Chapter 3 - Synapses Flashcards

1
Q

What is a reflex arc?

A

The circuit from sensory neuron to muscle neuron. Eg. In a leg reflex, a sensory neuron excites a second neuron, which in turn excites a motor neuron, which excites a muscle.

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2
Q

What are reflexes?

A

Automatic muscular responses to stimuli. This was studied by Sherrington who also named the synapse

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3
Q

What were 3 of Sherrington’s observations about reflexes?

A
  1. Reflexes are slower than conduction along an axon(an impulse traveling through a synapse is slower than an impulse travelling the same distance along an uninterrupted axon. Thus the synapse slows down the process)
  2. Several weak stimuli presented at slightly different times or locations produce a stronger reflex than a single stimuli does (temporal summation and spatial summation)
  3. When one set of muscles become excited, a different set becomes relaxed
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4
Q

Sherrington discovered temporal summation. What is it?

A

Repeated stimuli within a brief time have a cumulative effect. If they occur in quick succession then they will add up to a threshold before they decay. Note that this partial depolarisation is a graded potential. It can be either depolarisation (excitatory) or hyperpolarisation (inhibitory)

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5
Q

What is a presynaptic neuron?

A

The neuron that delivers the transmittion

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6
Q

What is a postsynaptic neuron?

A

The neuron that receives the transmittion

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7
Q

Explain excitatory postsynaptic potential (EPSP).

A

It is a graded depolarisation. It results from a flow of sodium ions into the neuron. If an EPSP does not cause the cell to reach its threshold, the depolarisation decays quickly.

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8
Q

Sherrington found that synapses have the property of spatial summation. What does this mean?

A

It is the summation over space. Synaptic input from separate locations combine their effects on a neuron. If a combined excitation exceeds the threshold an action potential will occur.

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9
Q

Why is spatial summation critical to brain functioning?

A

Sensory input to the brain arrives at synapses that individually produce weak effects. However, each neuron receives many incoming axons. Spatial summation ensures that a sensory stimulus stimulates neurons enough to activate them.

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10
Q

Sherrington found that when one muscles become excited, a different set becomes relaxed. What causes the muscles to relax?

A

At the synapses, input from an axon hyperpolarises the postsynaptic cell. This increase in negative charge moves it further from the threshold and decreases the probability of an action potential. This happens by allowing potassium to leave the cell or chloride to enter the cell. (IPSP)

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11
Q

Explain the inhibitory postsynaptic potential (IPSP).

A

An IPSP occurs when synaptic input selectively opens the gates for potassium ions to leave the cell or for the chloride ions to enter the cell

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12
Q

What is a spontaneous firing rate?

A

Most neurons have a spontaneous firing rate, a periodic production of action potentials even without synaptic input.

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13
Q

Outline the chemical event that occur at the synapse.

A
  1. The neuron synthesises chemicals that serve as neurotransmitters. It synthesises the smaller neurotransmitter in the axon terminals and synthesises neuropeptides in the cell body
  2. Action potentials travel down the axon. At the presynaptic terminal an action potential enables calcium to enter the cell. Calcium releases neurotransmitters from the tminals sand into the synaptic clef.
  3. The released molecules diffuse across the clef, attach to receptors, and alter the activity of the postsynaptic neuron
  4. The neurotransmitter molecules separate from their receptors
  5. The neurotransmitter molecules may be taken back into the presynaptic neuron for recycling or they may diffuse away
  6. Some postsynaptic cells send reverse messages to control the further release of neurotransmitters by presynaptic cells.
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14
Q

What are neurotransmitters?

A

A chemical released by one neuron that affects another neuron. There are suspected to be about 100.

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15
Q

List the main categories of neurotransmitters.

A

Amino acids, mono amines, acetylcholine, neuropeptides, purines, gases, nitric oxide

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16
Q

What are amino acids?

A

They are neurotransmitters. Acids containing a amine group. They include glutamate, GABA, glycine, asparate

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17
Q

What are monoamines?

A

Neurotransmitters. Chemicals formed by a change in certain amino acids. They include serotonin, dopamine, norepinephrine, epinephrine, insoles mines, catecholamines

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18
Q

What is acetylcholine?

A

It is a neurotransmitter. It is a modified amino acid.

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19
Q

What are neuropeptides?

A

Neurotransmitters. They are chains of amino acids. They include endorphins, substance P, neuropeptides Y

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20
Q

What are purines?

A

Neurotransmitters.a category of chemicals including adenosine and several of its derivatives. They include ATP, adenosine

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21
Q

What gases act as neurotransmitters?

A

Nitric oxide and possibly others. this gas is released by many small local neurons. In large quantities NO is poisonous. The nitric oxide relates to blood flow. It tells the blood which part of the brain is active and needs a greater supply.

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22
Q

Where do neurotransmitters come from?

A

Neurons synthesise nearly all neurotransmitters from amino acids, which the body obtains from proteins in the diet. Eg, acetylcholine is synthesised from choline found in milk, eggs, and peanuts. The amount of tryptophan in the diet controls the amount of serotonin in the brain. Serotonin levels rise after you eat food like soy and falls after maize.

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23
Q

What are catecholamines?

A

They are compounds. They contain a catecholamines group and a amine group. Compounds that are known as catecholamines are epinephrine, norepinephrine and dopamine.

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24
Q

How is serotonin created?

A

The amino acid tryptophan crosses the blood brain barrier by a special transport system that it shares with other large amino acids. To decrease the competition for use of the system and ensure that tryptophan gets across you could eat less phenylalanine, or eat more carbohydrates. Carbohydrates release insulin which takes several competing amino acids out of the bloodstream and into body cells. Once in the neuron tryptophan creates serotonin.

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25
Q

What are vesicles?

A

Most neurotransmitters are synthesised in the presynaptic terminal, near the point of release. They are stored in vesicles which are tiny nearly spherical packets. Not all neurotransmitters a kept in vesicles. And nitric oxide is released immediately (it is not stored)

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26
Q

What is MAO (mono amine oxidase)?

A

Sometimes neurons accumulate excess levels of neurotransmitters. Neurons that release serotonin, dopamine, or norepinephrine contain an enzyme, MAO that breaks down these transmitters into inactive chemicals.

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27
Q

How do neurotransmitters get released?

A

The action potential itself doesn’t release the neurotransmitters. The depolarisation opens voltage dependent calcium gates in the presynaptic terminal. After the calcium enters the presynaptic terminals, the neurotransmitters are released in bursts into the synaptic clef. It diffuses across the synaptic clef and attaches to a receptor.

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28
Q

What is exocytosis?

A

The release of the neurotransmitter in bursts from the presynaptic terminal. This is caused by the entry of the calcium into the presynaptic terminal.

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29
Q

How many types of neurotransmitters does each neuron have?

A

Many neurons release a combination of 2 or more neurotransmitters. Eg motor neurons in the spinal cord have one branch to the muscles where they release acetylcholine, and another branch to other spinal cord neurons where they release acetylcholine and glutamate. The combination makes the message more complex

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30
Q

What determines the effect of the neurotransmitter?

A

It depends on the receptor on the postsynaptic cell. The receptor may open a channel (exerting an ionotropic effect) or it may produce a slower but longer effect (a metabotropic effect)

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31
Q

Describe ionotropic effects.

A
  1. It has brief on/off effects
  2. When the neurotransmitter attaches to the receptor it opens a central channel, which is shaped to let a particular type so ion pass through (in contrast to the sodium and potassium channels which are voltage gated). these are transmitter gated or ligand gated channels
  3. The effects to begin quickly
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32
Q

What are transmitter gated or ligand gated channels?

A

They are channels controlled by neurotransmitters. A ligand is a chemical that binds to another chemical.

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33
Q

When is the ionotropic effect useful?

A

Well suited to conveying visual information and anything else that needs to be updated as quickly as possible.

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34
Q

Which neurotransmitters are used during the ionotropic effect?

A

Most of the Brian’s excitatory ionotropic synapses use the neurotransmitter glutamate. Most of the inhibitory ionotropic synapses use GABA (which opens chloride gates, enabling chloride ions jwith their negative charge to cross the membrane into the cells more quickly than usual) or glycine (mostly found in the spinal cord). Acetylcholine is also used, it is mostly excitatory.

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35
Q

Explain the metabotropic effect.

A

This is slower but longer lasting. It uses many different types of neurotransmitters.

  1. When the neurotransmitter attaches to a metabotropic receptor, it bends the receptor protein that goes through the membrane of the cell. The other side of the receptor is attached to a G protein.
  2. Bending the receptor detaches that G protein which is then free to make energy elsewhere in the cell. The result is an increased concentration of a second messenger inside the cell.
  3. The first messenger (the neurotransmitter) carries info to the post synaptic cell, the second messenger communicates to other areas within the cell. It may open or close ion channels in the membrane or activate a portion of a chromosome.
  4. Metabotropic effect is better suited for more enduring effects such as taste, smell, pain, where the exact timing is not important. It is important for aspect of arousal, attention, pleasure, emotion
36
Q

What is the G protein?

A

This is a protein coupled to guanosine tori phosphate ( GTP), an energy storing molecule.

37
Q

Explain the second messenger.

A

This carries information to many areas within the cell. Used by meta nootropic synapses.

38
Q

What are neuromodulators?

A

Neuropeptides are often referred to as neuromodulators. Neuropeptides are synthesised within the cell body. They are released mainly by dendrites, and also cell body and the side of the axon. Whereas a single a action potential may release other neurotransmitters, repeated stimulation is required for the release of neuropeptides. After a few dendrites release a neuropeptides, the released chemical primes other nearby dendrites to release the same neuropeptides also (including dendrites from other cells). Thus neuron containing neuropeptides do not release them often but when they do they release alot. When released they diffuse widely affecting many neurons. In this way they resemble hormones. The effects can last 20 mins. They are important for hunger, thirst, intense pain. Study table 3.2 p65 for comparisons.

39
Q

What is an A neuralgia form cell?

A

A kind of neuron, shaped like a glia that releases huge amounts of GABA all at once. It produces a widespread inhibituation

40
Q

What are hormones?

A

A chemical that is secreted by cells in one part of the body and conveyed by the blood to influence other cells. It is like a radio station, they convey info to any receiver tuned in. Neuropeptides are intermediate in that they only diffuse within the brain and blood doesn’t carry them to other parts of the body. Hormones are useful for coordinating long lasting changes in multiple parts of the body.

41
Q

What are endocrine glands?

A

They produce hormones

42
Q

What are protein hormones and peptide hormones?

A

They a types of hormones composed of chains of amino acids. (Proteins are longer chains, peptides are shorter). They attach to membrane receptors where they actives a second messenger within the cell (exactly like a mebotropic. Many chemicals serve as both neurotransmitters and hormones)

43
Q

What is the pituitary gland?

A

It is attached to the hypothalamus. It consists of 2 distinct glands, the anterior pituitary and the posterior pituitary which release different sets of hormones.

44
Q

What is the posterior pituitary?

A

It can be considered an extension of the hypothalamus. Neurons in the hypothalamus synthesise the hormones oxytocin and vasopressin which migrate down axons to the posterior pituitary which later releases the hormones into the blood.

45
Q

What is the anterior pituitary?

A

It is composed of glandular tissue, synthesises 6 hormones, although the hypothalamus controls their release. It does this by secreting releasing hormones which flow through the blood to the anterior pituitary where they still ate or inhibit the release of the hormones.

46
Q

What is oxytocin?

A

A hormone synthesised by the hypothalamus and released by the posterior pituitary

47
Q

What is vasopressin?

A

A hormones synthesised by the hypothalamus but released by the posterior pituitary.

48
Q

What is releasing hormones?

A

Something that is secreted by the hypothalamus, transported by blood to the anterior pituitary where they stimulate or inhibit the release of hormones

49
Q

Why do neurotransmitters not linger in the synapse?

A

Because they may continue he to excite and inhibit

50
Q

What happens to acetylcholine when it is finished?

A

Acetylcholine is broken down by the enzyme acetylcholinesterase into 2 fragments, acetate and choline. The choline diffuses back to the presynaptic neuron, which takes it up and reconnects it with acetate already in the cell to form acetylcholine again. This process takes time.

51
Q

What happens with serotonin and the catecholamines (dopamine, norepinephrine, and epinephrine)when they are finished?

A

They do not break down. They simply detach from the receptor. In some parts of the brain the presynaptic neuron takes up most of the released neurotransmitter molecules intact and reuse them. This process is called reuptake, occurs through special membrane proteins called transporters.

Dopamine transporters in the caudate nucleus are highly efficient and reuptake accounts for nearly all of the released dopamine. In other brain areas, fewer transporters are present, and reuptake is slower. If dopamine is released rapidly in these areas it accumulates and an enzyme called COMT breaks down the excess which then wash away.

52
Q

What happens to neuropeptides when they are finished?

A

They are neither inactivated, nor are they reabsorbed. They simply diffuse away. Because these large molecules are synthesised slowly, a neuron a temporarily exhaust it’s supply.

53
Q

What is negative feedback?

A
  1. Autoreceptors are receptors that respond to the released transmitters by inhibiting further synthesis and release.
  2. Some postsynaptic neurons respond to stimulation by releasing special chemicals that travel back to the presynaptic neuron, where they inhibit further release of transmitter. Nitric oxide does this.
54
Q

Do any synapses use electrical forms of communication?

A

Yes. Electrical transmission is faster. Some of the cells that control your breathing are synchronised by electrical synapses. (It’s important to inhale on the left side at the same time as the right side).

55
Q

What is a gap junction?

A

The place where the membrane comes into direct contact with the membrane of another (this synapse uses electrical transmissions). Fairly large pores of the membrane of one neuron line up precisely with similar pores in the membrane of another cell. These pores are large enough for sodium and other ions to pass through readily and are constantly open. Thus there is a fast reaction.

56
Q

What are the common drugs derived from?

A

Plants.lots of the neurotransmitters and hormones are the same.

57
Q

What is an antagonist?

A

A drug that blocks a neurotransmitter.

58
Q

What is an agonist?

A

A drug that mimics or increases the effects.

59
Q

What is a mixed agonist-antagonist?

A

It is an agonist for some effects of the neurotransmitter and an agonist for others or an agonist at. Some doses and an antagonist at others.

60
Q

What does affinity mean?

A

A drug binds to the receptor like a key

61
Q

What does efficacy mean?

A

A drugs tendency to activate the receptor. A drug that binds to a receptor but fails to stimulate it has a high affinity but low efficacy.

62
Q

In what ways do drugs influence the synapse?

A

A drug can

  1. Increase or decrease the synthesis of the neurotransmitter
  2. Cause it to leak from its vesicles
  3. Increase it’s release,
  4. Decrease it’s reuptake,
  5. Block it’s breakdown into inactive chemicals,
  6. Act in the postsynaptic receptors
63
Q

What is self-stimulation of the brain?

A

Olds and Milner implanted an electrode into a rats brain. They put the rate in a box with a lever where the rat could cause its own electrical stimulation within the brain

64
Q

Why is the nucleus accumbens important?

A

It is here that nearly all abused drugs affect. The axons here either directly or indirectly increase the release of dopamine or norepinephrine. Sexual excitement also stimulates this area and so does the taste of sugar. Just simply. Thinking of something pleasant activates the nucleus accumbens. Habits (including gambling) activate here. People with depression have less activity here.

65
Q

What are the 2 components of reinforcement?

A

Wanting (motivation) is not always the same as liking (pleasure). Small parts off the nucleus accumbens responds to pleasure (liking) but larger areas respond to motivation (wanting). Food, sex, addictive drugs all strongly activate thE nucleus accumbens by releasing dopamine or norepinephrine. People addicted to a drug show a strong drive to obtain even though it no longer provides any pleasure.

66
Q

What is a stimulant drug?

A

It increases excitement, alertness, and activity, while elevating mood and decreasing fatigue. Amphetamine and cocaine stimulate dopamine synapses in the nucleus accumbens and elsewhere by increasing the presence of dopamine in the synaptic terminal. Amphetamine and cocaine inhibit the dopamine transporter(a protein), thus decreasing the reuptake and prolonging the effects of the released dopamine.

Amphetamine has similar effects on the serotonin and norepinephrine transporters. Methamphetamine has effects similar to those of amphetamine but stronger.

Thus stimulant drugs increase the accumulation of dopamine in the synaptic clef. However, the excess dopamine in the synapse washes away faster than the presynaptic cell makes more to replace it. A few hours after taking the drug a user has a deficit of the neurotransmitter and enters a withdrawal state marked by reduced energy, reduced motivation, and mild depression.

67
Q

What are the behaviours associated with stimulant drugs?

A

Low doses enhance attention (used for ADHD sufferers). High doses impair attention and learning. Attention problems can linger for years after quitting. By altering the blood flow, cocaine also increases the risk of stroke and epilepsy.

68
Q

How do cocaine and methylphenidate differ?

A

They both block dopamine reuptake. Cocaine users inject and sniff to get a rapid rush, methylphenidate pills experience a gradual increase in the drug’s response and a slow decline. People who inject methylphenidate get the same rush as cocaine and the risk of addiction.

69
Q

Explain nicotine’s impact on the body.

A

It stimulates a family of acetylcholine receptors known as nicotinic receptors. Nicotine increases dopamine release mostly in the same cells that cocaine stimulate.

One consequence of repeated exposure to nicotine is that receptors in the nucleus accumbens become more sensitive to nicotine and less responsive than usual to other reinforcement. The same pattern emerges with cocaine and other addictions.

70
Q

Describe opiates impact on the body.

A

Derived from the opiate poppy. The drugs include morphine, heroin, and methadone. Because heroin enters the body quicker than morphine it produces a bigger rush and is more addictive. Opiates relax people, decrease their attention to real world problems, and crease their sensitivity to pain. Addiction depends on the person, the social setting , the dose, the reasons for taking the drug.

Neuropeptides called endorphins indirectly activate dopamine release. Endorphin synapses inhibit neurons that release GABA, a neurotransmitter that inhibits the firing of dopamine neurons. By inhibiting the inhibitor, the net effect is to increase dopamine release.

Medulla controls the breathing and heartbeat. Opiates have strong impacts on the medulla, hence overdoses are life threatening.

71
Q

What chemicals does marijuana contain?

A

Tetrahydrocannabinol (9-THC) and other cannabinoids (chemicals relating to 9-THC). Cannabinoids have been used medically to relieve pain or nausea, to combat glaucoma, and to increase appetite. Purified THC has been approved for medical use in the US.

72
Q

What are the effects of marijuana?

A

Intensification of sensory experience and an illusion that time has slowed down. It reportedly impairs memory, and cognition, especially in new and heavy users. Former users showed improved memory after 4 weeks. Cannabinoids receptors are among the most abundant receptors in many areas of the brain but there is not a strong presence in the medulla (which controls breathing and heartbeat) hence the post with not stop breathing nor the heart beating.

Two brain chemicals that bind to cannabinoid receptors are anandamide and sn-2 arachidonylglycerol (2-Ag). When certain neurons are depolarised they release anandamide or 2-AG as retrograde transmitters that travel back to the incoming axons and inhibit further release of either glutamate or GABA. These chemicals tell the presynaptic cell “the postsynaptic cell got your message, you don’t need to send it again”. The cannabinoids in marijuana attach to these same presynaptic receptors and send the message even though the original transmittion did not occur. Thus decreasing both excitatory and inhibitory messages.

By inhibiting the GABA release in the ventral regimental (in the midbrain) cannabinoids decrease inhibition of the neurons that release dopamine. In the nucleus accumbens.

Cannabinoids relieve nausea by inhibiting serotonin type 3 synapses. Cannabinoid receptors are abundant in areas of the hypothalamus and hypo amps that influence feeding and stimulation of these receptors increases the rewarding value of a meal.

73
Q

What are hallucinogenic drugs and how do they effect the body?

A

Hallucinogenic drugs distort perception. Many of them, like laserdisc acid diethylamide (LSD) chemically resemble serotonin. They attach to serotonin type 2A receptors and provide stimulation at inappropriate times or for longer than usual durations

74
Q

Explain MDMA.

A

MDMA is ecstasy. It is a stimulant at low doses, increasing the release of dopamine and producing effects similar to cocaine. At higher doses it also releases serotonin, altering perception and cognition like hallucinogenic drugs.

Many people use it at dance parties to increase their energy levels but after they feel lethargy and depression. Increased body’s temp is life threatening.

Indication of long term loss off serotonin receptors, persisting depression, anxiety and impaired learning and memory.

75
Q

What is alcoholism or alcoholic dependence?

A

The habitual use of alcohol despite medical or social harm.

76
Q

How does alcohol affect the body?

A

In moderate amounts it relaxes people and decreases anxiety.
Alcohol facilitates response at the GABA receptor the brains main inhibitory site. It also blocks activity at the glutamate receptors, the brains main excitatory site. This leads to a decrease in activity in the brain.

Alcohol increases stimulation at dopamine receptors in the nucleus accumbens.

77
Q

What is Type 1 (or type A) alcoholism?

A

People with this develop alcohol problems gradually, usually after 25 and may or may not have relatives with alcohol abuse.

78
Q

What is Type 2 (or Type B) alcoholism?

A

Those with this have more rapid onset, usually before age 25. Most are men, and most have close relatives with alcohol problems.

79
Q

Explain alcoholism and genetics

A

Twin studies confirm a strong influence of genes on vulnerability to alcoholism.

One identified gene controls variations in the dopamine type 4 receptor. The receptor has 2 forms, one short and one long. The long form are less sensitive and people with these report a stronger than average craving for additional alcohol after one drink.

Another key gene controls COMT, an enzyme that breaks down dopamine after its release. Those with the more active form of the enzyme break down more dopamine and therefore tends to decrease reinforcement. These people tend to be more impulsive, to choose immediate rewards rather than bigger rewards later.

Prenatal environment also contributes to the risk for alcoholism (drinking during pregnancy).

Stress, environment, and opportunities also impact.

80
Q

What are the risk factors for being an alcoholic?

A
  1. More likely in those who were impulsive, risk takers, easily bored, sensation seeking and outgoing as children.
  2. Sons of alcoholic fathers. They (a) show less intoxication after drinking a moderate amount, (b) it has a greater impact on reducing stress than it does in others, (c) smaller than normal amygdala in the right hemisphere
81
Q

What is the addiction paradox?

A

As the addiction progresses the pleasures become weaker while the costs and risks increase. Yet the person find it difficult to quit. Why?

82
Q

What is tolerance?

A

As an addiction develops, many of its effect, especially the enjoyable effects, decrease. Because of tolerance, heroin users use more, more frequently. Tolerance is to a large extent, learned. As the body comes to expect the drug, at least under certain circumstances, it acts strongly. When the drug is absent.

83
Q

What is withdrawal?

A

The effects of drug cessation. Symptoms include anxiety, sweating, vomiting, diarrhoea, fatigue, hallucinations. Even hAbitual video game players can have physical withdrawals.

84
Q

What is the relationship between craving and cues?

A

Hypothesis that drug users learn to associate cues with drugs. Later, even after years of abstinence, exposure to those cues trigger a renewed craving.

A drug related cue increases activity in the nucleus accumbens and several related was. People can decrease this arousal.

85
Q

How do drugs reorganise the brain?

A

Addictions hijack people’s motivations. It changes the brain so that other reinforcing experiences become less powerful. Epigenesis, certain events change the expression of genes. Cocaine increases the activity of certain genes that control changes in dendrites within the nucleus accumbens. The result is that the drug stimulates mores dendrites and other events stimulate fewer. It also induces changes that impair extinction.

86
Q

What is Antabuse?

A

It antagonises the effects of acetaldehyde dehydrogenase by binding to its copper ions. It makes people feel sick when they drink alcohol. It is moderately effective but some stop taking the pill.

Revia blocks opiate captors and thereby decreases the pleasure from alcsohol. This is also moderately effective. It works best for those with Type 2 alcoholism.

87
Q

Outline the medications used to combat opiate abuse.

A

Methadone is taken orally. The effects are slow and the withdrawal symptoms are also slow. Because methadone is already occupying the endorphin receptors, heroin can not add much stimulation to them. LAAM is similar to methadone and used to treat opiate addiction. These drugs do not end the addiction. They merely satisfy the craving in a less dangerous way.