Exam 2

Front 1

All of the catecholamines are derived from ___, which comes from dietary sources.

Back 1

tyrosine

Front 2

Parkinson's disease occurs because of the death of neurons in the _____.

Back 2

substantia nigra

Front 3

An enzyme responsible for the breakdown of catecholamines is ___.

Back 3

Both catechol-o-methyltransferase and monoamine oxidase

Front 4

First-generation neuroleptic (antipsychotic) drugs are ___.

Back 4

dopamine D2 receptor antagonists

Front 5

Most neurons in the CNS that produce norepinephrine arise from the ___.

Back 5

locus coeruleus

Front 6

Behavioral effects of norepinephrine include ___.

Back 6

enhanced memory of emotional events

Front 7

Methylphenidate (Ritalin) has been shown to increase activation of the ___.

Back 7

prefrontal cortex

Front 8

Cocaine ____ and methamphetamine ___.

Back 8

blocks DA transporters; causes DA transporters to operate in reverse

Front 9

Medical uses for amphetamines include all of the following except ___.

Back 9

schizophrenia

Front 10

Methamphetamine contains a methyl group that makes it more ___ than amphetamine.

Back 10

lipid soluble

stable

potent

all of the above

Front 11

Acute withdrawal from psychostimulants can produce symptoms including ___.

Back 11

depression

Front 12

MDMA is considered an entactogenic-empathogenic drug because it can cause ___.

Back 12

increased feelings of intimacy with others

Front 13

“Bath salts” typically contain ___.

Back 13

mephedrone

Front 14

Long-term or high-dose methamphetamine use can cause downregulation of ___.

Back 14

dopamine transporters

dopamine D2 receptors

both a and b

neither a nor b

Front 15

The rate-limiting enzyme in the synthesis of catecholamines is ________.

Back 15

Tyrosine hydroxylase (TH). High levels of catecholamines inhibit TH (negative feedback).

Front 16

Which of the following is true of MPTP?

Back 16

a. It can create Parkinsonian symptoms when given to primates.

b. It was accidentally created during illicit heroin synthesis and caused Parkinson's disease in the addicts who took it.

c. It selectively kills cells in the substantia nigra.

D. All the above.

Front 17

The major differences between the D₁ and D₂ dopamine receptor subtypes is that one

Back 17

Stimulates, and one inhibits adenylyl cyclase and thus cAMP.

Front 18

Which of the following is not true of norepinephrine (NE)?

Back 18

a. It acts in both the central nervous system and the autonomic nervous system.

b. It is thought to play a role in vigilance.

c. NE producing cell bodies are found in widespread brain regions.

d. NE terminals are found in widespread brain regions.

Front 19

Catecholamines:

Back 19

dopamine,norepinephrine, epinephrine.

Front 20

Catecholamines are synthesized in a multi-step pathway

Back 20

can be made by the body and is found in many kinds of food

Front 21

Vesicular monoamine transporter (VMAT)

Back 21

VMAT allows for the recycling of the neurotransmitter in a typical dopaminergic synapse.

Front 22

Role of catecholamine depletion in the behavioral depressant effects ofreserpine

Back 22

Reserpine blocks vesicular monoamine transporter (VMAT)

Animal model of depression and Parkinson's produced by reserpine

Arvid Carlsson showed that L- DOPA reverses these effects, leading to a Nobel Prize in Medicine

Front 23

Why not just give these depressed patients dopamine?

Back 23

Because Dopamine does not pass the blood-brain barrier, but L-DOPA does

Front 24

Catecholamines are degraded by two enzymes:

Back 24

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

- MAO inhibitors are used to treat depression.

Front 25

Catecholamines are monoamines, but notall monoamines are catecholamines.

Back 25

Serotonin is a monoamine, but not a catecholamine

Front 26

Two families of DA receptors:

Back 26

D1 and D2, both are metabotropic

- D1 receptors are stimulatory (coupled to Gs)

- D2 receptors are inhibitory (coupled to Gi)

- Their activation either increases (D1) or decreases (D2) adenylyl cyclase and thus, cAMP

- Affinities of D1 (low) and D2 (high) receptors are different

Front 27

Nigrostriatal dopamine pathway:

Back 27

movement

Front 28

Parkinson’s disease is characterized by a massive loss of cells in the

Back 28

substantial nigra.

Front 29

Mesolimbic dopamine pathway:

Back 29

reward.

Front 30

Mesocortical dopamine pathway:

Back 30

cognition.

Front 31

MPTP in a bad batch of homemade heroin caused

Back 31

rapid and permanent symptoms of Parkinson’s in several addicts in San Jose in 1982.

MPTP destroys cells in the substantia nigra, and as a result, mirrors the advanced stages of Parkinson's disease.

This led to a great deal of research into Parkinson’s.

Front 32

Adrenergic receptors are metabotropic receptors and are sensitive to both

Back 32

norepinephrine and epinephrine

Front 33

There are two families of adrenergic receptors:

Back 33

alpha (α) and beta (β), each with different subtypes.

- α2 are autoreceptors, coupled to Gi(inhibitory G protein)--so inhibit adenylyl cyclase.

- β (β1 and β2) are coupled to Gs(stimulatory G protein)-- so stimulate adenylyl cyclase.

Front 34

α1 adrenergic receptors increase phosphoinositide which activates

Back 34

phospholipase C (PLC).

- This produces an increase in intracellular Ca²⁺.

- α1 adrenergic receptors also activate protein kinase C.

Front 35

The noradrenergic system is important for wakefulness and arousal

Back 35

Noradrenergic agonists increase the amount of time spent awake

- Norepinephrine neurons are more active during waking than during sleep.

Front 36

Catecholaminergic drugs: L-DOPA

Back 36

Catecholamine precursor

Front 37

Catecholaminergic drugs: 6-OHDA

Back 37

•Neurotoxin (rodents)

Front 38

Catecholaminergic drugs: MPTP

Back 38

•Neurotoxin (primates)

Front 39

Catecholaminergic drugs: Reserpine

Back 39

•Depletes DA by inhibiting uptake into vesicles

Front 40

Catecholaminergic drugs: Propranolol

Back 40

Beta blocker

Front 41

The major catecholamine transmitters in the brain are

Back 41

Dopamine (DA) and norepinephrine (NE)

Front 42

Catecholamines are synthesized in several steps from the amino acid tyrosine. The first, and also rate-limiting, step in this biochemical pathway is catalyzed by the enzyme

Back 42

Tyrosine hydroxylase

Front 43

Once they have been synthesized, catecholamines are stored in

Back 43

synaptic vesicles for subsequent release.

Front 44

The process of release is controlled by inhibitory autoreceptors located on

Back 44

the cell body, dendrites, and terminals of catecholamine neurons.

Front 45

DA auto-receptors are of the

Back 45

D2 subtype

Front 46

NE auto-receptors are of the

Back 46

α2 subtype

Front 47

Catecholamines are inactivated by reuptake from

Back 47

the synaptic cleft mediated by specific DA and NE transporters, and also by enzymatic degradation.

Front 48

Monoamine oxidases (MAO) and Catechol-O- methyltransferase (COMT) are two enzymes that are important in

Back 48

catecholamine metabolism.

Front 49

The major catecholamine metabolites are

Back 49

homovanillic acid (HVA) for dopamine (DA) and methoxy- 4-hydroxy-phenylglycol (MHPG) and vanillymandelic acid (VMA) for norepinephrine (NE)

Front 50

Certain drugs can modify catecholaminergic function by acting on the processes of

Back 50

synthesis, release, reuptake, or metabolism.

- Some of these compounds are used either clinically to treat various disorders or experimentally to study the DA or NE system.

Front 51

The dopaminergic neurons of greatest interest to neuropsychopharmacologists are found near

Back 51

the base of the midbrain in the substantia nigra (A9 cell group) and the VTA (A10 cell group)

Front 52

Neurons in the substantia nigra send their axons to the

Back 52

striatum, thus forming the nigrostriatal tract.

- This pathway plays an important role in the control of movement and is severely damaged in Parkinson’s disease.

Front 53

Dopaminergic neurons in the VTA form two major dopaminergic systems:

Back 53

- the mesolimbic system, which has terminations in several limbic system structures (e.g., nucleus accumbens, septum, amygdala, hippocampus)

- the mesocortical system, which terminates in the cerebral cortex (particularly the prefrontal cortex).

-The mesolimbic and mesocortical DA systems have been implicated in mechanisms of drug abuse, as well as in schizophrenia.

Front 54

Caltecholamines

Back 54

Dopamine

Norepinephrine

Epinephrine

Front 55

Epinephrine from the periphery increases passive avoidance memory because it

Back 55

Activates the vagus nerve

Front 56

Crack cocaine can be smoked because it is

Back 56

More basic than cocaine HCL

Front 57

Methamphetamine can cause formication, which means

Back 57

The feeling of bugs crawling under the skin

Front 58

Effects of psychostimilants such as increases in heart rate, hypertension and hyperthermia are due to the actions as ______ drugs.

Back 58

Sympathomimetic

Front 59

Cocaine, the most potent stimulant of

Back 59

natural origin, is extracted from the leaves of the coca plant (EMhroxvjurn coca), Which is indigenous to the Andean highlands of South America

Natives in this region chew or brew coca leaves into a tea for refreshment and to relieve fatigue

Front 60

Catecholamines are degraded by two enzymes:

Back 60

monoamine oxidase (MAO)

and

catechol-O- methyltransferase (COMT)

MAO inhibitors are used to treat depression

Front 61

Catecholamines are

monoamines, but not all

Back 61

monoamines are

catecholamines.

Serotonin is a monoamine, but not a catecholamine

Front 62

Tyrosine hydroxylase (TH) is the _____ in catecholamine synthesis.

Back 62

Rate-limiting factor

Front 63

High levels of catecholamines inhibit

Back 63

Tyrosine hydroxylase, TH, (negative feedback).

Front 64

Coca paste from coca leaves is an _______, which is then converted to a _____ ______ form (______ HCL)

Back 64

Alkaloid

Water soluble

Cocaine

Front 65

Cocaine HCL is usually _____ or _____. It is very _______, so it readily crosses the blood brain barrier.

Back 65

Injected

Snorted

Lipophilic