DA neurons are found in the
(2)
- SN
- (substanstia nigra)
- VTA
- (ventral tegmental area)
Which of the following is believed to be increased in the nucleus accumbens by all drugs of abuse.
DA
Most antipsychotic drugs are
D2-like receptor antagonists
AADC
(5)
- Is also called dopa decarboxylase
- is required for the synthesis of DA, NE, and 5-HT (5-HT is serotonin).
- is inhibited by carbidopa
- converts L-DOPA to DA
- converts 5-HTP to 5-HT
Does NOT converts DA to NE
Parkinson’s disease is caused by the degeneration of
(3)
- DA neurons in the substantia nigra
- DA terminals in the basal ganglia
- nigrostriatal DA neurons
Not found in:
- DA terminals in the motor cortex
- mesolimbic DA neurons
- mesocortical DA neuron
- Striatal neurons
Which of the following is found in both serotonin and catecholamine neurons?
(4)
- AADC
- Dopa decarboxylase
- MAO
- VMAT
- The vesicular monoamine transporter acts to transport monoamine neurotransmitters – such as dopamine, serotonin, norepinephrine, epinephrine, and histamine – into the vesicles, which release the neurotransmitters into synapses as chemical messages to postsynaptic neurons.
In which of the following diseases is there reason to believe that the mesolimbic DA system is hypoactive?
Major depression
Notes: mesolimbic dopamine system is composed of the VTA (ventral tegumental area) and NAc (nucleus accumbens) and controls an individual’s responses to natural rewards, such as food, sex, and social interactions, and is therefore an important determinant of motivation and incentive drive.
Which of the following are used for the treatment of the motor symptoms of Parkinson’s disease?
(3)
-
D2 agonists
- Notes: act directly on dopamine receptors and mimicking the endogenous neurotransmitter.
-
MAO_B_ inhibitors
- Notes: help to block the break down of dopamine in the brain, thus making more dopamine available and reducing some of the motor symptoms associated with PD
-
mAchR antagonists
- Notes: muscarinic acetylcholine receptors
Are not aused for treatment of PD: MAOA inhibitors or D1 agonists
AADC is present in
almost all cell types in the body
Which of the following statements are true?
- D1-like receptors are Gi-coupled receptors
- D2-like receptors are Gi-coupled receptors
- DA autoreceptors are D2-like receptors.
- DA autoreceptors are D1-like receptors.
- Activation of DA autoreceptors inhibits DA neurons
- D1-like receptors are Gi-coupled receptors
- D2-like receptors are Gi-coupled receptors
- DA autoreceptors are D2-like receptors.
- DA autoreceptors are D1-like receptors.
- Activation of DA autoreceptors inhibits DA neurons
In which of the following diseases is there reason to believe that the mesocortical DA system is hypoactive?
Schizophrenia
Aripiprazole is an
(2)
- antipsychotic drug
- DA agonist
- Notes: is a D2-like receptor and partial D2 agonist
Which of the following are used for the treatment of the motor symptoms of Parkinson’s disease?
(2)
-
COMT inhibitors
- Tolcapone (xBBB), Entacapone
-
AADC inhibitors
- Given with L-Dopa
- Do not cross BBB
ARE NOT used for treatment of motor symptoms of PD:
- DAT inhibitors
- SSRIs
- Antipsychotic drugs
Extrapyramidal Syndromes (EPS)
(2)
- may be reduced by antiparkinsonian drugs
- L-Dopa
- DA agonists
- MAOB inhibitors
- Non-DA drugs
- are side effects of antipsychotic drugs
- typical antipsychotic drugs - 1st generation
- are D2 antagonists (Chlorpromazine, haloperidol, fluphenazine)
- also cause prolactin secretion
Most antipsychotic drugs are
(2)
- Effective in improving positive symptoms
- Capable of increasing DA release
Amphetamine-like psychostimulants increase the extracellular levels of
(3)
- NE
- 5-HT
- DA
Note: Cocaine and MDMA (Ecstasy) also increase these levels of reuptake inhibitors
The 5-HT-mediated synaptic transmission can be enhanced by the following except:
- Inhibition of COMT
- Inhibition of MAOA
- Inhibition of MAOB
- Blockade of VMAT
- Blockade of 5-HTT
- Blockade of 5-HT1A/1D autoreceptors
- Blockade of α1 receptors on 5-HT neurons
- Activation of tryptophan hydroxylase
The 5-HT-mediated synaptic transmission cannot be enhanced by:
- Inhibition of COMT
- Inhibition of MAOB
- Blockade of VMAT
- Blockade of α1 receptors on 5-HT neurons
The 5-HT-mediated synaptic transmission can be enhanced by:
- Inhibition of MAOA
- Blockade of 5-HTT
- Blockade of 5-HT1A/1D autoreceptors
- Activation of tryptophan hydroxylase
Triptans are
- 5-HT1B/D agonists
- drugs for treatment of migraine
Which of the following is found in both serotonin and catecholamine neurons?
(3)
- VMAT
- AAAT
- MAOA
(also AADC, Dopa decarboxylase, MAO is found in both serotonin and catecholamine neurons)
Which of the following are targets of antidepressant drugs?
MAOA**
(also DAT, 5-HTT, and NET are targets of antidepressant drugs)
(NOT targets: DBH, MAOB, LAT1, AAAT, TH)
Which of the following are target of antidepressant drugs?
(3)
- DAT
- NET
- 5-HTT
(MAOA is also a target)
NOT targets of antidepressant drugs: COMT, AADC, VMAT
Prozac is a
(2)
- antidepressant
- 5-HT reuptake blocker
(prozac is also an SSRI)
NOT the following:
- 5-HT antagonist
- direct 5-HT receptor agonist
Prozac is a
(1)
SSRI
(Prozac is also an antidepressant and 5-HT reuptake blocker)
Prozac is NOT the following:
- monoamine oxidase inhibitor
- SNRI
- Antipsychotic drug
- inhibitor of 5-HT synthesis
LSD is a
(abbreviated for D-Lysergic Acid Diethylamide)
(2)
-
5-HT2 agonist
- 5-HT2A/2C agonist
-
Hallucinogen
- other hallucinogens include amphetamine, cannabinoids, PCP, Salvinorin A, and Scopolamine
Most 5-HT neurons in the brain are located in the
raphe nuclei
Note: the CNS (sleep, mood, appetite)
Which of the following receptors requires activation by two different ligands?
NMDA receptor
Notes about NMDA receptor:
- NMDA receptor is a glutamate receptor and is ionotropic.
- Co-Agonist is Glycine
-
Long Term Potentiation
- Voltage-dependent blockade by Mg2+
- Activation by high frequency stimulation
- CaM – Ca2+-Calmodulin complex
- CaMK – CaM dependent- Kinase
GAD (Glutamic Acid Decarboxylase) is a key enzyme required for the synthesis of
GABA
Notes:
Allylglycine inhibits GAD
Benzodiazepines are useful in treating a number of brain disorders including anxiety and insomnia. The main mechanism of action of this class of drugs is to
increase the affinity of GABA for GABAA receptors
- Notes:*
- Benzodiazepines are GABA modulators*
- examples: Z drugs (Zolpidem), anticonvulsant, hypnotic, anxiolytic
- Benzodiazepines increase GAVA infinity (potency) while Barbiturates increase GABA efficacy*
- examples: anticonvulsant, anesthetic
In the brain, glutamine synthetase is primarily found in
(2)
- glial cells
- astrocytes
Ketamine is a
- non-competitive NMDA receptor antagonist.
- dissociative anesthetic.
- analgesic.
- “Vitamin K” (street name)
- fast acting antidepressant
- psychotomimetic.
- drug of abuse.
-
non-competitive NMDA receptor antagonist.
- a glutamate antagonist
- dissociative anesthetic
- analgesic
- “Vitamin K” (street name)
- fast acting antidepressant
- psychotomimetic.
- drug of abuse.
(All of the above)
Uptake is an important mechanism to remove released neurotransmitters from the synaptic cleft. Astrocytes play a critical role in uptake of
(3)
- Glycine
- Glutamate
- GABA
Drugs that increase the GABA-mediated transmission tend to produce the following effects:
(4)
- anxiolytic
- anticonvulsant
- causing drowsiness
- physical dependence
Glutamate is converted to GABA by
GAD
Which of the following receptors are coupled to Gi protein?
(5)
- α2
- D2
- 5-HT1A/D
- mGluR2
- GABAB
Which of the following statements is TRUE?
- Activation of GABAA receptors increases the membrane permeability to Cl-.
- GABA is synthesized from glutamate by the enzyme GABA transaminase
- All GABA receptors are ionotropic receptors.
- GABAC receptors are GPCRs.
- Most interneurons in the cortex are GABAergic, whereas most cortical projection neurons (i.e., pyramidal neurons) are glutamatergic.
- Activation of GABAA receptors increases the membrane permeability to Cl-.
- GABA is synthesized from glutamate by the enzyme GABA transaminase
- All GABA receptors are ionotropic receptors.
- GABAC receptors are GPCRs.
- Most interneurons in the cortex are GABAergic, whereas most cortical projection neurons (i.e., pyramidal neurons) are glutamatergic.
Which of the following statement is True?
- Glycine is an obligate co-agonist at NMDA receptors
- mGluR2/3 can function as inhibitory autoreceptors
- Almost all neurons are glutamatergic
- PCP is antipsychotic drug
- PCP is a competitive NMDA receptor antagonist
- Almost all neurons in the brain express glutamate receptors
- NMDA receptors are G-protein coupled receptors
- PCP is a non-competitive NMDA receptor antagonist
- PCP is psychotomimetic
- All glutamate receptors are ligand-gated channels
- PCP is a NMDA receptor agonist
- Glutamate always excites its target cells
- Glycine is an obligate co-agonist at NMDA receptors
- mGluR2/3 can function as inhibitory autoreceptors
- Almost all neurons in the brain express glutamate receptors
- PCP is a non-competitive NMDA receptor antagonist
- PCP is psychotomimetic
The major action of barbiturates is to
increase the efficacy of GABA, i.e., to prolong opening of Cl- channels when GABAA receptors are activated by GABA.
Which of the following are not glutamate receptors?
- and which ARE glutamate receptor?
- Glycine receptor
- Glutamine receptor
BELOW ARE GLUTAMATE RECEPTORS:
- Kainate receptor
- AMPA receptor
- mGluR1 receptor
- NMDA receptor
Glutamine synthetase converts
glutamate to glutamine
Which of the following is TRUE?
- Both NSAIDs and paracetamol inhibit COX and prostaglandin synthesis
- Morphine is a weak analgesic because it does not cross the BBB.
- Noxious stimuli directly activate PGE2 receptors on nociceptive fibers.
- Morphine is anti-inflammatory.
- Paracetamol is an analgesic agent, but it is not an NSAID as it has little anti-inflammatory action.
- TRP channels on nociceptive fibers are sensitive to high, but not low, temperatures.
- Both NSAIDs and paracetamol inhibit COX and prostaglandin synthesis
- Paracetamol is an analgesic agent, but it is not an NSAID as it has little anti-inflammatory action.
Common causes of neuropathic pain include
- chemotherapy
- amputation
- multiple sclerosis
- AIDS
- shingles
- diabetes
(all of the above)
All of the following have been recommended for treatment of pain except: (2 answers)
- Question 2: Which ARE recommended for treatment of pain?
Are NOT recommended for pain:
- fluoxetine
- SSRIs
ARE recommended for pain:
- clonidine
- gabapentin
- lamotrigine
- SNRIs
- NSAIDs
- morphine
- TCAs
Morphine produces its analgesic effect by
stimulating opiod μ receptors
Neuropathic pain is a result of:
disordered nerve function
Which of the following statements are TRUE?
- Acetaminophen has little anti-inflammatory effect because it does not inhibit Cox.
- All analgesics are anti-inflammatory
- Glucocorticoids such as cortisol are potent anti- inflammatory agents, but they are not classified as analgesics.
- All anti-inflammatory drugs are analgesics.
- Tylenol is not an NSAID because it is not anti-inflammatory.
- NSAIDs are both anti-inflammatory and analgesic.
- Paracetamol is not an NSAID because it does not inhibit Cox.
- Glucocorticoids such as cortisol are potent anti- inflammatory agents, but they are not classified as analgesics.
- Tylenol is not an NSAID because it is not anti-inflammatory
- NSAIDs are both anti-inflammatory and analgesic
Enkephalins, Endorphins, and Dynorphines:
- are ____ and ____.
- are released during ____
- bind to and activate ____
- produce ____
Enkephalins, Endorphins, and Dynorphines:
- are endogenous opioid peptides and are natural painkillers
- are released during long, continuous workouts
- bind to activate opioid receptors
- produce euphoria
Note: they do NOT bind to and inhibit opioid receptors