatory) Glutamate Glycine -- inhibitory GABA (gamma-amino-butyric acid) inhibitory
Discuss the role of second messengers in producing the metabotropic effects of neurotransmitters. What kinds of changes can they exert? (3.2)
3.2
They initiate a sequence of metabolic reactions that are slower and longer lasting than ionotropic. They emerge 30ms or more after the release of the transmitter
-second messengers communicate to many areas within the cell
What is a G-protein? What is the “first messenger”? Waht is one common second messenger? (3.2)
3.2
a protein couple to guanosine triphosphate=GTP an energy storing molecule
-first messenger is the neurotransmitter.
-Serotonin is a common second messenger.
What is a neromodulator? How does a neromodulator differ from most neurotransmitters? (3.2)
3.2
neuromodulators (aka neuropeptides) have several properties that set them apart from other transmitters
-neurons synthezise most other neurotransmitters in presynaptic terminal it synthesizes neuropeptides in the cell body and then slowly transports them to other parts of the cell.
-Neuropeptides are released mainly by dendrites or others are released at the axon terminal.
-effects for 20 mins and e.g.. impt for hunger thirst etc.
How are ACh, 5-HT, and the catecholamines inactivated? Why is inactivation important? (3.2)
3.2
acetylcholine is broken down by an enzyme actelycholinasesterase=>acetate and choline which are reabsorbed b the prey synaptic terminal.
inactivation is important otherwise->contd stimulation unchecked.
Why should there be multiple receptor rypes for each neurotransmitter? (3.2)
3.2
List six ways in which drugs may affect synaptic function.
3.3
increase or decrease the synthesis of neurotransmitters
cause it to leak from its vesicles
increase its release
decrease its reuptake
block its breakdown into inactive chemicals
acto on the postsynaptic receptors
What is an agonist? An antagonist?
3.3
Agonist: a drug that mimics or increases the effects
Antagonist: a drug that blocks a neurotransmitter
how can one drug be and agonist at a given receptor, while another drug, with similar affinity for that receptor is an antagonist?
3.3
a Drug has an affinity for a receptor if it binds to it but a drugs efficacy is its tendency to activate it.
The drug with high affinity but low efficacy is an antagonist because it occupied the binding site.
What is the effect of the drug AMPT (alpha-methyl-para-tyrosine)? Of tricyclic antidepressants?
3.3
antidepressant
Which brain area is especially important for reinforcement and addiction? What is the effect of dopamin in neurons there?
3.3
nucleus accumbens
addictive activities increase dopamine’s in this area
How were the brain meachanisms of pleasure and reinforcement discovered?
3.3
rates with implanted electrodes in their brain–when stimulated showed a favourable reaction => rats in a box allowed to press lever to produce self stimulus = all areas led to increase in dopamine or norepinephrine in nucleus accumbens
Is dopamine release always associated with pleasure? What evidence suggest that other processes are more closely associated with dopamine release in the nucleus accumbens?
3.3
yes dopamine release is associated with pleasure
-other evidence - sexual excitement stimulates the nucleus accumbens
-so does taste of sugar
-thinking of something pleasant
-gambling
What is the effect of amphetamine on synapses?
3.3
Behavioural effects-excitement, alterness, elevated mood and decreased fatigue
synaptic effects-blocks reuptake of dopamine and several other transmitters
Compare the effects of cocaine with those of amphetamine. What are the similarities and differences?
3.3
Behavioural effects- same excitement, alterness, elevated mood
Synaptic effects-blocks reuptake of dopamine and several other transmitters
-accumulation of dopamine in the synaptic cleft but the XS dopamine washes away faster.
Why do amphetamine and cocaine users frequently report a ‘crash’ a couple of hours after taking the drugs?
3.3
accumulationof dopamine in the synaptic cleft but the XS dopamine washes away faster than the presynaptic cell makes more to replace it. A few hours after taking a stimulate drug.
-a user has a deficit of the tramitters and enters a withdrawal state => reduced energy, decreased motivation and mild depression.
How does dynorphin affect cocaine use?
3.3
reduces the effects of cocaine so hopefully leads to protection against addiction
Why is methylphenidate (Ritalin) usually not abused?
3.3
related to dose and time course.
- the people on the drug take it and experience a gradual increase in the drugs [ ] over an hour then a slow decline so they don’t get that rush like cocaine users do.
What are the physiological effects of MDMA (Ecstasy)?
3.3
Hallucinogenic drug-Methylene dioxymethamphetamine is a stimulant at low dose increasing the release of dopamine and producing effects similar to amphetamine or cocaine.
At higher does it also releases serotonin, altering perception and cognition like hallucinogenic drugs.
What is the basis of nicotine’s reinforcing effects? Is stimulation of all types of acetylcholine receptors reinforcing?
3.3
stimulates a family of acetycholine receptors known as nicotinic receptors which are abundant on neurons that release dopamine in the nucleus accumbens so nicotine increases dopamine there.
What is an endorphin? What is the derivation of its name?
3.3
endogenous morphine
which are neuropeptides produced in the brain.
-indirectly activates dopamine release
How do opiates increase the release of dopamine? How do we know that not all opiate effects are produced by increasing dopamine release?
3.3
opiates relieve pain by acting on receptors in the brain
-opiates stimulate endorphins synapses which inhibits neurons that inhibit release of dopamine
By inhibiting an inhibitor, opiates increase the release of dopamine.
e.g. of opiates – morphine, heroin and methadone.
Which neurotransmitter has effects that are opposite those of dopamine in the nucleus accumbens?
3.3
GABA is a neurotransmitter that inhibits the firing of dopamine neurons
eg morphine, heroin and methadone
What is the main psychoactive chemical in marijuana? Why do marijuana users not experience a sudden crash several hours after taking the drug, as do amphetamine and cocaine users?
3.3
THC delta 9 tetrahydrocannabino and other cannabiniods
-cannabinoids released by the postsynaptic neurons where they inhibit further release of BOTH glutamate and GABA
Which two brain chemcals bind to cannabinoid receptors? How might marijuana decrease nausea?
3.3
1. anandamide
2. sn-2 arachidonylglycerol (2-AG)
decrease serotonin type 3 synapses (5-HT3) which are important for nausea.
Where is the brain are cannabinoid receptors located? Why do large doses of marijuana not threaten breathing or heartbeat?
3.3
located in many areas of the brain BUT are scarce in the medulla–which is the area that controls breathing or heartbeat (note: opiates have a strong effect here)
Which receptor does LSD stimulate? Can we explain the effects of LSD on behaviour?
3.3
a hallucinogenic drug-which distorts perception
-lysergic acid diethyl amine (LSD)–chemically resembles serotonin
-attaches to serotonin type 2A (5HT 2a) receptors and provide stimulation at inappropriate times or for longer than usual durations.
How does caffeine stimulate the nervouse system? What is a effect of adenosine?
3.3
increases metabolism in brain but decreases cerebral blood flow inducing a relative brain hypoperfusion
adenosine is a vasodilator
(information from web)
What are two effects of alcohol on membranes? What type of receptor is made more responsive by alcohol?
3.3
1. facilitates response at GABAa receptor –the brains main inhibitory site
2. blocks activity at the glutamate receptors the brains main excitatory site=> decrease in brain activity
alcohol also increases stimulation at dopamine receptors in nucleus accumbens
What sorts of behaviours have been linked with alternative forms of genes for the D2 and D4 dopamine receptors? How strong is the association?
3.3
stronger than average craving for additional alcohol after one drink
-people can be more impulsive
Δ9-tetrahydrocannabinol (Δ9-THC)
chemical contained in marijuana leaves
Synapse
a specialized gap as a point of communication between two neurons
