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Brain and Behaviour > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

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1
Q

How do neurons communicate?

A

through the release of neurotransmitters that are released into the synaptic cleft and onto receptors located on the cells they communicate with

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2
Q

What are neurotransmitters?

A

chemical messengers produced, stored and released by neurons

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3
Q

Where are neurotransmitters usually produced and released?

A

They are usually produced in terminal buttons and released into the synaptic cleft by exocytosis. They cross the synaptic cleft and bind to the postsynaptic membrane of the adjacent membrane

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4
Q

What do excitatory and inhibitory neurotransmitters do?

A

If they are excitatory they trigger an ESPS (depolarisation), if they are inhibitory they trigger an IPSP (hyperpolarisation)

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5
Q

Do most neurotransmitters have excitatory or inhibitory effects or both?

A

Both

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6
Q

What effects does glutamate have?

A

Only excitatory effects

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7
Q

What effects do GABA (and glycine in the spinal cord) have?

A

Only inhibitory effects

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8
Q

What sort of effect do most neurotransmitters have?

A
  • a modulating effect

- their release tends to activate or inhibit entire circuits of neurons that are involved in particular brain functions

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9
Q

What is Psychopharmacology?

A

The study of the effects of drugs on the nervous system and on behaviour

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10
Q

What are drug effects?

A

the changes a drug produces in animal’s physiological processes and behaviour. In the nervous system, most drugs affect synaptic transmission

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11
Q

What do a lot of drugs mimic?

A

Neurotransmitters

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12
Q

What is an antagonist?

A

a drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell

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13
Q

What is an agonist?

A

a drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell

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14
Q

What is acetylcholine?

A

Primary neurotransmitter secreted by the efferent axons of the CNS

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15
Q

Where is acetylcholine found and what does this mean?

A
  • Found on all neuromuscular junctions (place where neurons make connections with muscles)
  • All muscular movement is accomplished by the release of ACh
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16
Q

What is ACh involved in?

A

regulating REM sleep – dreaming (dorsolateral pons), perceptual learning (basal forebrain), and memory (hippocampus)

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17
Q

Where is ACh found?

A

At the target of the parasympathetic brain of the ANS - outside of the CNS

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18
Q

What are the ACh receptors?

A

Nicotinic and muscarinic receptors

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19
Q

What is a nicotinic receptor?

A
  • Ionotropic acetylcholine receptor stimulated by nicotine (opened from the outside)
  • Sodium ligand gated ion channel – sodium causes depolarisation and excitation of the cell
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20
Q

On which postsynaptic membranes are the nicotinic receptors found?

A

 All autonomic ganglia
 All neuromuscular junctions
 Some CNS pathways

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21
Q

Give features of the Muscarinic receptors

A
  • Metabotropic acetylcholine receptor (neurotransmitter binds to protein that either opens or closes the potassium channel – open causes hyperpolarisation, closed causes depolarisation)
  • Causes either inhibition or excitation
  • Produces parasympathetic nerve effects in the heart, smooth muscles and glands
  • G-protein coupled receptors
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22
Q

What are nicotinic receptors stimulated and blocked by?

A
  • stimulated by nicotine
  • blocked by curare
     Curare acts at the junction between nerve cells and muscles causing paralysis
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23
Q

What are muscarinic receptors stimulated and blocked by?

A
  • stimulated by muscarine
  • blocked by Atropine
     Atropine acts by preventing acetylcholine from depolarising the post-synaptic membrane in the parasympathetic branch – treatment of low heart rate
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24
Q

What is the Botulinum Toxin?

A

an acetylcholine antagonist: prevents release by terminal buttons – reduces muscles contractions, reduces wrinkles

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25
Q

What does Black Widow Spider venom do?

A

A poison produced by the black widow spider that triggers the release of acetylcholine causing convulsions – agonist. Can cause death

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26
Q

Give four neurotransmitters that belong to the Monoamides, what do they all effect?

A

Dopamine, norepinephrine, epinephrine and serotonin are four neurotransmitters that belong to a family of compounds called monoamides. All effect mood

27
Q

What is a precursor to the monoamides?

A

Tyrosine

28
Q

Why do some of the same drugs affect all of the Monoamines?

A

Because their structures are very similar

29
Q

How do you get from Tyrosine to Norepinephrine?

A

Tyrosine -> l-DOPA -> Dopamine -> Norepinephrine (enzyme helps in each of these stages)

30
Q

What are the main functions of Dopamine?

A
  • regulates reward

- involved in addiction pathways

31
Q

What happened when rats were in injected with Cocaine?

A
  • If they were injected in the periphery they would press the lever for more cocaine
  • If it were injected directly into the CNS they were even quicker to press the level for more Cocaine
32
Q

What are natural rewards?

A

food, water, sex, nurturing

33
Q

What is Addiction?

A

A state in which an organism engages in compulsive behaviour, behaviour is reinforcing (rewarding, pleasurable), loss of control for intake

34
Q

What is the path of the reward pathway?

A

Reward pathway starts deep in the midbrain (ventral tegmental area) -> Nucleus accumbent -> prefrontal cortex

35
Q

What is Tolerance?

A

 A state in which organism no longer responds to a drug

 A higher dose is required to achieve the same effect

36
Q

What is Dependence?

A

 A state in which organism functions normally only in the present of a drug
 Manifested as physical disturbance when the drug is withdrawn

37
Q

Why is it possible to be dependent on a drug without being addicted to it?

A

Because the processes work in different circuits in the brain

38
Q

Where are Cocaine binding sites?

A

in the nucleus accumbent

39
Q

What usually happens with dopamine?

A
  • Cocaine binding sites are in the nucleus accumbent (caudate nucleus with tail)
  • At the synapse dopamine comes to the presynaptic cell
  • The vesicles fuse with the presynaptic cell and release dopamine into synaptic cleft
  • Dopamine binds to postsynaptic receptor
  • Dopamine taken back to presynaptic cell (reuptake)
40
Q

What does Cocaine do?

A
  • blocks dopamine reuptake by binding to the proteins that facilitate reuptake
  • therefore you will have more dopamine
  • as it uses energy there is a glucose reduction due to Cocaine
41
Q

What other effects does Dopamine have apart from in the reward system?

A
  • Regulates movement and the control of attention
  • Nigrostriatal system: starts in the substantia nigra and terminates in the basal ganglia: plays a role in the control of movement
42
Q

What is Parkinson’s disease and how has it been treated?

A

Parkinson’s disease is a neurological condition characterised by tremors, rigidity of the limbs, poor balance and difficulty initiating movements; caused by degeneration of the nigrostriatal system; Parkinson’s disease has been treated with L-DOPA

43
Q

What is the function of Serotonin (5-HT)?

A
  • plays a role in the regulation of mood, the control of eating, sleep, dreaming and arousal
  • Involved in the regulation of pain
  • Plays a role in depression
44
Q

What are the Serotonin nerve pathways in the brain?

A

 Start in Raphe nuclei
 Either go down to spinal cord or go through the midbrain functions such as hippocampus, amygdala, thalamus, hypothalamus, then to prefrontal cortex and cerebellum
 Back to Raphe nuclei

45
Q

What does LSD do?

A

stimulates centres of the sympathetic nervous system in the midbrain which leads to pupillary dilation, increase in body temperate and rise in the blood sugar level

46
Q

What does MDMA do?

A

Serves as a serotonergic agonist, also known as ‘ecstasy’, has excitatory and hallucinogenic effects

47
Q

What happens with the Serotonin synapse?

A

Serotonin in vesicles, fuse with presynaptic cleft, bind to postsynaptic receptors, reuptake

48
Q

What are the effects of ecstasy on serotonin transporters?

A

 Prevent reuptake
 Binds to serotonin transporter protein
 Work in reverse mode: bring more 5-HT to the synapse

49
Q

What are the short term effects of ecstasy?

A

 Feel cold
 Experience jaw clenching
 Clouded thinking
 Disturbed behaviour

50
Q

What did they find from the experiment of ecstasy on monkeys?

A

 Monkeys had ecstasy twice a day for four days and then killed after two weeks or 7 years
 Dramatic lack of serotonin compared to control after two weeks
 A lot less serotonin after 7 years compared to control

51
Q

What are the long term effects of ecstasy?

A

 Degeneration of serotonin nerve terminals

 Impairments of verbal and visual memory – affects serotonergic synapses in hippocampus and prefrontal cortex

52
Q

Talk about serotonin and depression

A

 Low serotonin levels are believed to be the cause of many cases of mild to severe depression which can lead to symptoms such as anxiety, apathy, fear, feelings of worthlessness, insomnia and fatigue
 If depression arises as a results of serotonin deficiency then pharmaceutical agents that increase the amount of serotonin in the brain should be helpful in treating depressed patients. Anti-depressant medications increases serotonin levels at the synapse by blocking the reuptake of serotonin into the presynaptic cells: SSRIs (serotonin selective reuptake inhibitors)

53
Q

What is noradrenaline?

A

It is both a hormone and a neurotransmitter. As a hormone, secreted by the adrenal gland, it works alongside epinephrine/adrenaline to give the body sudden energy in times of stress, known as the fight or flight response

54
Q

What can medications that inhibit the reuptake of Noradrenaline be effective in treating?

A

Depression

55
Q

What is found in patients experiencing mania?

A

Elevated noradrenaline levels

56
Q

What is adrenaline?

A

a hormone secreted by the adrenal medulla; serves as a neurotransmitter in the brain

57
Q

Which amino acids are the most common neurotransmitters in the CNS?

A

glutamate, GABA and glycine

58
Q

What does Glutamate do?

A

 Binds to NMDA receptor: a specialised inotropic glutamate receptor: sodium ions cause depolarisation. Has many binding sites. Also has a blockage site (magnesium), magnesium needs to be released in order for receptor to be activated
 Most important excitatory neurotransmitter in the brain

59
Q

What is PCP?

A

angel dust synthetic drug, indirect antagonist. Won’t let magnesium be released

60
Q

What is GABA?

A

Most important inhibitory neurotransmitter in the brain

61
Q

Give features of GABA

A

 Involved in many different brain functions. Imbalances in GABA are relevant to bipolar disorder, schizophrenia, and anxiety disorder
 The GABA neurotransmitter and its receptors are critical to how humans think and act
 GABA is part of the brain system that allows us to fine-tune our moods, thoughts, and actions with an incredible level of detail
 GABA – driving a car. You need the accelerator but at every stage you need the brakes to work
 GABA provides the necessary inhibitory effects that we need in order to block our excessive brain activity that in depression may lead to excessive negative thinking (excessive GABA activity leads to depression)

62
Q

What are Benzodiazepines?

A

category of anxiolytic drugs (tranquilizers): an indirect agonist for the GABAA receptor; these drugs are used for their tranquilizing effects: Valium (diazepam)

63
Q

Give a summary of acetylcholine, GABA, dopamine, serotonin and glutamate

A
  • Acetylcholine is the transmitter at the NMJ connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors (nicotinic)
  • GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Corresponding glycine is the inhibitory transmitter in the spinal cord
  • Dopamine plays a critical role in the reward system, but dysfunction of the dopamine system is also implicated in Parkinson’s disease and schizophrenia
  • Serotonin regulates appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the cardiovascular system and endocrine system. It plays a role in depression
  • Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are ‘modifiable’ (capable of increasing or decreasing in strength.) Modifiable synapses are thought to be the main memory storage elements in the brain.

Brain and Behaviour (11 decks)

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