Pharmacology: Introduction To Cns

Front 1

What is Gamma amino butyric acid (GABA)

Back 1

major inhibitory transmitter in the CNS

Front 2

What does glutamic acid decarboxylase (GAD) do?

Back 2

converts l-glutamic acid into GABA

Front 3

Where is GABA stored?

Back 3

stored in synaptic vesicles in GABAergic neurons

Front 4

Who is GABA released?

Back 4

release is Ca++ dependent high-affinity reuptake pump in GABAergic nerve terminals

Front 5

What kind of receptors are GABA-A receptors?

Back 5

ionotropic Cl- channels

Front 6

What kind of receptors are GABA-B receptors? What ionic changes can they cause?

Back 6

metabotropic— increases K+ conductance & decreases Ca++ conductance to regulate neuronal excitability.

Front 7

Where can you find GABA-B receptors? What do they do at those locations?

Back 7

GABAB receptors are located both presynaptically where they inhibit transmitter release and post synaptically where they mediate a slow inhibitory post synaptic potential (IPSP) and reduce neuronal excitability.

Front 8

What is the major route of catabolism for GABA? What pharmaceutical agent inhibits the catabolism?

Back 8

GABA alpha-ketoglutarate Transaminase (GABA-T)
inhibited by Vigabatrin

Front 9

What determines the type of GABA-A receptors?

Back 9

GABA-A receptors come in different varieties depending on various combinations of α, β, & γ and others) subunits.

Front 10

Where do you find ligand-gated chloride channels (ionotropic) of GABA-A receptors? What change do they cause?

Back 10

for both pre &amp
post synaptic inhibition IPSPs from Cl- influx mainly

Front 11

What do benzodiazepines require to bind? What are they binding to?

Back 11

GABA-A receptors
requires gamma subunit

Front 12

What part of the GABA-A receptor do barbiturates act on? What is the result?

Back 12

act on part of β subunit located inside channel. BZD’s and Barbs bind to GABAA receptors and enhance GABA function.

Front 13

What do β carbolines bind to? What do they do?

Back 13

bind BZD receptor on α subunit (& so are BZD receptor agonists) of GABA-A receptor but cause opposite effects of BZD (panic instead): inverse agonists of BZD receptor

Front 14

What is Glutamate?

Back 14

major excitatory amino acid transmitter in brain

Front 15

Where do the neurons carrying glutamate function?

Back 15

a major output system from brain to peripheral autonomic and somatic NS and in many brain functions

Front 16

What do drugs that increase the release of glutamate or mimic its actions cause?

Back 16

can cause seizures, excitation, neurotoxicity/death of neurons w/ excess amts

Front 17

What are the classes of Glutamate receptors?

Back 17

AMPA/Kainate, NMDA

Front 18

What kind of receptor is the AMPA/Kainate glutamate receptor?

Back 18

ionophore selective for Na+ ions.

Front 19

What kind of receptor is the the NMDA glutamate receptor? What does this channel regulate? What happens in excessive stimulation?

Back 19

ionophore that conducts Ca++ & Na+. Ca++ entry through this receptor regulates synaptic strength (important for learning & memory), but excess Ca entry causes neuronal death through apoptotic ‘excititoxicity’.

Front 20

What is Rasmussen encephalitis?

Back 20

auto-Abs against type of AMPA glutamate receptor (GluR3) seizures, inflammation confined to a single cerebral hemisphere. This is like Graves dz since these anti-AMPA antibodies must stimulate glutamate-AMPA receptors (the way Graves antibodies stimulate TSH receptors).

Front 21

What is Glycine? Where is it found? What kind of receptors does it have? What drug targets this system?

Back 21

an inhibitory neurotransmitter, principally in spinal cord. Glycine receptors are ligand-gated chloride channels (similar pentameric structure to GABAA receptors), not a drug target except for poisons (strychnine).

Front 22

What is unique about Acetylcholine (ACh)?

Back 22

only nt that is not an amino acid or synthesized from one

Front 23

How is Acetylcholine formed? Degraded?

Back 23

choline acetyl transferase combines choline & acetate
AChEsterase separates them

Front 24

What kind of receptors are Acetylcholine nicotinic receptors?

Back 24

ligand-gated ion channels

Front 25

What kind of receptors are Acetylcholine muscarinic receptors? Where are they often found?

Back 25

2nd messenger systems

Front 26

What is the hallmark of Alzheimer's disease?

Back 26

loss of cholinergic neurons is a hallmark of Alzheimer’s

Front 27

What is Picrotoxin? What is it used for?

Back 27

GABA-A antagonist. It is a Analeptic-convulsant agent (for causing seizures in research animals) like bicuculline.

Front 28

What is Baclofen? What is it used for? How is it administered? What are its side effects?

Back 28

Good for spasticity
inhibits monosynaptic and postsynaptic reflexes
Good oral, increasing doses, or intrathecally via pump
SE - sedation, fatigue, and weakness

Front 29

What is Bicuculline? What is it used for?

Back 29

Specific GABA-A antagonist – research tool like picrotoxin. Causes seizures w/ small doses, reversed by GABA-mimetic agents.