Block D Lecture 2: CNS Chemical Messengers

Question 1

What are the 2 types of neurotransmitters?

Answer 1

Peptide and non-peptide neurotransmitters
(Lecture 2, Slide 2)

Question 2

What are the 3 first steps of a neurotransmitter acting?

Answer 2

1. Action potential reaches terminal
   2.Voltage-gated Ca2+ channels open
2. Calcium enters axon terminal
   (Lecture 2, Slide 4)

Question 3

What are the last 3 steps of a neurotransmitter acting?

Answer 3

4. The neurotransmitter is released and diffuses into the synaptic cleft
5. The neurotransmitter binds to postsynaptic receptors
6. The neurotransmitter is removed from the synaptic cleft
   (Lecture 2, Slide 4)

Question 4

What is the synaptic cleft?

Answer 4

The space between 2 neurons
(Lecture 2, Slide 4)

Question 5

What are the 6 criterial for a substance to be considered a neurotransmitter?

Answer 5

1. Synthesised within a neuron
2. Stored in nerve (axon) terminal
3. Released by nerve stimulation in Ca2+-dependent manner
4. Specific mechanisms exists for its inactivation
5. Exogenously applied substance mimics endogenous response to neurotransmitter (An exogenus substance and the neurotransmitter must have the same effect on the same receptor)
6. Antagonist inhibits both the neurotransmitter and exogenously applied substance
   (Lecture 2, Slide 6)

Question 6

What is a nerve/axon/synaptic terminal?

Answer 6

The end portion of an axon (the long, slender part of a neuron)
(Lecture 2, Slide 6)

Question 7

What is a exogenously applied substance?

Answer 7

A substance originating from outside the body which is introduced or applied externally
(Lecture 2, Slide 6)

Question 8

Is dopamine a neurotransmitter?

Answer 8

Yes
(Lecture 2, Slide 7)

Question 9

How is dopamine synthesised within a neuron?

Answer 9

Tyrosine is hydroxylated by tyrosine hydroxylase enzyme into L-DOPA (dihydroxyphenylalanine) which is then decarboxylated by the enzyme dopa decarboxylase into dopamine
(Lecture 2, Slide 7)

Question 10

What are the 4 dopaminergic projections?

Answer 10

Mesolimbic pathway
Mesocortical pathway
Nigrostriatal pathway
Tuberoinfundibular pathway
(Lecture 2, Slide 8)

Question 11

Where does the mesolimbic dopaminergic projection originate and project to, and what is it involved in?

Answer 11

It originates in the ventral tegmental area (VTA) and projects to various limbic structures such as the nucleus accumbens. This pathway is involved in reward, motivation and processing of emotional experiences
(Lecture 2, Slide 8)

Question 12

Where does the mesocortical dopaminergic projection originate from and project to, and what is it involved in?

Answer 12

Like the mesolimbic pathway, it originates from the ventral tegmental area (VTA) but its projections extend to the prefrontal cortex. This pathway is involved in cognitive function, executive control and emotional regulation
(Lecture 2, Slide 8)

Question 13

Where does the nigrostriatal dopaminergic projection originate from and project to, and what is it involved in?

Answer 13

It originates in the substantia nigra and projects to the striatum. This pathway is involved in motor control and co-ordination
(Lecture 2, Slide 8)

Question 14

Where does the tuberoinfundibular dopaminergic projection originate from and project to, and what is it involved in?

Answer 14

it originates in the hypothalamus (in the arcuate nucleus) and projects to the pituitary gland. This pathway regulates the secretion of prolactin (a hormone involved in lactation)
(Lecture 2, Slide 8)

Question 15

How does dopamine meet the mimicry requirement of being classified as a neurotransmitter?

Answer 15

cAMP measured in the striatum after nerve stimulation shows same levels as cAMP measured in the striatum after addition of dopamine
(Lecture 2, Slide 10)

Question 16

How does dopamine meet the inhibition by agonist requirement of being classified as a neurotransmitter?

Answer 16

D2-R antagonist inhibits both nerve stimulation and dopamine, as shown by cAMP levels staying high, (and the same between both nerve stimulation and dopamine addition) with levels not decreasing when dopamine is added or nerve stimulation occurs
(Lecture 2, Slide 11)

Question 17

Name 5 neurotransmitters in the brain.

Answer 17

Answers Include:
Noradrenaline
Dopamine
Serotonin (5-HT)
Acetylcholine
Glutamate
GABA
Glycine
(Lecture 2, Slides 13 and 14)

Question 18

What are 3 of the physiological functions of noradrenaline?

Answer 18

Answers include:
Reward pathway
Mood
Sleep / wakefulness
State of alertness
Blood pressure regulation
(Lecture 2, Slide 13)

Question 19

What are 3 physiological functions of serotonin?

Answer 19

Sleep/wakefulness
Temperature regulation
Mood
(Lecture 2, Slide 13)

Question 20

What are 3 physiological functions of acetylcholine?

Answer 20

Arousal
Learning
Motor control
(Lecture 2, Slide 14)

Question 21

What are 3 physiological functions of glutamate?

Answer 21

Memory
Epilepsy (an imbalance of glutamate can cause this)
Relay of sensory information
(Lecture 2, Slide 14)

Question 22

What are 2 physiological functions of GABA?

Answer 22

Manage anxiety + epilepsy
(Lecture 2, Slide 14)

Question 23

What are 3 similarities in neuropeptides and classical neurotransmitters?

Answer 23

Both are stored in vesicles, relay on Ca2+ ions for release and effect through2nd messengers or directly on ion channel activity
(Lecture 2, Slide 16)

Question 24

State 3 differences between neuropeptides and classical neurotransmitters.

Answer 24

Answers include:
Neuropeptides are synthesised in cell body (instead of in a neuron)

They are transported to the terminal

They are released at lower concentration

They have longer action
They are removed slowly from the synaptic cleft
(Lecture 2, Slide 17)

Question 25

What molecules does slow and fast neurotransmission use?

Answer 25

Slow neurotransmission uses neuropeptides whereas fast neurotransmission uses neurotransmitters
(Lecture 2, Slide 18)

Question 26

How long does slow neurotransmission take to take effect?

Answer 26

Seconds to minutes
(Lecture 2, Slide 18)

Question 27

Is slow neurotransmission direct or indirect acting?

Answer 27

Indirect, acts via G proteins and cytoplasmic 2nd messengers
(Lecture 2, Slide 18)

Question 28

How long does fast neurotransmission take to act?

Answer 28

10’s of milliseconds
(Lecture 2, Slide 21)

Question 29

Is fast neurotransmission direct or indirect acting?

Answer 29

Direct, via receptor-operated ion channels
(Lecture 2, Slide 21)

Question 30

What are excitatory and inhibitory post-synaptic potential?

Answer 30

They are changes in the membrane potential of a postsynaptic neuron or cell in response to the binding of neurotransmitters released by a presynaptic neuron
(Lecture 2, Slide 22)

Question 31

What are pre-synaptic and post-synaptic neurons?

Answer 31

A pre-synaptic neuron transmits a signal towards a synapse whereas a post-synaptic neuron transmits a signal away from a synapse
(Lecture 2, Slide 22)

Question 32

What is the difference between excitatory post-synaptic (EPSP) and inhibitory post-synaptic potential (IPSP)?

Answer 32

EPSP is a depolarising change in membrane potential whereas IPSP is a hyperpolarising charge in membrane potential
(Lecture 2, Slide 22)

Question 33

Do EPSP and IPSPs increase or decrease the chance of an action potential occuring?

Answer 33

An EPSP increases the chance of an action potential occurring whereas an IPSP decreases it
(Lecture 2, Slide 23)

Question 34

What is temporal summation?

Answer 34

When an individual EPSP is not enough to cross the threshold of an action potential occurring but if it occurs in rapid succession and overlap in time, the effects can break the threshhold
(Lecture 2, Slide 23)

Question 35

What is spatial summation?

Answer 35

The simultaneous stimulation of multiple different EPSPs to combine their effects to reach the threshold to trigger an action potential, as one EPSP enough may not be enough to trigger this
(Lecture 2, Slide 23)