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Psychopharmacology Flashcards

1
Q

What is psychopharmacology?

A
  • Psychopharmacology is the rule of drugs when they get into the brain, and how they influence behaviour and physiology.
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2
Q

What are neuromodulators?

A
  • They’re the same as NTs but with a more global effect.
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3
Q

How many neurons is the brain composed of?

A
  • Brain is composed of billions of neurons which do the things that make us ourselves.
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4
Q

What sort of things do the relationships between neurons allow us to do?

A
  • Breathe, think of childhood memories, think of future plans, think of falling in love, make connections, regenerate thoughts - it’s a broad and diverse range of abilities that are happening at the cellular level of the brain, and is very vast and complex.
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5
Q

How is information shared between neurons?

A
  • With NTs.

- Diff. neurons might send diff. neurotransmitters, or a multitude of neutrotransmitters.

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6
Q

Briefly describe the messaging process of the NTs.

A
  • NTs diffuse across the synaptic space, aiming to doc onto the receptor cells of the neighbouring neurons. If the signal is strong enough, the postsynaptic neuron is then activated to send a message to its neighbour and so on.
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7
Q

Where are NTs made?

A
  • NTs are made in the neurons and stored in the vesicles.
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8
Q

What happens if the info from a neighbouring neuron or network is strong enough?

A
  • It allows the vesicles to fuse with the presynaptic membrane, causing the release of NTs which diffuse along the synaptic cleft, docking to receptors in the neighbouring neuron, affecting the action. This could be an action potential to make something happen, or to stop a signal from spreading across the brain.
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9
Q

What is the site of action?

A
  • The site of action is the area of chemical transfer which is somehow influenced by the use of recreational drugs.
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10
Q

How many principles of psychopharmacology are there?

A
  • There are 5 principles.
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11
Q

What is psychopharmacology the study of?

PRINCIPLES

A
  • It’s the study of the effects of drugs on the nervous system and on behaviour.
  • Looks at the central nervous system (the brain and spinal cord), and also the peripheral nervous system.
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12
Q

What sort of effect do drugs have?

PRINCIPLES

A
  • Physiological and psychological.
    Physiological = increased heart rate and respiration.
    Psychological = euphoria, drowsiness.
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13
Q

What is exogenous?

PRINCIPLES

A
  • Exogenous is what classifies a drug as a drug; it’s something from the outside world that we have taken into our body.
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14
Q

What happens when the drugs reach our brains?

A
  • The drugs reaching out brains will change the cellular function in some way; either they will be compatible with the usual cellular function, thus strengthening it, or they will affect it negatively.
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15
Q

What are the sites of action?

PRINCIPLES.

A
  • The sites of action are also known as mechanism of action, and are targeted due to the chemical composition of the drugs.
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16
Q

What is pharmacokinetics?

A
  • It’s the study of the absorption of drugs into the body, and the distribution, metabolism and elimination of these drugs.
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17
Q

What must happen for a drug to have an effect?

PHARMACOKINETICS

A
  • The drug must be absorbed into the bloodstream and distributed to the site of action, which is in the central nervous system.
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18
Q

What is the life-length of a drug like?

PHARMACOKINETICS

A
  • There’s a particular half-life, meaning that over time, the effects will begin to diminish and the metabolism of the drugs will be broken down into a compound which can be eliminated from the body.
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19
Q

Where will evidence of drug consumption be?

PHARAMCOKINETICS

A
  • Evidence of drug consumption will be in your urine, most likely.
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20
Q

How many routes of administration are there?

ADMINISTRATION

A
  • There are 10 routes of administration.
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21
Q

What is an IV injection?

ADMINISTRATION

A
  • IV is the fastest route directly into the bloodstream.
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22
Q

What are intraperitoneal injections?

ADMINISTRATION

A
  • It’s an injection into the abdominal space.
  • It’s not very common in humans, but it allows the drug to bypass into the stomach.
  • It’s also rapid.
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23
Q

What are intramuscular injections?

ADMINISTRATION

A
  • The drug is absorbed through capillaries supplying muscle to the bloodstream (buttocks).
  • It completely avoids the stomach.
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24
Q

What are subcutaneous injections?

ADMINISTRATION

A
  • Subcutaneous injections sit just under the skin and are very slow release, for example, the contraceptive implant which slowly releases enough levels of the hormone to prevent conception.
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25
Q

What is oral ingestion?

ADMINISTRATION

A
  • Oral ingestion is the most common in human, but there is the possibility for the drug to be destroyed by stomach acid and other enzymes.
  • Swallowing leads to digestion into the bloodstream, however it can be a little bit slower.
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26
Q

What is sublingual administration?

ADMINISTRATION

A
  • Sublingual administration is when a drug is placed beneath the tongue and is absorbed through the blood capillaries.
  • The drugs placed underneath the tongue will dissolve.
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27
Q

What is intrarectal drug taking?

ADMINISTRATION

A
  • Intrarectal drug administration is a form of anal administration, avoiding the stomach and therefore preventing stomach upset.
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28
Q

What is inhalation?

ADMINISTRATION

A
  • Inhalation is when you inhale the drug, therefore giving it a direct route into the lungs.
  • It has very rapid effects.
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29
Q

What is topical administration?

ADMINISTRATION

A
  • Topical administration is the process of applying patches to the skin, for example, nicotine patches.
  • Patches can help stop withdrawal.
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30
Q

What is intracerebral administration?

ADMINISTRATION

A
  • Intracerebral administration is where the drug is administered directly to the brain.
  • This type of administration can have serious consequences if not done correctly, as anything exposing the brain can be incredibly dangerous.
  • An example of intracerebral administration would be in cases where an individual has meningitis.
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31
Q

How might administration influence the time course of the drug taking effect? Consider cocaine.

A
  • The method of administration influences the time course of the drug taking effect due to how quickly it enters the bloodstream and passes through the blood brain barrier. The time course of the drug depending on administration has differing effects into how the drug may behave once having arrived in the body.
  • Injection of cocaine is almost instant in creating feelings of euphoria, however the effects rapidly deplete.
  • Smoking the drug has rapid effects and reaches peak concentration in the bloodstream.
  • Intranasal administration increases the time course, taking roughly an hour before peak concentration is reached, widening the time course of effect on behaviour. This means that although the reaching of peak concentration takes longer, the effects will last longer.
  • Oral ingestion takes a while to pass through the digestive processes, however the effects may last longer.
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32
Q

What is the blood-brain barrier?

A
  • The blood brain barrier is the barrier between the circulating blood in the body and the blood in the brain.
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33
Q

What does the blood-brain barrier do?

A
  • The blood-brain barrier attempts to protect our brain from damaging external factors, such as exogenous drugs.
  • It aims to prevent chemicals from drugs from getting through, however some drugs that are ingested are able to get through the barrier.
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34
Q

What must drugs be in order to pass through the blood-brain barrier?

A
  • In order to pass through the barrier, the drugs must be lipid-soluble as the BBB is selectively permeable and so allows lipid-soluble substances to pass through, not water-soluble substances.
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35
Q

What does lipid-soluble mean?

A
  • Lipid-soluble means that the drugs are able to dissolve in fat.
  • The bigger the liquid soluble content of the drug, the easier it is for it to pass through the BBB.
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36
Q

What happens if blood doesn’t make its way to the brain?

A
  • If blood doesn’t make its way to the brain, we have no oxygen, meaning that the brain will starve, and so the blood is conscious about what is taken to the brain.
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37
Q

What is the blood-brain barrier made up of?

A
  • The BBB is made up of blood capillaries forming the network in the brain.
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38
Q

What is the difference between the capillaries in the body and the capillaries in the brain?

A
  • The capillaries in the brain are tightly woven, as opposed to the non-tightly woven molecules in the body which allow gases and other molecules to flow freely between them.
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39
Q

Give an example of drugs which only have an impact on the body.

A
  • Laxatives.
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40
Q

What is one of the most highly liquid drugs?

A
  • Heroin.
  • It diffuses through the BBB v. quickly and gives a v. intense high v. quickly.
  • When heroin gets into the brain it converts into morphine, but morphine doesn’t give you that high as it takes longer for it to diffuse in the barrier.
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41
Q

How do you get drugs out of the system?

A
  • Drugs are typically deactivated by enzymes in the blood, brain, or liver.
  • Most are excreted through urine, via the kidneys.
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42
Q

What are the effects of repeated exposure?

TOLERANCE

A
  • A tolerance to drugs is build.
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43
Q

Give an example of tolerance in terms of alcohol.

TOLERANCE

A
  • Originally, it wouldn’t take much alcohol to feel the effects of it, however repeated exposure to alcohol means that you need more of the substance to feel the same effects.
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44
Q

What is tolerance?

TOLERANCE

A
  • Tolerance to a particular substance means that you become used to the effects and so the effectiveness of the substance is decreased, meaning that more is required to experience the same effect.
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45
Q

What can tolerance lead to?

TOLERANCE

A
  • Tolerance can lead to withdrawal and symptoms of withdrawal.
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46
Q

Why does tolerance occur?

TOLERANCE

A
  • Tolerance occurs as our bodies are programmed to function at an optimal level which means that we have a baseline level of normality within our bodies, since our bodies know what is natural.
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47
Q

What is tolerance in relation to the optimal value?

TOLERANCE

A
  • Tolerance is our defence of the optimal value, meaning that we have to take more of the drug to experience the same feelings as our body is fighting back to reach the baseline level of normality.
  • Tolerance is activated in order to compensate for the loss of optimal value, producing the opposite effect.
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48
Q

What happens when the drug is stopped?

TOLERANCE

A
  • When the drug is stopped, the compensatory mechanism of the body, which has been fighting back against the drug, the effects are felt intensely, thus manifesting as withdrawal as a direct opposite to the effects of the drug.
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49
Q

Give an example of chronic opiate use and the effects when stopped.
TOLERANCE

A
  • Codeine, which is an opiate, has the effect of constipation when taken over time.
  • When you stop taking codeine, there is chronic diarrhoea as the sudden withdrawal manifests through the body in an attempt to reach normality.
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50
Q

What happens to drugs in their site of action?

COMPENSATORY MECHANISMS

A
  • Drugs often bind to receptors at their site of action.
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51
Q

What is the process of binding?

COMPENSATORY MECHANISMS

A
  • The presynaptic neuron released NTs which bind to the receptor across the synaptic cleft, which is where drugs often bind to affect that action.
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52
Q

What happens during the process of binding when tolerance is involved?
COMPENSATORY MECHANISMS

A
  • In cases of tolerance, either the affinity (readiness with which the two molecules bind together) for the drug decreases, or the receptors decrease in number.
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53
Q

What happens when affinity to the drug is experienced?

COMPENSATORY MECHANISMS

A

AFFINITY: To fight back, the brain has a tendency to reduce the affinity of the drug, and the drug no longer wants to bind with the receptor as it knows that some sort of negative effect is being experienced.

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54
Q

What happens when receptor decrease is experienced?

COMPENSATORY MECHANISMS

A
  • RECEPTOR DECREASE: Receptors might decrease in number if you’re constantly flooding your body with the drug, meaning that the action is happening all of the time and so your body attempts to get rid of some of the receptors so that there is less impact.
  • However, if you stop taking the drug, it takes a while for the balance to shift back to normality.
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55
Q

What happens in cases of chronic MDMA use?

COMPENSATORY MECHANISMS

A
  • If you’re a chronic MDMA user, the receptors will never recover.
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56
Q

What happens if the drug has gotten to the brain and has bound to a receptor?
COMPENSATORY MECHANISMS

A
  • If the drug has gotten to the brain and bound to a receptor, compensatory mechanisms stop the receptor opening so that the response can happen. Usually, the drug binds to the receptor, allowing the receptor to open and allowing ions to flow into the neuron, so the CM is to stop the receptor opening as freely as usual.
  • When bound to a receptor, an effect is initiated (either the ion channel is opened directly [ionotropic] or a secondary messenger is activated to do so [metabotropic]), and so with tolerance, either of these processes will become less effective.
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57
Q

What happens if a drug has more than one site of action?

TOLERANCE + SITES OF ACTION

A
  • If a drug has more than one site of action, it can produce tolerance at one action site and remain unchanged at another.
  • Dependent on the location of the brain, the same neurotransmitter might have a different function than it does elsewhere.
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58
Q

What happens in cases of Parkinson’s disease?

TOLERANCE + SITES OF ACTION

A
  • In cases of PD, the basil ganglia begins to degenerate and lose dopamine neurons which allow us to voluntarily walk and pick things up.
  • Dopamine is responsible for movement, however in other areas of the brain it is used to encode that something rewarding is happening.
  • These are 2 different processes mediated by the same NT.
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59
Q

What happens if a drug has different effects on a site of action?
TOLERANCE + SITES OF ACTION

A
  • If a drug makes one site of action tolerant and another site of action isn’t tolerant, the site of action that doesn’t become tolerance won’t have the same CMs, meaning you’ll need more of the drug, which can lead to complications like overdose.
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60
Q

Consider the effect of barbiturates which have multiple sites of action.
TOLERANCE + SITES OF ACTION

A
  • Barbs used to be taken to produce an anaesthetic effect, and were often prescribed for anxiety, depression and insomnia (however they aren’t typically used anymore).
  • The site of action for relaxation is susceptible for tolerance, meaning you need a higher dosage for the same effect.
  • However, there is also another site that leads to respiratory depression, which doesn’t show tolerance.
  • If you take more to feel the same effect of sedation in one site of action, and the other site of action doesn’t experience tolerance, you’re more susceptible to damaging the body and there is the heightened risk of respiratory depression, leading to breathing problems.
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61
Q

What happens when sensitisation to a drug is experienced as a result of repeated use?
SENSITISATION

A
  • Sensitisation is where the exact opposite effect of tolerance is produced, meaning that the drug produces larger and larger effects over time.
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62
Q

Give an example of sensitisation in relation to cocaine administration.
SENSITISATION

A
  • Stable cocaine administration can lead to an unaltered sense of euphoria, however there is an increased likelihood of producing ‘hyperkinetic’ movement disorders, which is similar to PD.
  • The euphoria is related to reward, so you continuously take cocaine to feel the reward in one site of action.
  • However, in the other side of action for dopamine, movement is increasingly more sensitised to cocaine in the brain, leading to effects like flailing limbs etc.
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63
Q

Historically, how were people with schizophrenia treated?

SENSITISATION

A
  • Historically, people with schizophrenia were treated with methods which had the ability to lead to hyperkinetic disorders.
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64
Q

What do sites of drug action look at?

SITES OF DRUG ACTION

A
  • Sites of drug action look at how the mechanics of drugs affect the transmission of message from one neuron to another.
65
Q

What happens when we take drugs?

SITES OF ACTION

A
  • When we take drugs, the synaptic transmission from one cell to another is affected. This means that the transmission of messages from one neuron to another neuron is affected via the synapse.
  • Drugs can either help or hinder synaptic transmission.
66
Q

What does it mean if a drug is an agonist?

AGONISTS

A
  • If a drug is an agonist, it facilitates the effects of a particular NT on the postynaptic neuron.
  • If the drug makes the process happen more, it keeps stimulation of the receptor cells and ramps up a process which is already happening through working with the NT, therefore making it an agonist.
67
Q

What does it mean if a drug is an antagonist?

ANTAGONIST

A
  • If a drug inhibits the effects of a particular NT on the postsynaptic neuron, it is known as an antagonist.
  • A drug is an antagonist is if effects the behaviour of a particular NT from behaving in its usual manner.
  • It works against the normal pattern.
68
Q

What is an important note to remember about agonism?

AGONISM

A
  • Agonism (facilitation) isn’t the same as neuronal excitation - some NTs have inhibitory effects, and an agonist of such an NT would enhance inhibitory neurotransmission.
    Some NTs have inhibitory effects, meaning they stop things from happening normally. A drug helping an NT from stopping certain things from happening is still an agonist.
  • If a drug is an agonist, it’ll do exactly what the NT does.
69
Q

What is an important note to remember about antagonism?

ANTAGONISM

A
  • Neural excitation where a drug begins to fire doesn’t necessarily mean that a drug is an agonist as an antagonist drug could also have the same effect.
  • Antagonism isn’t the same as neuronal inhibition - some NTs enhance inhibitory neurotransmission, and therefore an antagonist of such transmission would work to reduce inhibition.
70
Q

What is the FIRST step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The NT is synthesised within the presynaptic neuron.
71
Q

What is the SECOND step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The NT is then stored in the synaptic vesicles to be used when a message is sent.
72
Q

What is the THIRD step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The synaptic vesicles travel to the presynaptic membrane and dock there.
73
Q

What is the FOURTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • An axon is fired.
74
Q

What is the FIFTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • Voltage-dependent calcium channels in the presynaptic membrane open, allowing calcium ions to enter into the cell.
75
Q

What is the SIXTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The calcium ions interact with the docking proteins, opening the vesicles, initiating the release of NTs into the synaptic cleft where they can diffuse across the receptors of the new brain cells.
76
Q

What is the SEVENTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • Molecules of the NT bind with postsynaptic receptors of the new brain cell.
77
Q

What is the EIGHTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The binding of the molecules in the postsynaptic receptors of the new brain cell cause particular ion channels to open.
78
Q

What is the NINTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The opening of the ion channels changes the electric potential of the postsynaptic membrane and dependent on the influx/eflux of particular ions, either excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) are generated.
  • Both processes are important in the mechanisms of the brain.
79
Q

What is the TENTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • EPSPs or IPSPs happen.
  • EPSPs elicit a depolarisation, making the neuron more likely to fire, whilst IPSPs elicit a hyperpolarisation, making the neuron less likely to fire.
80
Q

What is the ELEVENTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • The action of the NT is quite brief, as surplus is removed from the synaptic cleft by transporter molecules in the presynaptic membrane, or the surplus is destroyed by enzymes.
  • Basically, surplus NTs are either removed by enzymes in the synaptic space, or transporter molecules on the presynaptic neuron take the surplus NT into the emitting neuron.
81
Q

What is the TWELFTH step of synaptic transmission?

SYNAPTIC TRANSMISSION

A
  • NT synthesis and release is regulated by presynaptic autoreceptors on the terminal button.
  • Autoreceptors are little cells which monitor what is happening in the synaptic cleft by trying to detect if an NT is present. If they can detect an NT, they do nothing. If they can’t detect an NT, they initiate the cell to produce more of that NT.
82
Q

What happens in cases of PD with the BBB?

A
  • Dopamine cannot cross the BBB, and dopamine is influential in PD.
  • There’s a drug which makes its way into the remaining dopamine neurons and it allows the remaining cells to increase their output of dopamine.
  • It’s an agonist as it activates the cell.
83
Q

What is L-Dopa used for and what type of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • L-Dopa is administered for PD to alleviate ‘frozen’ movement.
  • It is a precursor to dopamine, which is depleted in PD patients.
  • Dopamine can’t be given directly as it cannot cross the BBB.
  • L-Dopa is an agonist.
84
Q

What is PCPA used for and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • PCPA is used experimentally to relieve serotonin-mediated-side-effects of certain types of tumours, but the side effects of the drug are too high.
  • PCPA inactivates synthetic enzymes which inhibit the synthesis of the serotonin NT; it stops the production of serotonin.
  • PCPA an antagonist.
85
Q

What is reserpine used for and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • Reserpine is used as snake bite treatment, alongside being used to treat high blood pressure, but there are side effects.
  • Reserpine prevents the storage of NT in vesicles.
  • It blocks the monoamine transporters.
  • Reserpine in an antagonist.
86
Q

What is ACh used for in relation to black widow venom and what sort of drug is it?
DRUGS AND SYNAPTIC TRANSMISSION

A
  • ACh is often used in cases such as black widow spider venom in the body, and is able to relieve muscle cramps, spasms and restlessness.
  • ACh stimulates the release of neurotransmitters.
  • ACh is an agonist.
87
Q

What is ACh used for in relation to botulinum toxin and what sort of drug is it?
DRUGS AND SYNAPTIC TRANSMISSION

A
  • Botulinum toxin causes paralyses and suffocation.

- ACh acts as an antagonist and inhibits the release of NTs.

88
Q

What is ACh used for in relation to nicotine and muscarine, and what sort of drug is it?
DRUGS AND SYNAPTIC TRANSMISSION

A
  • Muscarine is found in fly fungus and other fungi of Inocybe species, and is a toxic alkaloid.
  • Nicotine and muscarine both bind to receptors and activate cholinergic receptors, and have a stimulant effect.
  • ACh acts as an agonist and stimulates the postsynaptic receptors.
89
Q

What is ACh used for in relation to curare and atropine, and what sort of drug is it?
DRUGS AND SYNAPTIC TRANSMISSION

A
  • Curare has the opposite effect to nicotine, and causes paralysis. It’s used to coat the tips of arrows.
  • Atropine is a medication used to treat certain types of nerve agent and pesticide poisoning as well as types of slow heart rate and to decrease saliva production during surgery.
  • ACh acts as an agonist and blocks the postsynaptic receptors.
90
Q

What is apomorphine and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • Apomorphine is a type of morphine derivare which primarily affects the hypothamalic region of the brain.
  • Drugs of this nature are sometimes used in the treatment of PD and erectile dysfunction, and are highly effective emetics.
  • There are also possible uses in opiate addition but this is yet unconfirmed.
  • Depending on dosage, apomorphine can be an antagonist or an agonist, however in this case there are autoreceptor antagonist effects as it creates a reduction in dopamine synthesis and release.
  • The drug stimulate autoreceptors and inhibits the synthesis/release of the NT dopamine.
91
Q

What is idazoxan used for and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • Idazoxan might enhance the therapeutic effects of antipsychotic medication in schizophrenia, however the effects are still being tested.
  • The drug is an agonist which blocks autoreceptors and increases the synthesis/release of the NT norapinephrine.
92
Q

What does cocaine do and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • Cocaine produces euphoric effects.

- It’s an agonist and blocks the reuptake of dopamine.

93
Q

What is physotigmine used for and what sort of drug is it?

DRUGS AND SYNAPTIC TRANSMISSION

A
  • Physotigmine is used in countering the effects of atropine overdose, and is a muscle relaxant.
  • Physotigmine is an agonist and inactivates acetylcholinsterase.
94
Q

What are the different types of drug influences of NTs?

A
  • There are drugs which influence specific NTs and have effects on them.
  • Depending on the NT that drugs interact with and what molecules of the drug interact with that specific neuron, the effects will be different.
  • Drugs must work with what is naturally occurring.
  • Some NTs transmit info between neurons.
  • Some NTs have modulatory effects on entire circuits of neurons - often called neuromodulators.
95
Q

How will drugs influence behaviour?

A
  • Drugs will influence behaviour dependent on the type of NT with which they interact.
  • Example: if an NT sends messages about muscles, the relevant drug will interact with that message about muscles.
96
Q

What is acetylcholine (ACh)?

ACh

A
  • Acetylcholine is responsible for all muscular movement, both voluntary and involuntary.
  • It is easy to access and easy to diffuse.
97
Q

How does botulinum toxin enter the body?

ACh

A
  • Botulinum toxin enters the body endogenously, and is sometimes found in soil and can enter things like glass jars, and can cause botulism.
  • Botulism is v. dangerous and causes paralysis and suffocation.
98
Q

Is the botulinum toxin an agonist or an antagonist?

ACh

A
  • Botulinum toxin is an acetylcholine antagonist which inhibits the release of ACh, causing botulism.
  • ACh is required for muscular movements and so an antagonist will prevent this from happening.
99
Q

What is the botulinum toxin an active ingredient in?

ACh

A
  • It’s an active ingredient in botox; paralyses the muscles to stop them from contracting.
  • Injection works on neurobindings of the face to cause a small level of paralysis from miniscule doses.
  • More research suggests it might be able to cross the blood-brain barrier.
100
Q

What is black widow spider venom?

ACh

A
  • It’s an ACh agonist so it stimulates the release of ACh.
  • If you’re given an agonist, it sends the muscles into spasm due to the high firing.
  • It causes muscle pain and causes you to become very weak, eventually leading to paralysis.
  • Because it’s an agonist, it’s depleting the resources faster than we can reproduce the ACh.
101
Q

What are the two types of ACh receptors?

ACh

A
  • Ionotropic nicotine receptors.

- Curare.

102
Q

What does nicotine do to ACh?

ACh

A
  • Nicotine is an agonist of nicotinic receptors, causing a stimulus effect, and one of the outcomes can be that you feel stimulated quickly.
  • Nicotine causes presynaptic facilitation of ACh release, thus leading to addictive properties, not only as it directly binds to the receptors of ACh, it upregulates the production of ACh and this might be how it causes addiction. It’s a complicated relationship
103
Q

What is curare?

ACh

A
  • Curare is another molecule in the external world and is in the poison in poison dart frogs. The poison is used to be wiped on the tip of spears in the hunting of animals, and the curare is a nicotinic receptor antagonist, and ach is responsib le for movement. If an antagonist is introduced, it will cause paralysis so the animals will be wounded and paralysed.
104
Q

What is dopamine?

MONOAMINES

A
  • Dopamine is an NT with several dopaminergic systems in the brain.
105
Q

What is the nigrostriatal system?

MONOAMINES

A
  • Nigrostriatal system: important for voluntary movement – it’s the degeneration of this system which causes Parkinson’s disease.
106
Q

Can dopamine pass through the BBB?

MONOAMINES

A
  • No, and so it cannot be administered directly to the brain.
  • Dopamine can’t cross BB barrier, so it has to have a way of bypassing this, for example through L-DOPA, which passes through and upregulates dopamine in the basal ganglia.
    L-DOPA is a dopamine agonist.
107
Q

What happens to L-Dopa?

MONOAMINES

A
  • L-DOPA is synthesised into dopamine and increases dopamine release in surviving dopaminergic neurons.
108
Q

How does L-Dopa work in relation to PD?

MONOAMINES

A
  • Parkinson’s disease is increasingly degenerative and the L-DOPA depends on there being dopamine neurons in the basil ganglia to work on, however eventually there wont be enough dopamine so the L-DOPA will become less effective.
109
Q

How does dopamine work within the mesolimbic system?

MONOAMINES

A
  • Mesolimbic system: some drugs inhibit the reuptake of dopamine, like cocaine.
  • Once dopamine is released, some drugs prevent that dopamine from being taken back into it’s emitted cell, so it cannot be recycled and used again as it usually would.
  • As well as having an impact on movement, dopamine is used in encoding rewarding events, which some drugs target as it creates a sense of euphoria.
110
Q

What happens in the reuptake of dopamine in the mesolimbic pathway?
MONOAMINES

A
  • Reuptake by the emitting neuron is required so when dopamine has exerted its effect at the postsynaptic receptors, the excess dopamine in the synaptic cleft is mopped up so neurotransmission effects don’t continue without regulation.
111
Q

What is cocaine?

MONOAMINES

A
  • Coke is a potent dopamine agonist; stops the dopamine going back into the neuron that sent it out, building a sense of euphoria.
  • It exerts its effect by blocking the reuptake transports on the presynaptic membrane, leading to more dopamine being available in the synaptic cleft, thus binding to dopamine receptors and creating euphoria.
112
Q

How do amphetamines work?

MONOAMINES

A
  • Amphetamines work similarly to cocaine, but instead of just blocking the transporters, it makes the transports work in reverse so there’s more and more spill into the synaptic cleft which creates a feeling of euphoria.
113
Q

What effect does the dopamine coding of reward cause?

MONOAMINES

A
  • When dopamine’s released in some areas of the brain, it brings along with it a subjective experience of pleasure.
114
Q

What is methylphenidate (ritalin)?

MONOAMINE

A
  • Methylphenidate can be used medically to treat ADHD, suggesting ADHD might be an abundance of reuptake transporters which mean that dopamine is taken back into the cells far too quickly.
  • Suggestion that overabundance of reuptake transporters is a risk-factor for ADHD = low levels of dopamine which create an inability to maintain reward-focused behaviour.
  • Treating children with a depletion of dopamine with a drug that increases that dopamine in the system should bring those levels back up to baseline.
115
Q

What is an overabundance of dopamine hypothesised to do in relation to schizophrenia?
MONOAMINES

A
  • Hypothesised to be a major contributing factor to some of the positive symptoms of schizophrenia, such as hallucinations etc.
  • Overabundance of dopamine in reward system = leads to unusual beliefs and hallucinations.
116
Q

What does chloropromazine bind to?

MONOAMINES

A
  • It binds to particular dopamine receptors, known as D2 receptors.
117
Q

What is chloropromazine?

MONOAMINES

A
  • It’s a dopamine antagonist and therefore reduces the effects of dopamine.
  • Reduce the positive symptoms of schizophrenia through decreasing dopamine.
  • Agonist; removes dopamine rather than facilitating it.
118
Q

What can chronic abuse of psychostimulants such as cocaine and amphetamines cause?
MONOAMINES

A
  • The positive symptoms of schizophrenia are a result of too much dopamine, and there are often parallels in people who abuse psychostimulants, thus causing the effects of paranoia which are seen in schizophrenia.
119
Q

What is serotonin?

MONOAMINES

A
  • Serotonin is closely related to dopamine, but does different things.
  • Many neurons in the brain release both serotonin and dopamine.
120
Q

What is serotonin important in?

MONOAMINES

A
  • Serotonin is important in the regulation of mood, control of eating, sleep and arousal, alongside the regulation of pain.
  • It is also linked to depression.
  • There’s a hypothesis that people with extended chronic episodes of depression have depleted levels of serotonin, however there are drugs that can counter this.
121
Q

What is fluoxetine?

MONOAMINES

A
  • It’s commonly known as prozac, and is a serotonin agonist (SSRI).
  • Serotonin agonist which blocks the reuptake transporters so that more serotonin is kept in the system, which might lead to an elevation of mood.
  • Inhibits the reuptake of serotonin.
  • Also used to treat some forms of anxiety disorder and OCD.
122
Q

What type of recreational drugs have an effects on the serotonergic system?
MONOAMINES

A
  • Hallucinogenic drugs like LSD (acid), psilocibyn (shrooms) and MDMA (ecstasy).
123
Q

What are LSD and psilocibyn?

MONOAMINES

A
  • They’re postsynaptic serotonin receptor agonists, meaning that they can induce an altered perception of meaning.
  • These drugs can make you experience things which aren’t reality, and they all affect the serotoninergic system, and are post synaptic receptor agonists and will attach themselves to the receptors in the brain without there being serotonin there. It seems that this leads to an altered perception of meaning.
124
Q

What does MDMA do?

MONOAMINES

A
  • MD causes serotonergic transporters to run backwards which causes the hallucinogenic effect.
  • It also causes excitatory effects through the noradrenergic transporters; causes them to run backwards = creating a feeling of motivation and creating a dual effect of hallucinations and an upsurge of energy.
125
Q

How could hallucinogenic drugs be used to treat depression?

MONOAMINES

A
  • Could play a crucial role in therapeutic use for depression as they allow you to explore an altered perception of the world, acting as a reset mechanism.
  • If you have intense depression, being able to enter an altered world might lead to positive effects of leaving feelings of depression.
126
Q

What are amino acids?

AMINO ACIDS

A
  • They’re categorised by their chemical composition which are the building blocks of proteins.
127
Q

What is glutamate?

AMINO ACIDS

A
  • It’s the most abundant excitatory NT in the brain and one of the most important; we need it to make most things happen.
128
Q

What does glutamate seemingly play a role in?

AMINO ACIDS

A
  • Depending on the neurons it is interacting with it will have different effects. It seems it is v. important in synaptic plasticity (which is vital in learning), and also may play a role in memory.
  • It enables us to form connections between new things in the world, and to store memories etc.
129
Q

Are glutamate receptors complex?

AMINO ACIDS

130
Q

What can antagonist drugs binding to the glutamate receptor NMDA cause?

A
  • Can cause anaesthetic effects, which means that if glutamate is causing excitatory effects and is making you be you, an antagonist binding to this receptor will have an anaesthetic effect as it will bring you down.
131
Q

How does the drug PCP (angel dust) bind to NMDA?

AMINO ACIDS

A
  • PCP will bind to glutamate’s NMDA receptor, which was originally used in anaesthetic but was discontinued as it made people experience dissociative hallucinations.
132
Q

Is alcohol an NMDA agonist or antagonist?

AMINO ACIDS

A
  • Alcohol is also an NMDA antagonist and so it stops glutamate doing its job effectively, and so chronic alcohol abuse can cause seizures if you stop drinking due to the compensatory mechanism of the brain as the excitatory mechanism has been ramped down, the brain will try to fight back and cause as much excitation as possible, and so the reaction that ensues can lead to seizures, thus meaning that chronic alcohol drinkers must be monitored carefully.
133
Q

What is ketamine?

AMINO ACIDS

A
  • Ketamine is a recreational drug originally designed as a horse tranquilliser.
134
Q

What does ket do to the NMDA glutamate receptors?

AMINO ACIDS

A
  • Antagonises the NMDA receptor for glutamate leading to a dissociation of the brain and body. It seems this dissociation frees your mind to enter into an expanded state of consciousness.
135
Q

How can ket be used therapeutically?

AMINO ACIDS

A
  • Entering into an expanded state of consciousness can have therapeutic advantages for people with acute levels of depression, and particularly for people who are suicidal in the moment.
  • It seems that in people with depression, there may be increased levels of glutamate, so an antagonist will ramp down the levels of glutamate and may have a therapeutic advantage.
  • Treating suicidal people with ketamine might bring them up to a baseline level.
  • One study found that less than 2 hours after ketamine injection, 71% of patients showed improvement in symptoms, and 20% showed remission of symptoms.
  • It’s especially hopeful for those who are otherwise treatment-resistant.
136
Q

What is GABA?

AMINO ACIDS

A
  • GABA is the most abundant inhibitory NT, which turns things off in the brain and stops things firing uncontrollably as a result of excitatory transmission
137
Q

What is epilepsy thought to be?

AMINO ACIDS

A
  • It is thought that one of the causes of epilepsy is the result of a default of GABA receptors as the brain is unfettered with regard to its electrical activity which can be problematic and cause seizures.
  • Epilepsy = abnormality in GABA secreting neurons or GABA receptors.
138
Q

Are GABA receptors complex?

AMINO ACIDS

139
Q

What do agonist drugs binding to the GABA receptor GABA-A cause?
AMINO ACIDS

A
  • Can cause tranquillising effects, thus meaning that GABA is ramped up as GABA is inhibitory.
140
Q

What are benzodiazepines?

AMINO ACIDS

A
  • They’re agonist for GABA-A receptors (includes valium), and are useful as anxiolytics.
  • Valium is a useful agonist for GABA as it helps with anxiety through boosting the levels of GABA to alleviate feelings of anxiety.
141
Q

What are barbiturates?

AMINO ACIDS

A
  • They’re GABA-A agonists and are still used today in the lethal injection for execution.
142
Q

What is alcohol?

AMINO ACIDS

A
  • Alcohol is a GABA-A agonist, so it ramps down the brain to make you feel tired.
143
Q

What are peptides?

PEPTIDES

A
    • We have a system in the brain which we have to make sure that if we’re injured, we have some natural way of relieving the pain to get us to seek help or run away.
144
Q

What are endogenous opioids?

PEPTIDES

A
  • We need this naturally occurring system in our brains to help us promote survival; it’s an endogenous opioid system in the brain which works to ensure our safety.
145
Q

What neural systems are activated when opiate receptors are stimulated?

A
  • One system produces analgesia.
  • One system inhibits ‘flight’ responses.
  • One system stimulates dopamine neurons involved in reinforcement (the reward system).
146
Q

What is an endorphin rush?

PEPTIDES

A
  • Endorphin rush is where the opioid system releases endorphins to counteract pain.
147
Q

What do opiate drugs such as heroin, morphine and opium act as?
PEPTIDES

A
  • They act as opiate receptor agonists.

- The activation of the reward system is responsible for addiction.

148
Q

What is analgesia?

PEPTIDES

A
  • Analgesia is pain relief.
  • This works well with the system which inhibits ‘flight’ responses as it ensures that you have pain relief for the fight response.
149
Q

Can heroin cross the BBB?

PEPTIDES

A
  • Yes, it crosses the BBB very quickly, creating an intense feeling of euphoria.
150
Q

What is naloxone?

PEPTIDES

A
  • It’s an opiate receptor antagonist and reverses heroin overdose and therefore helps people recover.
151
Q

What drugs work on lipids?

OTHER DRUGS

152
Q

Give an example of endocannabinoids?

OTHER DRUGS

A
  • Anandamide is a prominent example, and cannabis works as an agonist.
153
Q

What is anandamide involved in?

OTHER DRUGS

A
  • Anadamide is involved in memory, reading behaviour, reward behaviour and pain relief.
154
Q

How is cannabis implicated in anandamide?

OTHER DRUGS

A
  • Cannabis creates changes in time perception and causes the munchies as anadamide is directly related to feeding behaviour.
155
Q

What is SPICE?

OTHER DRUGS

A
  • Synthetically manufactured; also works on the endocannibinoid system in the brain and has a similar effects.
  • It’s a designer drug.
156
Q

What are nucleosides?

OTHER DRUGS

A

-Adenosine, which has an inhibitory effect and dilates blood vessels, and an accumulation of adenosine causes sleepiness.

157
Q

What sort of effect does caffeine have?

OTHER DRUGS

A
  • Caffeine has an antagonist of adenosine which has an inhibitory effect and accumulation of it in the day causes sleepiness, but caffeine stops this from happening.
158
Q

What are soluble gases?

OTHER DRUGS

A
  • Nitric oxide, which dilates blood vessels and induces penile erection, and also may be involved in learning.
159
Q

What is viagra?

OTHER DRUGS

A
  • Viagra (sildefanil) reduces destruction of nitric oxide’s secondary messenger (cyclic GMP) and sustains erections, making it an agonist.

Biological Psychology (2 decks)

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