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YEAR 1 - Physiology and Pharmacology (Anton) > 6. Excitable Cells: Neural Communication (HT) > Flashcards

6. Excitable Cells: Neural Communication (HT) Flashcards

1
Q

Describe how the divisions of the spinal cord that are sympathetic and paraympathetic.

A

Remember: PSP

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2
Q

What are catecholamines?

A
  • Hormones made by your adrenal glands, which are located on top of your kidneys.
  • Examples: dopamine, noradrenaline, adrenaline
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3
Q

What are the main catecholamines?

A
  • Dopamine
  • Noradrenaline
  • Adrenaline
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4
Q

Describe how catecholamines are synthesised.

A

Tyrosine -> L-Dopa -> Dopamine -> Noradrenaline -> Adrenaline

  • Tyrosine is converted to L-Dopa by tyrosine hydroxylase
  • L-Dopa is converted to dopamine by DOPA decarboxylase
  • Dopamine is converted to noradrenaline by dopamine beta-hydroxylase
  • Noradrenaline is converted to adrenaline by phenylethanolamine N-methyl transferase
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5
Q

Describe where each stage of the synthesis of catecholamines occurs in the cell.

A
  • Low concentrations of catecholamines are free in the cytosol
  • Conversion of tyrosine to L-DOPA and L-DOPA to DA occurs in the cytosol
  • DA then is taken up into the storage vesicles
  • In NE-containing neurons, the final β hydroxylation occurs within the vesicles.
  • In the adrenal gland, NE is N-methylated by PNMT in the cytoplasm. Epinephrine is then transported back into chromaffin granules for storage.
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6
Q

Which is the step in catecholamine synthesis which is typically regulated and why?

A
  • Conversion of tyrosine to L-DOPA by tyrosine hydroxylase
  • This is because this is the slowest step, so it is the rate-limiting step
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7
Q

How is tyrosine moved into the nerve varicosity?

A

Sodium-dependent aromatic L-amino acid transporter

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8
Q

Describe the properties of tyrosine hydroxylase.

A
  • Cytoplasmic, but loosely associated with the endoplasmic reticulum
  • Fe2+ and tetrahydro(bio)pteridine are cofactors
  • Enzyme is subject to feedback inhibition by noradrenaline (end-product inhibition) and activity regulated by phosphorylation
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9
Q

Describe the acute and long-term regulation of tyrosine hydroxylase.

A
  • Acute -> Noradrenaline reduces tyrosine hydroxylase activity (end-product inhibition)
  • Long-term -> Up-regulation by de novo synthesis of tyrosine hydroxylase
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10
Q

Describe the properties of DOPA decarboxylase and dopamine β-hydroxylase.

A
  • DOPA decarboxylase
    • Cytoplasmic
  • Dopamine β-hydroxylase
    • Located in storage vesicles
    • Specificity not high so will convert many phenylethylamine derivatives e.g octopamine from tyramine
    • Ascorbate is a co-factor
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11
Q

Describe the properties of phenylethanolamine N-methyltransferase.

A
  • Located in the chromaffin cells of the adrenal medulla
  • Also converts other hydroxylated phenylethylamines e.g synephrine from octopamine
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12
Q

What are some ways in which the synthesis pathway for catechaolamines can be targetted clinically?

A
  • α-methyltyrosine
    • Competitive inhibitor of conversion of tyrosine to L-DOPA by tyrosine hydroxylase.
    • Was used to treat the effects of tumours of the adrenal medulla (pheochromocytoma) by reducing the systemic release of catecholamines.
    • There is a wide range of side effects of reduced systemic catecholamines and α-methyltyrosine is not specific to a single catecholamine, so the drug is not widely used.
  • L-DOPA
    • Used to bypass tyrosine hydroxylase, which is usually the rate-limiting step
    • Clinically, used to treat Parkinson’s because concentration of dopamine in the brain can be increased
  • Carbidopa
    • Inhibits conversion of L-DOPA to dopamine by DOPA decarboxylase.
    • Clinically, carbidopa is used alongside L-DOPA in treating Parkinson’s disease because carbidopa cannot be taken into the brain, so it only inhibits the conversion of L-DOPA in the periphery and not the brain. This means that L-DOPA can be used to increase dopamine secretion selectively in only the brain.
  • Disulfiram
    • Inhibits conversion of dopamine to NA by dopamine β-hydroxylase
    • Not used much for this application due to many side effects
    • Clinically, disulfiram is used in inhibiting aldehyde dehydrogenase in treating alcohol dependence, since it stimulates the effects of a hangover almost immediately upon alcohol consumption.
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13
Q

Give an example of a false transmitter in the synthesis of catecholamines.

A
  • α-methyldopa is a false substrate for the noradrenaline synthesis pathway
  • It isconverted to α-methylnoradrenaline, which is released alongside noradrenaline into the junction
  • It has higher affinity for α2 receptors (but not α1) than noradrenaline
  • So it is used clinically to treat hypertension in a selective manner.
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14
Q

Describe how catecholamines are stored.

A
  • Noradrenaline -> In vesicles, using vesicular monoamine transporters
  • Adrenaline -> In chromaffin cells of the adrenal medulla
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15
Q

Describe the storage of catecholamines in vesicles.

A

Dopamine and NA that has been reuptaken are moved into storage vesicles by vesicular monoamine transporters (VMAT), utilising a proton gradient set up by a proton pump.

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16
Q

Give an example of a drug that inhibits the storage of catecholamines in vesicles.

A
  • Reserpine can be used to block the amine binding site of VMAT, preventing the uptake of catecholamines into vesicles, so that their content is depleted by leakage.
  • Clinically, reserpine is used as an antihypertensive drug since the lack of catecholamines contributes to reduced heart contraction and vasodilation in certain blood vessels.
  • The side effects of reserpine may include depression due to the decreased release of, for example, dopamine in the brain, but this mechanism for onset of depression has been subject to much debate.
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17
Q

Compare the release sites of adrenaline and noradrenaline.

A
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18
Q

Describe the process of the release of noradrenaline. How is this regulated endogenously?

A
  • NA exocytosis is triggered by calcium influx following an action potential (as well as a small amount of spontaneous release).
  • All sympathetic nerve terminals have a α2 adrenoceptors on the prejunctional membrane, which are Gi-coupled GPCR that result in decreased levels of cAMP (via adenylate cyclase stimulation) when activated. This reduces PKA activity, causing decreased phosphorylation of voltage-gated calcium channels, so that calcium influx upon action potentials is weaker and less NA is released.
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19
Q

Describe how the release and action of noradrenaline can be regulated clinically.

A
  • Clonidine
    • Agonist of α2 receptors on the nerve terminal membrane
    • Used to treat hypertension by reducing NA release in the peripheral nervous system and the brain stem.
  • α-methyldopa
    • False substrate for the noradrenaline synthesis pathway and is converted to α-methylnoradrenaline, which is released alongside noradrenaline into the junction.
    • It has higher affinity for α2 receptors (but not α1) than noradrenaline, so it is used clinically to treat hypertension in a selective manner.
  • Guanethidine
    • Taken up into vesicles, decreasing stored levels of NA in vesicles and inhibiting exocytosis by a poorly understood mechanism.
  • Bretylium
    • Acts in the same manner as guanethidine
    • Also a blocker of potassium channels, so it is used as an antiarrhythmic drug.
  • Amphetamines
    • Used to treat ADHD, since they help increase release of dopamine and NA at sites of the brain responsible for attention
    • Use at high doses is associated with a risk of addiction.
  • Tyramine
  • Trimetaphan
    • Non-depolarising competitive antagonist of nAChRs at autonomic ganglia
    • Due to its action on both the sympathetic and parasympathetic system it is not highly specific in action and is rarely used clinically.
  • Tyramine
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20
Q

What are indirectly acting sympathomimetics (IAS)?

A

Drugs that indirectly increase the release of catecholamines.

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21
Q

Describe how catecholaminergic transmission is terminated.

A

It is mostly done MOSTLY by uptake of the neurotransmitter, rather than its hydrolysis like with ACh.

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22
Q

Describe the process of catecholamine reuptake after release.

A

There are two main pathways:

  • Uptake 1
    • This is the more significant pathway
    • It involves reuptake of the neurotransmitter into the presynaptic variscosity
  • Uptake 2
    • This is the lesser pathway, mostly intended to prevent horizontal loss of the neurotransmitter
    • It involves uptake of the neurotransmitter into the postsynaptic neurone
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23
Q

Describe uptake 1 (in terms of reuptake of noradrenaline).

A
  • Main mechanism of reuptake -> Responsible for reuptake of 70% of NA by pumping it into the prejunctional nerve terminal.
  • Enabled by the sodium-dependent NET (norepinephrine transporter).
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24
Q

Describe how uptake 1 (in relation to noradrenaline) can be regulated by drugs.

A
  • Cocaine + Tricyclic antidepressants
    • Block NET (norepinephrine transporter)
    • So increase the concentration of NA in the junction
    • Used to treat ADHD, depression and obesity, due to their psychostimulant and appetite supressing effects in the brain.
    • Cocaine is not routinely used because of the high likelihood of dependence, which is also a risk with the use of ritalin.
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25
Q

Describe uptake 2 (in terms of reuptake of noradrenaline).

A
  • Extraneuronal uptake
  • The more minor mechanism, although it is also carries dopamine and other catecholamines.
  • Involves the ENT pump, which is on the postjunctional cell membrane and is not sodium-dependent.
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26
Q

Describe how uptake 2 (in relation to noradrenaline) can be regulated by drugs.

A
  • Corticosteriods
    • Block ENT (extra-neuronal transporter)
    • Used to treat many systemic conditions
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27
Q

Describe the recycling of catecholamines that are reuptaken by uptake 1 and 2.

A
  • In the nerve terminal, NA may be packed into vesicles without being broken down, which means it can be used again.
  • NA may also be broken down into a variety of products, with the initial breakdown being catalysed by MAO or COMT enzymes:
    • MAO (monoamine oxidase)
    • COMT (catechol O-methyl transferase)
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28
Q

What is MAO and how can it be regulated clinically?

A
  • MAO (monoamine oxidase) is found in the outer mitochondrial membrane (but some is also found extracellularly)
  • Functions by deaminating catecholamines, with MAO-A being primarily responsible for degradation of NA, adrenaline and dopamine, while MAO-B degrades dopamine and some other minor catecholamines.
  • MAO inhibitors are used in increasing cytoplasmic NA, and therefore their packing into vesicles and exocytosis. They are used in treatment of Parkinson’s disease (such as selegiline, which is selective for MAO-B) and depression (such as clorgiline, which is selective for MAO-A).
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29
Q

What is COMT and how can it be regulated clinically?

A
  • COMT (catechol O-methyl transferase) is a cytoplasmic enzyme typically associated with uptake 2 in liver, kidney and other cells.
  • Most catecholamines in circulation are converted by COMT.
  • Clinically, entacapone is a COMT inhibitor used as part of therapy for Parkinson’s disease.
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30
Q

Draw the graph to show the relative reuptake of adrenaline and noradrenaline by uptakes 1 and 2 at various concentrations.

A
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31
Q

What are the different ways in which catecholamines are degraded?

A
  • MAO (Monoamine oxidase) -> Uses oxygen to remove amine group -> This is a mitochondrial enzyme
  • COMT (Catechol-O-methyltransferase) -> Inserts a methyl group into the catecholamine -> This is soluble or membrane bound
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32
Q

Name some inhibitors of the degradation of catecholamines and how they work. State their medical uses.

A
  • MAO inhibitors
  • Inhibit the activity of monoamine oxidase, thus preventing the breakdown of catecholamines and thereby increasing their availability
  • Uses: Antidepressants, Panic disorders, Social phobia
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33
Q

What are the types of adrenoceptors you need to know about?

A
  • α1
  • α2
  • β1
  • β2
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34
Q

What type of receptor are adrenoceptors?

A

GPCR

35
Q

In general, summarise the rank order of agonist potency for alpha and beta adrenoceptors.

A
  • α : Noradrenaline≥Adrenaline>>>>Isoprenaline
  • β : Isoprenaline>Adrenaline>>Noradrenaline
36
Q

Compare the structure of adrenaline and noradrenaline.

A
37
Q

Draw the graphs showing how the arterial pressure, heart rate and total peripheral resistance change upon infusion of adrenaline, noradrenaline and isoprenaline.

A
38
Q

What are some clinical uses of catecholamines?

A

Treating:

  • Anaphylactic shock -> Reverse bronchspasm + Vasoconstriction
  • Acute heart failure -> Heart stimulation
39
Q

For α1 receptors, describe the distribution, mechanism of action, relative potency of agonists and function.

A
  • Distribution: Smooth muscle that needs to contract upon sympathetic stimulation
  • Mechanism of action: Gq (IP3 increase pathway)
  • Agonist potency order: Noradrenaline > Adrenaline > Isoprenaline
  • Function: Causes smooth muscle contraction, Salivary secretion, Glycogenolysis
40
Q

For α2 receptors, describe the distribution, mechanism of action, relative potency of agonists and function.

A
  • Distribution: Nerve terminal (pre-synaptic)
  • Mechanism of action: Blocks neurotransmitter release / Gi (downregulation of adenylate cyclase)
  • Agonist potency order: Noradrenaline = Adrenaline > Isoprenaline
  • Function: Inhibits neurotransmitter release, Vasoconstriction (to a small extent)
41
Q

For β1 receptors, describe the distribution, mechanism of action, relative potency of agonists and function.

A
  • Distribution: Heart
  • Mechanism of action: Gs (upregulation of adenylate cyclase)
  • Agonist potency order: Isoprenaline > Noradrenaline = Adrenaline
  • Function: Increases heart rate
42
Q

For β2 receptors, describe the distribution, mechanism of action, relative potency of agonists and function.

A
  • Distribution: Smooth muscle that needs to relax upon sympathetic stimulation (e.g. trachea)
  • Mechanism of action: Gs (upregulation of adenylate cyclase)
  • Agonist potency order: Isoprenaline > Adrenaline > Noradrenaline
  • Function: Relaxes smooth muscle, Glycogenolysis
43
Q

Summarise the distribution, effect, mechanism and main body activator of each adrenoreceptor type.

A
  • α1 -> Smooth muscle, Contraction, Gq, Noradrenaline
  • α2 -> Nerve terminal, Inhibition of NT release, Gi, Noradrenaline and Adrenaline
  • β1 -> Heart, Contraction, Gs, Noradrenaline and Adrenaline
  • β2 -> Smooth muscle, Relaxation, Gs, Adrenaline
44
Q

For these tissues, name the adrenoceptor types and the effect of their stimulation.

A
45
Q

Describe the mechanism by which α1 receptors produce their effects.

A
  • Gq-coupled
  • Activate phospholipase C
  • Increases IP3 and DAG
  • IP3 leads to calcium release
  • DAG activates protein kinase C activity
  • Effects: Smooth muscle contraction, Salivary secretion, Glycogenolysis
46
Q

Describe the mechanism by which α2 receptors produce their effects.

A
  • Gi-coupled
  • Inhibits adenylate cyclase
  • Decreased cAMP
  • Leads to lower PKA activity
  • So voltage-gated calcium channels are less open
  • Less calcium influx leads to less neurotransmitter release
  • Effects: Inhibited release of catecholamines
47
Q

Describe the mechanism by which β1 receptors produce their effects.

A
  • Gs-coupled
  • Stimulate adenylate cyclase
  • Increase cAMP
  • cAMP leads to:
    • Increased funny current (If) -> Heart contraction is faster
    • Increased PKA activity -> Increased calcium influx, so increased contractility of heart
48
Q

Describe the mechanism by which β2 receptors produce their effects.

A
  • Gs-coupled
  • Stimulate adenylate cyclase
  • Increased cAMP -> Inhibits myosin light chain kinase (MLCK)
  • Increased PKA activity -> Phosphorylation removes inhibition of SERCA
  • Effect: Smooth muscle relaxation
49
Q

Beta-1 and beta-2 adrenoreceptors both function using the Gs mechanism and yet have totally opposite effects. Why?

A

The Gs mechanism causes an ultimate increase in cAMP and PKA:

  • With beta-1 adrenoreceptors in the heart, the PKA activates calcium channels in the plasma membrane, leading to contraction
  • With beta-2 adrenoreceptors on smooth muscle, the cAMP normally inhibits myosin light chain kinase (enzyme responsible for phosphorylating smooth muscle myosin and causing contraction)
50
Q

Compare the effects that endogenous catecholamines and acetylcholine have on the heart.

A
  • Catecholamines
    • Increase both the heart rate and contractility
    • Due to there being sympathetic innervation of the whole heart
  • Acetylcholine
    • Decreases only the heart rate
    • Due to there only being parasympathetic innervation of the SAN
51
Q

What are the effects of noradrenaline and acetylcholine on blood pressure?

A
  • Noradrenaline increases blood pressure
  • Acetylcholine decreases blood pressure (although there is no parasympathetic innervation of blood vessels so it raises questions about why M3 receptors are present)
52
Q

Describe how acetylcholine leads to vasodilation.

A
  • Acetylcholine acts on the epithelial cells (not the muscle cells in the vessel wall)
  • Binds to M3 receptors, which are Gq-coupled
  • This activates PLC, which increases IP3
  • This leads to increased intracellular calcium
  • This stimualtes nitric oxide synthase (NOS)
  • Nitric oxide is released, which acts on the smooth muscle cells in the vessel wall by activating guanylate cyclase
  • This leads to increased cGMP
  • cGMP leads to relaxation due to inhibition of MLCK by phosphorylation
53
Q

Give some examples of α1 agonists and their clinical uses.

A
  • Phenylephrine
    • Counter acute hypotension
    • Treat nasal decongestion
    • Cause mydriasis (ocular examination)
  • Xylometazoline
    • Nasal decongestion
  • Metaraminol
    • Acute hypotension, partially IAS
54
Q

Give some examples of α2 agonists and their clinical uses.

A
  • Clonidine
    • Anti-hypertensive
  • Xylazine
    • Sedative effects via CNS
55
Q

Give some examples of β1 agonists and their clinical uses.

A
  • Isoprenaline (mixed beta 1 and 2 agonist)
    • Cardiac stimultant, although non-selectivity limits use
  • Dobutamine
    • Cardiogenic shock
    • Inotropic support in infarction
56
Q

Give some examples of β2 agonists and their clinical uses.

A
  • Isoprenaline (mixed beta 1 and 2 agonist)
    • Cardiac stimultant, although non-selectivity limits use
  • Salbutamol + Terbutaline
    • Short acting bronchodilators
  • Salmeterol
    • Long acting, preventive bronchodilators
57
Q

Give some examples of α adrenoceptor antagonists and their clinical uses.

A

Selective:

  • Prazosin
    • Selective α1 antagonist
    • Antihypertensive agent, Raynaud’s phenomenon, Phaeochromocytoma (catecholamine-secreting tumour of chromaffin tissue)

Non-selective:

  • Phentolamine
    • Non-selective, superceded by selective α1‑antagonists
    • Use associated with heart rate (blocks α2 presynaptic feedback)
  • Phenoxybenzamine
    • Irreversible, non-selective antagonist • phaeochromocytoma: combination with β-blocker to prevent BP and heart rate during surgery
  • Labetalol
    • Combined α1-and β-antagonist, racemic mixture used
58
Q

What are some problems that typically arise alongside alpha adrenoreceptor antagonist use?

A

Increase the likelihood of postural hypotension, which occurs since vasoconstriction cannot occur as part of the normal baroreflex.

59
Q

Aside from cholinergic and catecholaminergic transmission, what are some other types of signalling? Define each and give an example of each.

A
  • Purinergic -> Extracellular signalling mediated by purine nucleotides and nucleosides (e.g. adenosine and ATP)
  • Gaseous -> Signalling mediated by gases (e.g. nitric oxide)
  • Neuropeptide -> Signalling mediated by small protein-like molecules (peptides) used by neurons to communicate with each other (e.g. Neuropeptide Y and vasoactive intestinal peptide)
60
Q

Give some examples of β adrenoceptor antagonists and their clinical uses.

A
  • Propranolol
    • Non-selective
    • Used to treat tremors, angina, hypertension, heart rhythm disorders, and other heart or circulatory conditions
    • Risk of bronchoconstriction, other effects include fatigue and claudication
  • Atenolol
    • β1 selective
    • Used to treat hypertension, angina, etc.
    • Less likely to give bronchoconstriction

Both selective and non-selective antagonists give cold hands and feet, unmask vasoconstriction

61
Q

What is the concept of co-transmission?

A
  • The control of a single target cell by two or more substances released from one neuron in response to the same neuronal event, does occur in experimental situations.
  • It has not been shown to occur in the normal operation of an animal, but the likelihood that it does is great.
62
Q

What are the categories of the other neurotransmitters (non-ACh and non-adrenergic) that you need to know about?

A
  • Co-transmitters
  • Other non-adrenergic, non-cholinergic (NANC) transmitters
63
Q

What is a co-transmitter?

A

A substance that is released from a nerve ending along with a primary neurotransmitter in order to modify the action of the latter.

64
Q

What are the categories of the other neurotransmitters (non-ACh and non-adrenergic) that you need to know about?

A

Co-transmitters:

  • With acetylcholine -> ATP, VIP
  • With noradrenaline -> Dopamine, ATP, NPY

Other non-adrenergic, non cholinergic (NANC) transmitters:

  • Neuropeptides -> Enkephalin
  • Nitric oxide
65
Q

In which nervous system are other neurotransmitter common?

A

Autonomic

66
Q

How can other neurotransmitters be identified?

A
  • When the nerves in a preparation are electrically stimulated to trigger action potentials, the neurotransmitters released can be identified.
  • Repeat in the presence of a selective blocker to see whether
67
Q

Name some co-transmitters with acetylcholine.

A
  • ATP
  • VIP (vasoactive intestinal peptide)
68
Q

Transmission using ATP is known as what?

A

Purinergic transmission

69
Q

Give an example of a situation when ATP is important as a co-transmitter in the parasympathetic nervous system.

A
  • In the detrusor muscle of the urinary bladder
  • ATP and ACh are released together into the synapse
  • ATP binds to P2X receptors
  • Purinergic transmission and cholinergic transmission occur simulatneously and cause the same effect, so that one neurotransmitter acts as a “back-up” for the other one
70
Q

Name some co-transmitters with noradrenaline.

A
  • Dopamine
  • ATP
  • NPY (Neuropeptide Y)
71
Q

Describe how ATP can act as a co-transmitter with noradrenaline.

A
  • ATP made from adenosine in cytoplasm of nerve ending and stored in vesicles with noradrenaline, then released together
  • Extracellular ATP is rapidly broken down to ADP, AMP and adenosine via ectonucleotideases:
    • ATP acts at P2X (ionotropic) and P2Y (Gq-coupled) receptors
    • ADP acts at P2Y (Gq-coupled) receptors
    • Adenosine can act at pre- and postsynaptic A receptors (Gi or Gs-coupled)
72
Q

Give an example of a situation when ATP is important as a co-transmitter in the sympathetic nervous system.

A
  • In blood vessels that can contract
  • ATP acting at P2X receptors (ionotropic) depolarizes smooth muscle and evokes rapid contraction (which desensitizes)
  • ATP can also act at smooth muscle P2Y (Gq-coupled) receptors to stimulate sustained, slower contraction
  • Also have purinergic receptors on endothelial cells (linked to relaxation)
73
Q

Describe the synthesis of ATP as a co-transmitter.

A

It is synthesised from adenosine in the cytoplasm.

74
Q

Describe the synthesis and breakdown of neuropeptides.

A
  • De novo synthesis at the cell body level
  • Breakdown by enzymatic hydrolysis of the released peptide
75
Q

Give some examples of neuropeptides.

A
  • Substance P
  • Enkephalin
  • Neuropeptide Y
  • VIP
76
Q

What are enkephalins?

A

Neuropeptides that mimick the actions of morphine.

77
Q

What are some of the effects of VIP (vasoactive intestinal peptide) transmission?

A
  • Stimulates contractility in the heart
  • Vasodilation
  • Increases glycogenolysis
  • Lowers arterial blood pressure
  • Relaxes the smooth muscle of trachea, stomach and gall bladder
78
Q

Along with which sort of neurotransmitter is VIP released?

A

ACh from parasympathetic nerves

79
Q

Give an example of a situation where VIP is important as a co-transmitter in the parasympathetic nervous system.

A
  • In the salivary glands
  • Parasympathetic supply increased blood flow and secretions
  • The VIP is important in increasing the blood flow to the salivary gland
80
Q

Along with which sort of neurotransmitter is NO released?

A

None specifically.

81
Q

Describe the importance of NO as a (neuro)transmitter.

A
  • NO is released by endothelial cells to relax smooth muscle
  • In some autonomic nerves, NO is made following rises in Ca2+ levels in the nerve ending -> Released to act on adjacent smooth muscle
82
Q

What are some of the effects of NPY (neuropeptide Y)?

A
  • Strong vasoconstrictor
  • Growth of fat tissue
  • Also acts on the brain
83
Q

Along with which sort of neurotransmitter is NPY released?

A

Noradrenaline

YEAR 1 - Physiology and Pharmacology (Anton) (13 decks)

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