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Neurobio II (Fys) > T4 (Fys) Sås och kopplingar > Flashcards

T4 (Fys) Sås och kopplingar Flashcards

0
Q

What is the general rule for the action fo neurotransmitters.

A

“the action of a transmitter drives the postsynaptic membrane potential toward E_rev for the particulsr ion channel being activated.

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1
Q

Define the EPC.

A

End plate current. The macroscopic current created by the brief opening of a large number of ion channels as a result of release of transmitter substance onto the post synaptic membrane.

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2
Q

What are the conditions for PSPs being depolarizing vs. hyperpolarizing in the case of EPP at the neuromuscular junction?

A

Depolarizing: when E_rev is more positive than the PSMP

Hyperpolarizing: when the E_rev is more negative than the PSMP

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3
Q

Define EPSP and IPSP based on their reversal potentials relative to threshold potentials.

A

EPSP (e.g. glutamate): reversal potential is more positive than threshold potential

IPSP (e.g. GABA): reversal potential more negative than threshold

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4
Q

Are IPSPs always hyperpolarizing? If not, can IPSPs cause depolarization past the threshold value?

A

IPSPs are not always hyperpolarizing. A reversal potential more positive than the membrane potential can increase the PSP but will, however, not do so past the threshold value and thus not cause depolarization.

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5
Q

What is the term of the process with which neurons in the brain are able to cause action potentials despite most synapses evoking only fractions of millivolts in EPSPs?

A

Summation.

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6
Q

What are responses of glial cells in the brain to stimulation from GABA, ACh and some other neurotransmitters?

A

They exhibit calcium induction waves, releasing neurotransmitters (gliotransmitters) and ATP. Release is performed in the same way as in neuronal synapses (vesicular exocytosis) but also through “unconventional release mechanisms such as permeability through certain ion channels”.

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7
Q

Explain the concept of the ‘tripartate’ synapse.

A

A synapse concistency not only of a pre- and postsynaptic part but also of a joining glial cell. The glial cell may regulate presynaptic release of transmitter substance as well as regulate transmission through release If ‘gliotransmitters’.

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8
Q

Compare and give examples of neuropeptides and small-molecule neurotransmitters.

A

Neuropeptides: larges molecules made up of 3-36 amino acids.

Small-molecule neurotransmitters: individual amino acids (glutamate, GABA, ACh, serotonine, histamine), biogenic amines (dopamine, norepinephrine, epinephrine, serotonin, histamine).

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9
Q

List the major neurotransmitters, their postsynaptic effects and type of storing vesicle.

A

ACh: excitatory, small clear

Glutamate: excitatory, small clear

GABA: inhibitory, small clear

Glycine: inhibitory, small clear

Catecholamines: excitatory, small dense-core/large irregular dense-core

Serotonin: excitatory, large dense-core

Histamine: excitatory, large dense-core

ATP: excitatory, small clear

Neuropeptides: excitatory and inhibitory, large dense core

Endocannabinoids: inhibit inhibition, none

Nitric oxide: excitatory and inhibitory, none

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10
Q

In what synapses does ACh function as a transmitter substance?

A

Skeletal neuromuscular junctions, neuromuscular synapse between vagus nerve and cardiac muscle fiber, ganglia of visceral motor system, varoitus other sites of nervous system.

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11
Q

How is ACh removed from the synaptic cleft?

A

Through the action of acetylcholinesterase.

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12
Q

Outline the steps of ACh recycling in the synapse.

A
  1. Exocytosis into synaptic cleft
  2. Breakdown by acetylcholinesterase into acetate and choline
  3. Transfer into presynaptic cell by action of ChT (proton-choline exchanger)
  4. Recombining of choline with Acetyl CoA (derived from glycolysis) by action of choline acetyltransferase.
  5. Packing into vesicles by action of VAChT (vesicular transporter, acidic pH inside vesicle aids in transportation).
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13
Q

What is the relationship between Sarin and ACh?

A

Sarin, like many organophosphates, reacts with cholinergic enzymes. This inhibits ACh breakdown in synaptic cleft leading to neuromuscular paralysis following the prolonged refractory period brought on by continual depolarization.

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14
Q

What type of receptor is nAChr?

A

Ionotropic neurotransmitter receptor: a non-selective cation channel.

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15
Q

What is the difference between nAChRs and mAChRs?

A

Muscarinic ACh receptors are metabotropic whilst nicotinergic ACh receptors are ionotropic.

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16
Q

Where are mAChRs mostly found?

A

In synapses in e brain.

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17
Q

Give examples of excitatory and inhibitory functions of mAChRs.

A

Excitatory: In the hippocampus mAChRs close KCNQ-type K ion channels ( also found in ganglia of peripheral nervous system).

Inhibitory: In the stratum and other forebrain regions mAChRs activate inward rectifier K ion channels or Ca ion activated K ion channels.

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18
Q

What areas’ peripheral responses are mAChRs responsible for?

A

Autonomic effector organs (heart, smooth muscle, exocrine glands), heart rate inhibition through nervus vagus.

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19
Q

Name some mAChR antagonists.

A
  • atropine (dilates pupils)
  • scopolamine (prevents motion sickness)
  • ipratromium (treatment of asthma)
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20
Q

Which is the most abundant neurotransmitter in the brain? What can it cause when released in an accident that causes brain damage?

A

Glutamate. Excitotoxism.

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21
Q

Outline the circulation of glutamate in the synapse.

A
  1. Release from vesicle into synaptic cleft (glutamate-glutamine cycle)
  2. Transportation by EAATs ( excitatory amino acid transporters) into presynaptic and also glial cells (there converted to glutamine)
  3. Glutamine ia transported to presynaptic cell and converted to glutamate by glutaminase.
  4. Glutamate is packed into vesicles by VGLUT
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22
Q

Name some ionotropic glutamate receptors. What are the functions of these?

A

AMPA receptors, NMDA rceeptors, kainate receptors etc. They are glutamate gated cation channels which allow the flow of Na ions and K ions (similarly to nCHhR). AMPA (slower and long-lastin EPSC) and NMDA (quicker and faster EPSC, main mediators of excitatory transmission) are usually found together. Kainate receptors can act on the presynaptic membrane as feedback mechanisms for glutamate release, and on postsynaptic membranes as mediators of quickly rising but more slowly decaying transmissions than AMPA.

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23
Q

How do NMDA receptors differ from other ionotropic glutamate receptors?

A
  • allow Ca ion movement in addition to those of Na and K
  • Mg ions block the pore at hyperpolarized membrane potentials making voltage dependant on current flow through receptor (role in cell plasticity since channel flow is dependent on polirization)
  • requires co-agonist glycine for activation
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24
Q

How do metabotropic glutamate receptors differe from ionotropic ones?

A
  • activation of many of these inhibit postsynaptic Ca and Na ion channels
  • slower, either excitatory or inhibitory, postsynaptic responses
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25
Q

How widespread is the use of GABA in synapses in the brain?

A

Ca one third of neurons use GABA inhibitory transmission.

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26
Q

Why is vitamin B6 so vital for GABA synthesis?

A

It acts as a co-factor for GAD (glutamin acid decarboxylase, “found almost exclusively in GABAergic neurons”).

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27
Q

Outline the GANA circulation in the synapse.

A
  1. Exocytosis of vesicles
  2. Endocytosis via GAT (Na ion-dependent cotransporter) into presynaptic neuron or glial cell.
  3. Conversion to succinate and entering mitochondrial ATP-producing cycle, or to γ-hydroxybutyrate
  4. Production of GABA from glucose-glutamate-GABA
  5. Packing by VATT into vesicles
28
Q

What sub-groups of GABA receptors are there and how Do they differ from one another?

A

3 subgroups: GABA_A, GABA_B and GABA_C. A and C are ionotropic , anion-gated (usually CL ion) receptors, whilst B is metabotropic.

29
Q

Give an example of paradoxical responses for GABA receptors.

A

In evolving neurons postsynaptic CL ion concentration can be high, and GABA_A/C receptor response can be excitatory.

30
Q

What drugs act upon GABA receptors?

A

Benzodiazepines, barbiturates, steroids, picrotoxin, alcohol (alterates ionotropic GABA receptors).

31
Q

What is the inhibitory action of GABA_B receptors based on?

A

Activation of K ion channels or blocking of Ca ion channels.

32
Q

What is the role of glycine in neural transmission?

A

It functions as an inhibitory transmitter substance, found in half of the inhibitory synapses of the spinal chord.

33
Q

How is glycine synthesized, packaged and how is it removed from the synaptic cleft?

A

Synthesis: from serine by mitochondrial isoformer of serine hydroxymethyltransferase.

Packaging: same mechanism as for GABA

Removal: removed by glycine transporters in plasma membrane

34
Q

Which are the three main biogenic amine neurotransmitters?

A

The catecholamines dopamine, noradrenaline and adrenaline, and histamine and serotonin.

35
Q

What is the basis for the synthesis of the catecholamines?

A

The amino acid tyrosine is converted with the aid of the enzyme tyrosine hydroxylase into DOPA (dihydroxyphenalanine), then into dopamine, noradrenaline and ultimately adrenaline.

36
Q

Outline the production of dopamine and ultimate removal of it from the synaptic cleft.

A

Dopamine is produced through the action of DOPA decarboxylase on DOPA. Dopamine is removed from the synaptic cleft trough action of the Na ion-dependent dopamine co-transporter (DAT).

37
Q

What receptor does dopamine activate?

A

Dopamine acts exclusively on GPCRs (activating), e.g. D_3 dopamine receptor.

38
Q

Compare the areas of the brain after upon by dopamine, noradrenaline and adrenaline respectively.

A

Dopamine: produced in substantia nigra and ventral tegmentum area it affects the superior part of the brainstem, the foetal and parenteral lobe.

Noradrenaline: produced in the locus coeruleus it affects the whole brain.

Adrenaline: produced in the medullary epinephrine neurones it affects solely the brain stem

39
Q

How is dopamine removed from the synaptic cleft?

A

Enzymatically (MAO monoamine oxidase and COMT catechol O-methyltransferase).

40
Q

Name prominent areas of neurotransmitter activity for noradrenaline.

A

The locus coruleus nucleus in the brain stem (projections to various locations in the forebrain) and sympathetic ganglion cells of the visceral motor system.

41
Q

How is noradrenaline removed from the synaptic cleft?

A

Through action of NET (norepinephrine transporter) and MAO and COMT (similar as for dopamine).

42
Q

What distinguishes adrenaline from other catecholamine neurotransmitters in the brain?

A

It’s found in a far smaller quantities and fewer neurons in the bain. The function of adrenaline-secreting neurons is also not known, affecting mainly in the lateral tegmentum system, projections to the hypothalamus and thalamus.

43
Q

Where is histamine found in the brain and what is its function?

A

In neurons of the hypothalamus, projecting all over the body. It controls alertness and blood flownof the brain.

44
Q

What type of receptor thus histamine bind to? Which are these?

A

Metabotropic receptors, e.g. H_1 and H_2.

45
Q

Compare the areas of affect of serotonin and histamine.

A

Histamine: the entire brain, stemming from the tuberomammilary nucleus of hypothalamus

Serotonin: the entire brain, stemming from the Raahe nuclei of the brain stem

46
Q

What is is VMAT?

A

Vesicular amine transporter. Responsible for loading most monoamine neurotransmitters into vesicles in the presynaptic cell.

47
Q

What types of receptors does 5-HT (serotonin) bind to and activate?

A

Mostly metabotropic ones. These control behaviour, emotion, circadian ryhtymään, mental arousal etc. The only ionotropic serotonin receptor, 5-HT_3, are non-selective cation channels, mediation excitation.

48
Q

What are the precursors of histamine and serotonin respectively? Are these essential amino acids?

A

Histamine: histidine (non-essential)

Serotonin: tryptophan (essential)

49
Q

Where does ATP act as a neurotransmitter?

A

In motor neurons in the spinal chord (excitatory), and sensory and autonomic ganglia. Also in the CNS in dorsal born neurons and a subset of hippocampal neurons.

50
Q

Why can’t ATP be considered a Classical neurotransmitter?

A

Because it is not stored in synaptic vesicles and also because its degradation product adenosine also functions as a signaling substance.

51
Q

How is ATP removed from the synaptic cleft?

A

Through degradatory enzymes and nucleotide transporters.

52
Q

What types of purinergic receptors are there for ATP and where are they found?

A

The receptors for ATP and adenosine are “widely distributed in the nervous system as well as in many other tissues”. Three classes are known:

P2X receptor: the only ionotropic ATP receptor, non-selective cation channel, mediates excitatory responses

2 other metabotropic receptors: one stimulated by adenosine, the other by ATP

53
Q

What is the common homologuous structure for ENDOGENOUS opioid peptides?

A

Tyr-Gly-Gly-Phe

54
Q

What are some basic concepts of peptide neurotransmitters?

A

Regulate sympathetic ganglions of the viscera motor system (induce constitution), receptors often found in conjunction with other receptors (GABA, HT-5), required in minute amounts compared to other transmitter substances compared to those needed for small-molecule neurotransmitters.

55
Q

What are some unconventional neurotransmitters?

A

Endocannabinoids: modulate GABA responses and mediate retrograde (post- to presynaptic) messagubg

NO: diffuses few tenths of micrometers from area of production, making it a good synchronizing signal

56
Q

Ahdistuneisuus between short- and long-term synaptic plasticity.

A

Short-term: lasting a few minutes or less

Long-term: lasting up to days, weeks or longer

57
Q

Outline the forms of short-term synaptic plasticity.

A

Synaptic facilitation: Two successive action potentials yield a second greater EPSP due to readily available Ca ion from the first EPSP.

Synaptic depression: the opposite of synaptic faciliation, based on rate of vesicle exocytosis and vesicle reforming.

Synaptic potentiation/augmentation: enhance the ability of Ca ions to fuse transmitter vesicles with presynaptic membrane, the former during a period of a few seconds, the latter over tens of seconds to minutes.

58
Q

Give examples of behavioural plasticity.

A

Hanituation and sensitization.

59
Q

What’s the physiological basis for habituation?

A

Decreased glutamergic response in synapses.

60
Q

What’s the physiological basis for sensitization?

A

Long term: Increase in serotonin release from interneurons onto sensory neurons and following gene expression.

Short term: based on prolonged K ion channel opening on presynaptic membrane and thus prolonged depolarization, PKA mediated

61
Q

What is the relevance of LTP (long-term potentiation) and LTD (long-term depression) for memory? Where does it occur?

A

Cells in the hippocampus show these phenomenons and they are most probably part of memory formation through alteration fo synapse plasticity. This occurs at the synapses of entorhinal cortex-granule cell, granule cell(mossy fiber)-CA3 pyramidal cell and CA3 pyramidal cell-CA1 pyramidal cell

62
Q

What is the associativity of LTP?

A

The ability of parallel neurons (Schaffer collaterals) to influenced each others potentiation. A neuron receiving intense stimulus will experience LTP, and if there is a parallell neuron synapsing upon a common cell, then that parallel neuron will also experience LTP (associativity). Weak stimulation of the parallell neuron along will not yield LTP (specificity, p. 173).

63
Q

What is basis for LTP?

A

The glutamergic receptors NMDA and AMPA. Since NMDA is blocked by Mg ion when the postsynaptic potential is at resting potential, the AMPA receptor mediated depolarization allows increase in strength of depolarization through NMDA receptors which let in Ca ions.

64
Q

How can LTP in hippocampal CA1 neurons be modulated/maintained?

A

Through adding of AMPA receptors by excitatory synapses.

65
Q

When does LTD occur?

A

When Schaffer collaterals are stimulated at low rates of about 1Hz.

66
Q

How can it be determined that the mechanisms of LTP and LTD act through a common site? What is this common factor?

A

They act reversible upon each other, one aleviates the effects of the other. Both act through postsynaptic Ca ion cascades, where a slowly rising cascade makes for LTD, and vice versa, acting upon protein phosphates and kinases ( CREB and PKA).

67
Q

Where else than in the hippocampal CA3-CA1 synapse has LTD been indicates and what is special about it?

A

Purkinje cells od cerebellum where complex movements are stored. The LTD is here associativity, rising from dual activation of climbing fibers and parallell fibers.

68
Q

Explain STDP (spike-timing dependent plasticity).

A

The form of plasticity, LTP vs. LTD, is determined by the relative times of EPSP produced in the postsynaptic membrane, as a result of Ca ion levels fluctuating.

Neurobio II (Fys) (10 decks)

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