Final Psychopharm Exam
Arousal spectrum - answer as it spans around an awake, alert, creative and problem
solving person
from deficient arousal to excessive arousal
Sleep wake switch - answer set of circuits in the hypothalamus that regulate sleep and
wake discontinuously
Tubermamillary nucleus (TMN) - answer Wake promoter (on)
Ventrolateral preoptic nucleus (VLPO) - answer Sleep promoter (off)
Lateral hypothalamus (LAT) - answer orexin containing neurons
these are lost in narcolepsy
especially narcolepsy with cataplexy
Suprachiasmic nucleus (SCN) - answer melatonin sensitive neurons
brains internal clock
pacemaker
regulates circadian input to the sleep wake switch
Histamine - answer key neurotransmitter regulating wakefulness
ultimate target of many drugs
produced from histidine
H1 and H3 receptors in brain
also acts on NMDA, but unclear how
all histamine neurons arise from a single small are of hypothalamus, the TMN
Homeostatic - answer sleep drive
Circadian - answer wake drive
Sleep regulation - answer small number of interconnecting systems or centers that are
located chiefly in the brainstem and that mutually activate and inhibit one another.
Norepinepherine - answer controlling sleep patterns
locus ceruleus
drugs and manipulations focused here reduce REM sleep
Acetylcholine - answer particularly in the production of REM sleep
disturbances in central cholinergic activity are associated with sleep changes in
depression
Alzheimers dementia - answer reduced REM and slow wave sleep from loss of
cholinergic neurons in basal forebrain
Melatonin - answer secretion from pineal gland inhibited by bright light
,Final Psychopharm Exam
lowest serum concentrations during day
Suprachiasmatic nucleus - answer hypothalamus
anatomical site of a circadian pacemaker that regulates melatonin secretion and the
entrainment of the brain to a 24 hour sleep wake cycle
Dopamine - answer has an alerting affect
Serotonin - answer prevention of synthesis or destruction of its house (raphe nucleus)
reduces sleep for a considerable time.
circadian rhythm - answer
Histamine synthesis - answer Histidine taken into histamine nerve terminals via a
histidine transporter and converted into histamine by enzyme histidine decarboxylase
(HDc) and packed into vesicles
Histamine metabolism - answer Termination: broken down intracellularly by histamine n-
mehtly-transferase (histamine NMT) which converts histamine into n-mehtly-histamine,
which then is converted by MAO-B into the inactive substance n-methly-indoleacetic
acid.
Histamine receptor H1 - answer H1 - really involved in sleep
G-protein linked receptor
Variety of intermediate steps to promoting sleep
Histamine receptor H2 - answer -does not appear to be directly related to wakefulness
-G protein linked
Histamine receptor H3 - answer autoreceptor
presynaptic
MOA of caffeine - answer -Antagonist of endogenous neurotransmitters (Purines)
-caffeine antagonizes purine receptor and prevents adenosine from binding resulting in
increased dopamine action
pharmacokinetics - answer -how the body acts upon drugs
-mediated through hepatic and drug metabolism
Pharmacodynamics - answer -What is the action of the drug on the body?
Accounts for therapeutic action and side effects of drug.
Half-life serum - answer -takes about 5 half-life cycles for drug to be eliminated
-concentrations may be higher in brain
, Final Psychopharm Exam
steady state - answer -Balance between addition of drug and action of CYP
metabolization.
-Takes about 5 half-life cycles to reach.
drug transportation - answer -Many drugs transported on proteins (albumen).
-If another drug added, tries to knock off old one.
-So, may be higher concentration of old drug in bloodstream.
NMDA glutamate receptor - answer glutamate is recycled and regenerated
glutamate released - answer taken into glial cells (excitatory amino acid
transporter/EAAT)
glutamate converted glutamine - answer by glutamine synthetase
Glutamine released from glial cells (glial SNAT) - answer by reverse transport and taken
into Glutamate neuron by SNAT.
Glutamine converted to Glutamate by glutaminase . - answer Taken into vesicles by
vesicular glutamate transporter (vGluT) and stored
NMDA receptor - answer -dependent upon co-transmitters -One is Glycine (produced
either in glycine neuron or glial cells).
Magnesium - answer negative allosteric modulator at NMDA glutamate receptor
If magnesium is present, even with glycine and glutamate - answer depolarization must
occur for the channel to be open (allows for long-term potentiation and synaptic
plasticity)
Schizophrenia - answer abnormal NMDA action and reduced glutamate inhibition, can
lead to increased dopamine
First generation antipsychotics - answer D2 Antagonism
High risk of neurological side effects (EPS, tardive dyskinesia, dystonia)
Second Generation Antipsychotics - answer 5HT2A/D2 Antagonism
High risk of metabolic side effects (hyperglycemia, weight gain, dyslipidemia etc.)
Mesolimbic pathway - answer overactive, leading to positive symptoms
D2 partial agonists modulate the overactivity of dopamine and reduce symptoms
Mesocortical pathways - answer overactive, leading to negative, cognitive, and affective
symptoms
partial D2 agonists increase dopamine activity and restore function
Arousal spectrum - answer as it spans around an awake, alert, creative and problem
solving person
from deficient arousal to excessive arousal
Sleep wake switch - answer set of circuits in the hypothalamus that regulate sleep and
wake discontinuously
Tubermamillary nucleus (TMN) - answer Wake promoter (on)
Ventrolateral preoptic nucleus (VLPO) - answer Sleep promoter (off)
Lateral hypothalamus (LAT) - answer orexin containing neurons
these are lost in narcolepsy
especially narcolepsy with cataplexy
Suprachiasmic nucleus (SCN) - answer melatonin sensitive neurons
brains internal clock
pacemaker
regulates circadian input to the sleep wake switch
Histamine - answer key neurotransmitter regulating wakefulness
ultimate target of many drugs
produced from histidine
H1 and H3 receptors in brain
also acts on NMDA, but unclear how
all histamine neurons arise from a single small are of hypothalamus, the TMN
Homeostatic - answer sleep drive
Circadian - answer wake drive
Sleep regulation - answer small number of interconnecting systems or centers that are
located chiefly in the brainstem and that mutually activate and inhibit one another.
Norepinepherine - answer controlling sleep patterns
locus ceruleus
drugs and manipulations focused here reduce REM sleep
Acetylcholine - answer particularly in the production of REM sleep
disturbances in central cholinergic activity are associated with sleep changes in
depression
Alzheimers dementia - answer reduced REM and slow wave sleep from loss of
cholinergic neurons in basal forebrain
Melatonin - answer secretion from pineal gland inhibited by bright light
,Final Psychopharm Exam
lowest serum concentrations during day
Suprachiasmatic nucleus - answer hypothalamus
anatomical site of a circadian pacemaker that regulates melatonin secretion and the
entrainment of the brain to a 24 hour sleep wake cycle
Dopamine - answer has an alerting affect
Serotonin - answer prevention of synthesis or destruction of its house (raphe nucleus)
reduces sleep for a considerable time.
circadian rhythm - answer
Histamine synthesis - answer Histidine taken into histamine nerve terminals via a
histidine transporter and converted into histamine by enzyme histidine decarboxylase
(HDc) and packed into vesicles
Histamine metabolism - answer Termination: broken down intracellularly by histamine n-
mehtly-transferase (histamine NMT) which converts histamine into n-mehtly-histamine,
which then is converted by MAO-B into the inactive substance n-methly-indoleacetic
acid.
Histamine receptor H1 - answer H1 - really involved in sleep
G-protein linked receptor
Variety of intermediate steps to promoting sleep
Histamine receptor H2 - answer -does not appear to be directly related to wakefulness
-G protein linked
Histamine receptor H3 - answer autoreceptor
presynaptic
MOA of caffeine - answer -Antagonist of endogenous neurotransmitters (Purines)
-caffeine antagonizes purine receptor and prevents adenosine from binding resulting in
increased dopamine action
pharmacokinetics - answer -how the body acts upon drugs
-mediated through hepatic and drug metabolism
Pharmacodynamics - answer -What is the action of the drug on the body?
Accounts for therapeutic action and side effects of drug.
Half-life serum - answer -takes about 5 half-life cycles for drug to be eliminated
-concentrations may be higher in brain
, Final Psychopharm Exam
steady state - answer -Balance between addition of drug and action of CYP
metabolization.
-Takes about 5 half-life cycles to reach.
drug transportation - answer -Many drugs transported on proteins (albumen).
-If another drug added, tries to knock off old one.
-So, may be higher concentration of old drug in bloodstream.
NMDA glutamate receptor - answer glutamate is recycled and regenerated
glutamate released - answer taken into glial cells (excitatory amino acid
transporter/EAAT)
glutamate converted glutamine - answer by glutamine synthetase
Glutamine released from glial cells (glial SNAT) - answer by reverse transport and taken
into Glutamate neuron by SNAT.
Glutamine converted to Glutamate by glutaminase . - answer Taken into vesicles by
vesicular glutamate transporter (vGluT) and stored
NMDA receptor - answer -dependent upon co-transmitters -One is Glycine (produced
either in glycine neuron or glial cells).
Magnesium - answer negative allosteric modulator at NMDA glutamate receptor
If magnesium is present, even with glycine and glutamate - answer depolarization must
occur for the channel to be open (allows for long-term potentiation and synaptic
plasticity)
Schizophrenia - answer abnormal NMDA action and reduced glutamate inhibition, can
lead to increased dopamine
First generation antipsychotics - answer D2 Antagonism
High risk of neurological side effects (EPS, tardive dyskinesia, dystonia)
Second Generation Antipsychotics - answer 5HT2A/D2 Antagonism
High risk of metabolic side effects (hyperglycemia, weight gain, dyslipidemia etc.)
Mesolimbic pathway - answer overactive, leading to positive symptoms
D2 partial agonists modulate the overactivity of dopamine and reduce symptoms
Mesocortical pathways - answer overactive, leading to negative, cognitive, and affective
symptoms
partial D2 agonists increase dopamine activity and restore function
