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Psych2221B > Synapses > Flashcards

Synapses Flashcards

1
Q

reflex arc

A

Reflex arc = reflex action to stimuli
What reflex arc looks like, at the level of the spinal cord: sensory neuron get info from tactile info at skin –> propagates the signal to an interneuron –> interneuron becomes excited –> excites motor neuron –> excites the muscle.

a reflex must require communication between neurons, thus reflex can be used to study synapses!

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2
Q

Sherrington’s (3) observations

A
  1. Reflexes are slower than conduction along an axon
  2. Several weak stimuli present at slightly different times or slightly different locations produce a stronger reflex than a single stimulus
  3. As one set of muscles becomes excited, another set relaxes = there are inhibitory and excitatory synapses.
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3
Q

Which as faster, conduction solely along axon, or conduction including a synapse?

A

Conduction along axon (40 m/s).

conduction along a synapses is slower, approx 15 m/s

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4
Q

Temporal summation

A

Pulses that occur at approximately the same time on a membrane are summed. (temporal and spatial often occur concurrently)

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5
Q

Spatial summation

A

Pulses that occur different places on a membrane (somewhat same time) are summed (temporal and spatial often occur concurrently)

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6
Q

Excitatory postsynaptic potential (EPSP)

A

Graded depolarization of postsynaptic neuron - creates action potential if depolarization is strong enough.
EPSPs are associated with the opening of sodium channels: allows influx of Na+.
EPSP and IPSP occur at level of synapse

• EPSPs increase the number of action potentials above the spontaneous (what they would do without synaptic input) firing rate

Shown by Eccles (1964) - attached microelectrodes to stimulate axons of presynaptic neurons while he recorded from the postsynaptic neuron. He made one, two, three, etc stimulations, at 3 exceeding threshold

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7
Q

graded depolarization

A

depolarization isn’t JUST an all or nothing: depolarization occurs (-70, -65, -55 etc = graded) , and when reaching the threshold of -55 = action potential.

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8
Q

Inhibitory Postsynaptic Potential (IPSP)

A

• Temporary hyperpolarization of a membrane
• Serves as an active “brake” that suppresses excitation
• IPSPs are associated with the opening of potassium channels (allows an efflux of K+ (flows OUT of cells = cell becomes even more negative = hyperpolarization) or with the opening of chloride channels (allows an influx of Cl−).
EPSP and IPSP occur at level of synapse

• IPSPs decrease the number of action potentials below the spontaneous firing rate

Sherrington noted in studies of reflex arc, when one dog leg contracted, the other legs extended. (excitatory message to one leg, inhibitory to other legs)

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9
Q

Summation of Graded Potentials – relationship between EPSP, IPSP and Action Potential

A

EPSP and IPSP occur at level of synapse (at dendritic tree (and cell body)) –> all get integrated and summated at axon hillock
• The axon hillock
• Junction of cell body and axon

EPSPs increase the number of action potentials above the spontaneous (what they would do without synaptic input) firing rate

IPSPs decrease the number of action potentials below the spontaneous firing rate

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10
Q

Neurotransmitters

A

chemicals that travel across the synapse allow for communication

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11
Q

How was it “established” that neurons communicate via chemicals? (at least majority of neurons)

A
  • Otto Loewi’s experiment (1921)
  • Frog heart in saline bath –> electrically stimulated vagus nerve
  • Transfer of fluid from container with stimulated heart to container with non-stimulated heart
  • Stimulating heart = decreased heart rate –> also decreased rate in non-stimulated container
  • = chemicals (Acetylcholine) from fluid transferred to non-stimulated heart –> decreased the HR
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12
Q

nitric oxide

A

neurotransmitter - gas - poisonous in large quantities - many neurons contain an enzyme that enables them to make it efficiently – stimulates nearby neurons to release nitric oxide + dilates the nearby blood vessels, thereby increasing blood flow to that brain area.

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13
Q

How are neurotransmitters synthesized?

A

Neurons synthesize nearly all neurotransmitters from amino acids, which the body obtains from proteins in the diet.

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14
Q

How is acetulcholine synthesize?

A

Acetylcholine is synthesized from choline, which is abundant in milk, eggs, and peanuts

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15
Q

How are catecholamines (dopamine, norepinephrine, and epinephrine) synthesized?

A

amino acids phenylalanine and tyrosine, present in proteins, are precursors of dopamine, norepinephrine, and epinephrine (catecholamines). (phenylalanine –> tyrosine –> dopa –> catecholamines)

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16
Q

What NTs are included in the concept “catecholamines”?

A

dopamine, norepinephrine, and epinephrine

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17
Q

How is serotonin synthesized?

A

the amino acid tryptophan –> 5-hydroxytryptophan –> serotonin

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18
Q

Can drugs alter synthesis of NTs?

A

Yes, several drugs act by altering the synthesis of transmitters. L-dopa, a precursor to dopamine, helps increase the supply of dopamine. It is a helpful treatment for people with Parkinson’s disease

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19
Q

The 6 types of NTs

A

amino acids, modified amino acids, monoamines (First 3 are “small molecule NTs”), Neuropeptides, Purines, gasses

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20
Q

Amino acid NTs include…

A

Glutamate, GABA;glycine, asparate, maybe others

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21
Q

Modified amino acid NTs include…

A

Acetylcholine

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22
Q

Monoamine NTs include…

A

Serotonin, catecholamines (dopamine, norepinephrine, and epinephrine)

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23
Q

Neuropeptide NTs include…

A

Endorphins, substance P, neuropeptide y, others

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24
Q

Purine NTs include…

A

ATP, adenosine, others

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25
Q

Gas NTs include…

A

Nitric oxide (NO), maybe others

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26
Q

Where are NTs stored?

A

Most neurotransmitters are synthesized in the presynaptic terminal, near the point of release - small molecyule NTs typically stored in vesicles.

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27
Q

Glutamate

A

Main excitatory NT

28
Q

GABA

A

Main inhibitory NT (Gamma aminobutyric acid)

29
Q

Noepinephrine

A

Catecholamine - help control alertness and arousal

30
Q

Serotonin

A

affects mood, hunger, sleep, arousal

31
Q

Dopamine

A

Catecholamine - influences movement, emotion, learning and attention

32
Q

Acetylcholine

A

muscle action, learnign, memory (slows down HR)

33
Q

Vesicles

A

(for small molecule NTs) tiny spherical packets located in the presynaptic terminal where neurotransmitters are held for release

34
Q

MAO (monoamine oxidase)

A

breaks down excess levels of some neurotransmitters (so they don’t become toxic) - Neurons that release serotonin, dopamine, or norepinephrine contain
an enzyme, MAO
– there are drugs MAOI’s (I = inhibitor) that inhibit, so it leaves more NT in synaptic cleft –> drug treatment of e.g. depression (increase of serotonin)

35
Q

Exocytosis

A

bursts of release of neurotransmitter from the presynaptic terminal into the synaptic cleft (Triggered by an action potential)

36
Q

Endocytosis

A

Neuron “intakes” an NT.

37
Q

How does Release and Diffusion of Transmitters occur?

A

At the end of an axon, an action potential itself does not release the neurotransmitter. Rather, depolarization opens voltage dependent calcium gates in the presynaptic terminal. Within 1 or 2 milliseconds (ms) after calcium enters the terminal,
it causes exocytosis—bursts of release of neurotransmitter from the presynaptic neuron. An action potential often fails to release any transmitter, and even when it does, the amount varies.–> Neurotransmitter diffuses (takes approx 0.01 ms in time) across the synaptic cleft (20-30 nanometers wide) to the postsynaptic membrane, where it attaches to a receptor (quite quick process). Often, neurons release a combination of two or more transmitters at a time (simultaneous or slightly later), sometimes different NTs from different branches. What NTs a neuron release may change over time (e.g. summer and winter)  all of this makes neuronal behavior flexible.

Effect of an NT depends on the RECEPTOR it binds to

38
Q

Ionotropic receptor

A

A pore that regulates ion flow to directly and rapidly change membrane voltage - Allows ions such as Na+, K+, and Ca2+ across a membrane.

When NT binds to receptor = opens pore = influx of ions = change of membrane potential. This effect is faster, but not so long in duration.

An ionotropic synapse has effects localized to one point on the membrane

For vision and hearing, the brain needs rapid, up-to-date information, the kind that ionotropic synapses bring where timin is important)

Typic NTs for ionotropic receptors: glutamate (typically excitatory) and GABA (typically inhibitory)
The ionotropic effects begin quickly, typically less than a millisecond after the transmitter attaches. The effects decay with a half-life of about 5 ms.

39
Q

Metabotropic receptor (and second messenger systems)

A

A receptor that has a more complex signalling system - instead of directly opening a pore, when an NT binds, it provokes a “second messenger” inside the cell to start an act, causing an effect inside the cell, e.g. opening pores somewhere - this effect is slower, but also longer in duration.
a metabotropic synapse, by way of its second messenger, influences activity in much or all of the cell and over a longer time.
• Metabotropic events include such behaviors as taste, smell, and pain
examples: Dopamine, Norepinephrine, Serotonin

metabotropic synapses are better suited for more enduring effects such as taste, where exact timing isn’t as important (e.g. thirst, hunger)

When a neurotransmitter
attaches to a metabotropic receptor, it bends the receptor
protein that goes through the membrane of the cell. The other
side of that receptor is attached to a G protein—that is, a
protein coupled to guanosine triphosphate (GTP), an energystoring
molecule. Bending the receptor protein detaches that G protein, which is then free to take its energy elsewhere in
the cell. The result of that G protein is increased concentration of a second messenger, such as cyclic
adenosine monophosphate (cyclic AMP), inside the cell.
Just as the “first messenger” (the neurotransmitter) carries
information to the postsynaptic cell, the second messenger
communicates to areas within the cell. It may open or close
ion channels in the membrane or activate a portion of a chromosome.

40
Q

Neuropeptides

A
  • Neuropeptides are often called neuromodulators
  • Synthesized in soma rather than at presynaptic terminal and transported to other parts of the neuron.
  • neuropeptides are released mainly by dendrites, and also by the cell body and by the sides of the axon.
  • Release requires repeated stimulation (opposed to typical small-molecule NT only require one action potential)
  • Released peptides trigger other neurons to release same neuropeptide
  • Diffuse widely and affect many neurons via metabotropic receptors.
  • longer lasting effects (approx 20 minutes)
41
Q

Agonist drug

A

Substance that enhances the function of a synapse – mimics the effect of the NT

42
Q

Antagonist

A

Substance that blocks or decreases the function of a synapse - works counter to the NT

43
Q

hallucinogenic drugs

A

Chemically resemble serotonin in their molecular shape (e.g., LSD) –> able to bind onto serotonin receptor.

Stimulate serotonin type 2A receptors (5-HT2A) at inappropriate times or for longer duration than usual, thus causing their subjective effect

44
Q

Nicotine

A

stimulates acetylcholine receptors - also known as nicotinic receptors. Because nicotinic receptors are abundant on neurons that release dopamine, nicotine increases dopamine release nicotine is rewarding.

45
Q

Opiate drugs

A
  • The brain produces certain neuropeptides now known as endorphins (endorphins = important for pain management)
  • Opiate drugs exert their effects by binding to the same receptors as endorphins –> give us the high, as if you overproduced a naturalistic endorphin.
  • Opiates used medically for pain management.
46
Q

Stimulant drugs

A

mostly dopamine agonists

  • Amphetamine and cocaine - Stimulate dopamine synapses by increasing the release of dopamine from the presynaptic terminal (they can also do this by decreasing the reuptake of dopamine = more dopamine in synapse)
  • Methylphenidate (Ritalin) (often prescriped, is a type of dopamine agonist I understand) - Also blocks the reuptake of dopamine but in a more gradual and more controlled rate. - Often prescribed for people with ADD (also for schizophrenia, it improves psychosis)
47
Q

Amphetamine and cocaine

A

Stimulate dopamine synapses by increasing the release of dopamine from the presynaptic terminal (they can also do this by decreasing the reuptake of dopamine = more dopamine in synapse)

48
Q

Methylphenidate (Ritalin)

A

blocks the reuptake of dopamine but in a more gradual and more controlled rate (comapred to amphetamine and cocaine).

49
Q

Reuptake

A

The presynaptic neuron takes up much or most of the released neurotransmitter molecules intact and reuses them. The process occurs through special membrane proteins called transporters.  transmitter molecules that the transporters do not take will instead break down by an enzyme called COMT (not sure if this is only for serotonin and catecholamines) and are washed out. OBS stimulant drugs (like cocaine) can inhibit the transporters, decreasing reuptake and prolonging effects of NTs (possibly this only applies to dopamine, serotonin and noepinepphrine).  COMT breaks down excess faster than presynaptic cell can reproduce  dopamine deficiency  small depression after cocaine use.

50
Q

How does “Negative feedback” occur?

A
  1. Autoreceptors (on the presynaptic neuron): respond to the released transmitter and inhibit further synthesis and release
  2. Postsynaptic neurons: release chemicals (“reverse transmitters”) that travel back to the presynaptic terminal where they inhibit further release
    • E.G. Anandamide and 2-AG (sn-2 arachidonylglycerol)
51
Q

Autoreceptors (on the presynaptic neuron):

A

espond to the released transmitter and inhibit further synthesis and release

52
Q

reverse transmitters

A

Postsynaptic neurons release chemicals (“reverse transmitters”) that travel back to the presynaptic terminal where they inhibit further release
• E.G. Anandamide and 2-AG (sn-2 arachidonylglycerol)

53
Q

Cannabinoids

A
  • The active chemicals (THC) in marijuana bind to anandamide or 2-AG receptors on presynaptic neurons or GABA
  • Cannabinoids attach to the receptors and the presynaptic cell stops sending neurotransmitter (both the excitatory and inhibitory NTs)
  • Chemicals in marijuana decrease both excitatory and inhibitory messages from many neurons –> just less brain activity I guess
  • Typical behavioral effects might be decrease in anxiety.
54
Q

Electrical Synapses

A
  • A few special-purpose synapses operate electrically
  • Faster than all chemical transmissions
  • Gap junction: the direct contact of the membrane of one neuron with the membrane of another
  • Fairly large pores of the membrane of one neuron line up precisely with similar pores in the membrane of the other cell. These pores are large enough for sodium and other ions to pass readily, and unlike the other membrane channels we have considered, these pores remain open constantly. Therefore, whenever one of the neurons is depolarized, sodium ions from that cell can pass immediately into the other neuron and depolarize it, too.
  • Depolarization occurs in both cells (neurons act as if they were one – they act in synchrony – important for functions such as rhythmic breathing)
55
Q

Hormones

A

• Chemicals secreted by a gland or other cells that is transported to other organs by the blood where it alters activity
• Produced by endocrine glands
• Important for triggering long-lasting changes in multiple parts of the body
Two types of hormones
are protein hormones and peptide hormones, composed
of chains of amino acids. (Proteins are longer chains
and peptides are shorter.) Protein and peptide hormones
attach to membrane receptors, where they activate a
second messenger within the cell—exactly like a metabotropic synapse.

56
Q

Amphetamine

A

blocks reuptake of dopamine (blocks transporters) (and others)

57
Q

Cocaine

A

blocks reuptake of dopamine (blocks transporters)

58
Q

Methylphenidate (Ritalin)

A

blocks reuptake of dopamine (GRADUALLY!)

59
Q

MDMA / ecstasy

A

release dopamine + serotonin

60
Q

Nicotine

A

stimulates nicotinic-type acetylcholine receptor  increase dopamine release in nucleus accumbens (= why nicotine is rewarding)

61
Q

Opiates (heroin, morphine)

A

stimulates endorphin receptors

62
Q

Cannabinoids

A

excites negative-feedback receptors (normally responding to anandamide and 2AG) on presynaptic cells  signals to cell that it should stop producing NTs  decreased overall activity.

63
Q

Hallucinogens (e.g. LSD)

A

stimulates serotonin (type 2A) receptors

64
Q

Alcohol

A

Alcohol enters the brain and interacts with GABA receptors to make them more inhibitory. Second it binds to glutamate receptors preventing them from exciting the cell.
AGONIST for GABA (enhancing inhibitory effects) ANTAGONIST for glutamate (decrease excitatory effects)

65
Q

Heroin

A

natural opiates shuts down release of inhibitory NTs (which normally inhibit dopamine from being released) dopamine can be released = heroin MIMICS opiate. (create feeling of immediate wellbeing)

Psych2221B (9 decks)

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