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Neurology and Neuroscience > NS Pharmacology > Flashcards

NS Pharmacology Flashcards

Pharmacology and Neurotransmitters

1
Q

Pharmacology defination?

A

Chemical substance that interacts with a specific target within a biological system to produce a physiological effect

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2
Q

How drugs produce effects?

A

What is the target for the drug?
Where is the effect produced?
What is the response produced after interaction with this target

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3
Q

Why do side effects happen?

A

Dependent on dose of drug

Can be due to effect on other targets in the body or the same target ( in the same or different tissue e.g. dopamine receptors in gut can cause constipation from pramipexole - structurally similar to dopamine - agonist) - can happen as dose increases, enough receptors will increase to see side effect

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4
Q

What makes a drug safe?

A

Having a large difference between dose required for required effect and dose required for side effects

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5
Q

Atorvastatin drug target class

A

Enzyme HMG coA

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6
Q

Amlodipine drug target class

A

Ion channel

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7
Q

Salbutamol drug target class

A

Receptor Beta 2 in lung = bronchodilation

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8
Q

Citalopram drug target class

A

Transport protein

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9
Q

Why might selectivity be more important for drugs than endogenous compounds e.g. dopamine, noradrenaline

A

Neurotransmitters are released from nerves specifically to the corresponding nerve receptors so this overcomes issue of similar shaped neurotransmitters.

Drugs, however go into bloodstream and so can cause effects to multiple receptors if the drug looks alike. (lock and key)

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10
Q

As dose increases…

A

Selectivity decreases

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11
Q

What are the small membranous protrusions from a neuron’s dendrite ?

A

Protein molecules called spine = increase SA to increase information coming in

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12
Q

What are the two important amino acid neurotransmitters?

A

Glutamate - excititory transmitter

y-aminobutryric acid - (GABA) - inhibitory transmitter

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13
Q

Amines as neurotransmitters?

A

Noradenraline and Dopamine

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14
Q

What Neuropeptides can act as Neurotransmitters?

A

Opioid peptides

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15
Q

Activation of synapse:

Action potential reaches ‘x’ and causes ‘y’. This activated voltage sensitive ‘z’ channels. ‘z’ floods into terminal and activates exocytotic release of NT into cleft. Fusion and release is aided by ‘a’ on the vesicles, presynaptic

A

x = axon terminal

y = depolarisation

z = calcium ions

‘a’ = vesicular proteins (e.g. synapsin, SNAP 25 - SNARE proteins)

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16
Q

How much Calcium increase is required for synaptic transmission?

A

200 microMolars from around 1 microMolar

  • has the highest concentration gradients
17
Q

How many molecules of NT in each vesicle

A

4000-10,000 loaded into vesicles before release = idea of NT release of Quanta

18
Q

Alpha Latrotoxin and muscular paralysis

A

from black widow spider, stimulates transmitter release to depletion. targets for the vesicular proteins to do so

19
Q

Zn2+ dependent endopeptidases?

A

Inhibit transmitter release

e.g. Tetanus toxin inhibits glycine and GABA - spasms and pralysis

20
Q

Botulinum toxin causing flaccid paralysis?

A

From clostridium botulinum

Due to muscle relaxation, can cause respiratory arrest in fatal doses or lethal food poisoning. Botux uses this method.

Bi-chain molecule, one part binding to nerve terminal, 2nd chain penetrates nerve terminal and cleaves peptide bonds on vesicular proteins. no more exocytosis.

21
Q

What are ion channel linked receptors in synapses?

A

Fast responses in msecs, mediate all fast excitatory and inhibitory transmission

e.g. in CNS glutamate, GABA
in NMJ Acetylcholine at nicotine receptors

22
Q

What NT receptor mediates slow responses?

A

G-protein-coupled receptors. secs/mins

CNS and PNS : ACh at muscarinic receptors, dopamine, noradrenaline, serotonin, neuropeptides, 5HT, endorphins

23
Q

Why are G-protein coupled receptors named as such?

A

When the agonist reaches the receptor the receptor will couple with g-protein, which will couple with the effector e.g. enzymes or channels

24
Q

Do the NT go through ion-linked channels and what are subunits?

A

No,
E.g. Glu binds and causes Na+ influx = depolarisation
GABA binds and causes Cl- influx and Gly causes Cl- influx = hyperpolarisation

Multiple subunit combinations lead to distinct functions

25
Q

Explain EPSP vs IPSP?

A

Excitatory postsynaptic potential (depolarisation) from e.g. glutamate

Inhibitory postsynaptic potential (hyperpolarisation) e.g. GABA

26
Q

What are the two main types of Glutamate receptors?

A

AMPA Receptors : fast excitatory responses, rapid onset and offset and desensitisation

NMDA Receptors : Permeable to Na+ but also Ca2+
slow component of excitatory transmission. Serve as coincidence detectors

27
Q

What role to Glial cells play in an excitatory Glu synapse?

A

After transmission Glu needs to be taken up by the presynaptic axon and loaded back into vesicles.

It can also be taken up into Glial cells by excitatory amino acid transporters EAATs

Glutamine synthetase creates it into glutamine

28
Q

What measures electrical activity in the brain?

A

EEG

Electroencephalography

29
Q

Epileptic Seizures

A

Abnormal cell firing leads to seizures associated with excess glutamate in synapse increasing brain activity as well as physical seizures.

Recurrent activity

30
Q

How is GABA synthesized?

A

Decarboxylation of glutamate by glutamic acid decarboxylase - GAD

31
Q

GABA in Glial cells?

A

GABA transporters take in GABA and modified by GABA-transaminase to succinic semialdehyde = succinate which goes into TCA

32
Q

Why is GABA receptor units considered?

A

Pentameric organisation

Different drugs can bind to different subunits and can facilitate transmission of GABA
E.g. Antiepileptic
Anxiolytic
Sedative
Muscle relaxant

Neurology and Neuroscience (21 decks)

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