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neuropharmacology test 3 > Metabotropic Glu receptors > Flashcards

Metabotropic Glu receptors Flashcards

1
Q

<p>what is the initial compound that is converted to glutomate in mitochondria? </p>

A

<p>L-glutamine </p>

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2
Q

<p>how is glutamine transported to mitochondria? </p>

A

<p>using glutamine transported </p>

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3
Q

<p>how is glutamate transported out side of mitochondria? </p>

A

<p>there is no transported for glutamate in mitochondria and that_s why glutamate has to be converted to alpha-ketoglutarate then it can be transported out </p>

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4
Q

<p>which enzyme converts glutamate to ketoglutarate? </p>

A

<p>AA enzyme </p>

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5
Q

<p>what molecule transports ketoglutarate out of mitochondria? </p>

A

<p>dicarboxylate carrier </p>

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6
Q

<p>conversion of glutamate ro ketoglutarate is reversabel? T/F</p>

A

<p>T</p>

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7
Q

<p>how is ketoglutarate converted back to glutamate when it leaves mitochondria (in cytosol)? </p>

A

<p>AA enzyme converts the ketoglutorate back to glutamate aspartate aminotransferase </p>

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8
Q

<p>if glutamate stays in mitochondria, where does it go to? </p>

A

<p>it goes to kreb cycle for ATP production </p>

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9
Q

<p>why is glutamate structure very simmilar to GABA? </p>

A

<p>because glutamate is the initial compound for production of GABA </p>

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10
Q

<p>how is glutamate converted to GABA? </p>

A

<p>if glutamate is transported to an inhibitory neuron, then it is converted to GABA using GAD enzyme </p>

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11
Q

<p>what happens to glutamate after it is released in to synapses? </p>

A

<p>then is is picked up by the anzyme EAA-T and sent in to Glial cell </p>

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12
Q

<p>what is the role of glial cell at the synapses? </p>

A

<p>reuptake of glutamate </p>

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13
Q

<p>what happens to glutamate when it is transported to glial cell? </p>

A

<p>then it is converted back to glutamine using the glutamine synthase </p>

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14
Q

<p>what are the four different amino acid transporters? </p>

A

<p>EAAC-1, GIT-1, VGlu-T, Gln-T, DCC</p>

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15
Q

<p>which ion is EAAC depended on? </p>

A

<p>Na+</p>

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16
Q

<p>which ion is GIT-1 depended on ? </p>

A

<p>Na+</p>

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17
Q

<p>which ions is Vglu-T depended on? </p>

A

<p>H+ and Mg++</p>

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18
Q

<p>which ion is Gln-T depended on? </p>

A

<p>H+ and Na+</p>

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19
Q

<p>what is the structural model of mGluRs? </p>

A

<p>7 Transmembrane segment receptors </p>

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20
Q

<p>what is the modern structural model of mGluRs? </p>

A

<p>14 Transmembrane segment, mGluRs are homodimer, they interact with one another to form one binding site </p>

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21
Q

<p>what is the hill coefficient of modern structural model of mGlueRs??</p>

A

<p>hill coefficient 1 </p>

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22
Q

<p>how many G-protein binding site can you find on mGluRs? </p>

A

<p>1 to 2 G-protein binding site </p>

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23
Q

<p>what is the typical expression of mGluR1 in different region of brain? </p>

A

<p>1-highly expressed in neurons of dentate gyrus of hippocampus
2-lower levels in CA3
3-lowest level of expression in pyramidal of CA1
4-cerebellum _ in granule cells and Purkinje</p>

24
Q

<p>what is the typical expression of mGluR1 in epileptic patient? </p>

A

<p>large increase in expression of mGluR5 in epileptic</p>

25
Q

<p>how are GluRs defined by their effectors? </p>

A

<p>they are defined in 2 group, excitatory and inhibitory </p>

26
Q

<p>which group of GluRs enhances the the enzyme activity? </p>

A

<p>group 1 which is excitatory. Gq enhances the PLC activity </p>

27
Q

<p>which group of GluRs decrease the the enzyme activity? </p>

A

<p>group 2 which is inhibitory. Gi decreases the AC activity </p>

28
Q

<p>based on gene expression how many class og mGluRs do we have? </p>

A

<p>there are 3 classes, </p>

29
Q

<p>define each class of mGluRs based on their gene expression? </p>

A

<p>calss 1: it consists of mGluR1 and mGluR5. Class 2: consists of mGluR2 and mGluR3. Class 3: consists of mGluR4 and mGluR 6 to 8</p>

30
Q

<p>what do you know about class 1 mGluRs? </p>

A

<p>>this class consists of mGluR1 & mGluR5
>they increases the levels of IP3 and Ca
>the Gq _ (PLC acts on PIP2 to created DAG and IP3)
>Only 2 excitatory mGluR</p>

31
Q

<p>what do you know about class 2 mGluRs? </p>

A

<p>>this class consists of mGluR2 & mGluR3
>they decreases cAMP levels in neurons
>ATP is substrate
>Gi</p>

32
Q

<p>what do you know about class 3 mGluRs? </p>

A 
<p class="large" style="text-align: center;">>this class consists of mGluR4 & mGluR6-8
>they decrease cAMP levels (Gi)
>structurally dissimilar from class 2</p>
33
Q

<p>what other processes are mGluRs involved in? </p>

A

<p>>perception of pain
> mood/affect, especially anxiety
> learning and/or memory
>blood flow/headache</p>

34
Q

<p>what other activites are modulated by mGluRs? </p>

A

<p>>voltage-dependent ion channels
>transmitter release
>Ca-dependent ion channels (K)
>Ligand-gated ion channels</p>

35
Q

<p>what is the Group 1 effector mehcanism? </p>

A

<p>Glu _mGluR1/mGluR5 _ Gq _ PLC _ PIP2 _ IP3 + DAG _ IP3R and PKC (protein kinase)</p>

36
Q

<p>what are the Group 1 agonists?</p>

A

<p>Glu, Ibotenic acid, DHPG, ACPD, HCPCC, CHPG, </p>

37
Q

<p>name an endogenous agonsit for group 1 mGluRs? </p>

A

<p>Glu</p>

38
Q

<p>name an organic agonist for group 1 mGluRs? </p>

A

<p>Ibotenic acid </p>

39
Q

<p>how is the potency of Ibotenic acid? </p>

A

<p>it is a very potent agonis (over-excitation causes apoptosis); it is used to create legions in different portions of the nervous system but glia aren_t sensitive to it</p>

40
Q

<p>the HCPCC is specific to which mGluRs? </p>

A

<p>mGluR1 specific </p>

41
Q

<p>the CHPG is specific to which mGluRs? </p>

A

<p>mGluR 5 specific </p>

42
Q

<p>what are the 2 competitve antagonsits of group 1 metabotropic receptors? </p>

A

<p>EMQMCM, MPEP, MTEP</p>

43
Q

<p>the EMQMCM antagonsit is specific to which mGluR? </p>

A

<p>mGluR1 specific </p>

44
Q

<p>the MPEP and MTEP antagonist are specific to which mGluR? </p>

A

<p>mGluR5 specific </p>

45
Q

<p>how can group 1 agonists increase excitability? </p>

A

<p>if a neuron fires and has a large AHP, when DHPG is applied, the neuron will fire many more APs with the same input and will have no AHP (significantly more excitable)</p>

46
Q

<p>how does phosphorylation of VDCCS effects Ca2+ influx and how does it effect IAHP and IsAHP? </p>

A

<p>>phosphorylation of VDCCs could severely reduce Ca influx, block IAHP or direct effect on sAHP
>probably not an IP3 mediated effect (alpha subunit effect)</p>

47
Q

<p>how is Ca2+ hypothesis disproven? </p>

A

<p>>Ca increases when DHPG is applied
>Phosphorylation of IAHP</p>

48
Q

<p>explain step by step how Group I agonists can further enhance excitability? </p>

A

<p>1-NMDAR are bound to PSD-95
2-mGluR (group I) are bound to Homer
3-if Glu is stimulating an mGluR1 or 5, it can subsequently enhance activity of NMDAR by phosphorylation
4-Ca amplification system
5-VDCC have decreased current flow when they_re phosphorylated
6-nAChR current is decreased by phosphorylation
7-GABAAR current is increased by phosphorylation</p>

49
Q

<p>explain how does group 1 agonist causes headaches? </p>

A

<p>1-they are also located on the end feet of astrocytes
2-At the other end of the glial cell, where it helps form the BBB (by surrounding blood vessels) an increase of prostaglandin production occurs through increase of AA</p>

50
Q

<p>how does asprin help with the headache? </p>

A

<p>Aspirin inhibits production of prostaglandin</p>

51
Q

<p>how does Group I agonists reduce transmitter release?</p>

A

<p>group 1 can reduce NT release by a presynaptic drug
when we Apply DHPG in synapse to bind on receptors on the presynaptic terminal,
This will create a smaller IPSC,
then If you measure the amount of Ca being released post synaptically, there is a much lower influx (the IPSC)</p>

52
Q

<p>in effector mechanism concept how does group 2 and 3 decrease AC activity?</p>

A

<p>>they both use Gi alpha subunits to decrease AC activity,
and this will use up less ATP and produce less cAMP (and thus less PKA activation and less phosphorylation of whatever PKA is phosphorylates)
>Group IIs on presynaptic terminals can enhance Glu release</p>

53
Q

<p>what are the Group II (mGluR2,3) agonist?</p>

A

<p>1-Glu (endogenous) 2-NAAG</p>

54
Q

<p>what is the Group II (mGluR2,3) competitive antagonist?</p>

A

<p>ethylGlu</p>

55
Q

<p>what are the Group III (mGluR4,6,7,8) agonist? </p>

A

<p>1-Glu (endogenous), 2-AP4</p>

56
Q

<p>what are the Group III (mGluR4,6,7,8) competitive antagonist? </p>

A

<p>MAP4</p>

neuropharmacology test 3 (4 decks)

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