Psychopharmacology

Front 1

Cortical neurons serve as _____ to networks in the brain and are called this for 2 reasons....

Back 1

"engines"
Able to take simple inputs n create complex output
Each address in the network is a node

Front 2

3 dimensional/planes of brain anatomy

Back 2

Horizontal (transverse) - gives top -superior and bottom -inferior
Coronal (frontal) gives ventral and dorsal
Sagittal gives left and right

Front 3

What are Broadmann Areas?

Back 3

Structurally different areas labeled by numbers. Several are related to PFC, Hippo, and Amygdala

Front 4

Abbreviations of functional Divisions of the brain...

Back 4

PFC= prefrontal cortex
H=hippocampus
A=Amygdala
Th=Thalamus
Ht=Hypothalamus
BF=Basal forebrain
S=Striatum
NA=Nucleus Accumbens

Front 5

What are the 4 divisions of the PFC and the functions?

Back 5

1. Dorsolateral PFC= DLPFC = cognitive function, problem solving analyzing
2. Orbital Frontal Cort=OFC=impulses, compulsions, drives
3. Anterior Cingulate Cortex=ACC=emotions such as depression and anx
4. Ventromedial PFC= emotional processing

Front 6

What is the primary function of H?

Back 6

Hippocampus is memory and neurogenesis

Front 7

What is function of A?

Back 7

Amygdala is fear processing

Front 8

What is primary function of NT Nodes

Back 8

•Cell bodies in brainstem, etc. or nuclei in the area where spinal cord enters brain stem. There are NT nodes outside brainstem but many clustered here.
•Projections to PFC, etc. that branch out to other areas
•Some overlap, some unique

Front 9

Where do DA projections project from? To?

Back 9

VTA vetral tegmental area and substantia nigra.
PFC, NA (imp in addictions), Th to neorcortex, st, A

Front 10

What is the functions of DA projections?

Back 10

regulate movement
pleasure and reward
cognition
psychosis
Sleep arousal in Th DA

Front 11

Where do NE Projections descend project from? To?

Back 11

Locus Coeruleus ascending to PFC
Lateral Tegmental NE cell system descending in SC in brainstem

Front 12

Functions of NE projections?

Back 12

Regulates mood, arousal, cognition
Descending regulates pain pathways

Front 13

5HT Projections from where? to where?

Back 13

From brainstem to PFC and SC- similar to NE w addition of S and NE

Front 14

What are the functions of 5HT projections?

Back 14

regulates mood, anx, sleep and pain

Front 15

ACh Projections project from where? to where?

Back 15

Brainstem NT center ot PFC regulating arousal and cognition
From BF to PFC and A and H regulating memory

Front 16

HA projections from where to where?

Back 16

From tuberomammilary Nucleus (TMN) in Hy to PFC, SC
regulating arousal, wakefullness and sleep. "Sleep-wake switch"

Front 17

What is the primary NT in cortical circuits aka loops?

Back 17

Glu

Front 18

What is the implication for activating one area of a loop?

Back 18

Ripple effect and see activity down the circuit.

Front 19

What is the oreder of the main loop?

Back 19

DLPFC
ACC
OFC
H

Front 20

What is CSTC?

Back 20

Cortico striatal thalamic cortical loops.
Downstream info with feedback. PFC to S to T to PFC

Front 21

What is the role of pyramidal cells in loops?

Back 21

They are the engines and targets for meds. both for NT input and output. We can deal with them indirectly by targetting NTs that are part of the circuit.

Front 22

What do pyramidal celss use as excitatory outputs and inputs?
Inhibitory inputs?

Back 22

Glu
GABAergic connect at various points on cortical pyramidal cells.
 Note that it is possible to inhibit the inhibitory cells if they are strung together (net effect = disinhibition in this case)

Front 23

What other NTs can be used to modulate the actions of Glu (on) and GABA (off)?

Back 23

MAs, ACh, HA

Front 24

Pyramidal inputs occur mostly on _____.

Back 24

Basilar dendrites

Front 25

What are 2 obvious targets of MAs that tune pyramidal cells/circuits?

Back 25

1. reuptake transporters (SERT, DAT, NET)
2. Enzymes that break down NTs (COMT, MAO-A)

Front 26

What is meant by a malfunctiong circuit?

Back 26

Inefficient info processing in the circuit

Front 27

Repeated stress that overloads the circuit can lead to stress_______.

Back 27

Sensitization. There is no Sx, but there is loss of resiliency - presymptomatic

Front 28

What are potential intervention target times?

Back 28

Presymptomatic
Prodromal
Subsyndromal

Front 29

Each of the lobes of the brain can be broken down into at least 2 cortical areas. List 2 areas for each lobe.

Back 29

Frontal Lobe - Prefrontal cortex; Primary motor cortex
Parietal Lobe – Primary somatosensory cortex; somatosensory association cortex
Temporal Lobe – Primary auditory cortex; Auditory association cortex
Occipital Lobe – Primary visual cortex; Visual association cortex

Front 30

What are the primary functions associated with histamine? What other NT has similar associated functions?

Back 30

The primary functions associated with histamine are arousal, wakefulness and sleep. The neurotransmitter with similar associated functions is dopamine, specifically the thalamic dopamine system which regulates sleep and arousal.

Front 31

What does CSTC stand for? What loop is hypothetically associated with emotions? What role do pyramidal cells play in these loops?

Back 31

CSTC stands for Cortico-striatal-thalamic-cortical circuits. The CSTC loop hypothetically associated with emotion originates in the ventral or Subgenual ACC Nucleus AccumbansThalamusCortex. Pyramid cells are the drivers of cortical circuits and each loop begins and ends with a pyramid cell.

Front 32

Compare and contrast Glu and GABA. How does this compare to the actions of monoamines?

Back 32

Glu is the neurotransmitter output of all cortical pyramidal neurons. Conversely, GABAergic interneurons provide inhibitory input to pyramidal neurons. Glu excitatory projections synapse with apical dendrites while monoamines and other neurotransmitters synapse with basilar dendrites. Monoamine projections can be either excitatory or inhibitory and their actions may be more subtle than the actions of Glu and GABA. Namely, Glu and GABA exert more of an “on-off” effect on pyramidal neurons, while monoamines exert a more “fine-tuning” action.

Front 33

What are the two common targets for fine-tuning monoamine function?

Back 33

Two common targets for fine-tuning monoamine function are 1) presynaptic transporters for monoamines and, 2) catabolic enzymes for monoamine degradation.

Front 34

What is diabolical learning? Explain how psychotherapy and/or psychopharmacology could have important short term and long term benefits.

Back 34

Diabolical learning is a model of learning which suggests that a psychiatric symptom that is allowed to persist over time will create worsening of circuit breakdown. This circuit breakdown leads to an eventual worsening of symptoms or to relapse. The main idea of this model is that “symptoms beget symptoms” and circuits learn to become inefficient and overly activated.

Front 35

What is an N-back test (i.e., how is it conducted and why would we use it) and what would it mean if someone had little to moderate prefrontal activity during this type of test?

Back 35

An N-back test is a functional neuroimaging strategy that uses a mental task during imaging. The N can be any number and the subject is presented with the sequence of “N” stimuli during the imaging. On a 0-back task the subject views a number and then is asked to repeat or identify the number just seen. This can get more difficult on 1-back where the subject is asked to identify the stimulus that was the one prior. On a 2-back the subject identifies the stimulus that was two numbers back, and so on. When the subject performs the tasks, the activated cortical areas “light up.” Little to moderate prefrontal activity during this type of test suggests processing efficiency.

Front 36

are the steps in the rational selection and combination for treatments according to Stahl? What happens if a particular symptom does not remit?

Back 36

1)Construct a diagnosis,
2) Deconstruct diagnosis into component symptoms,
3) Match symptom to hypothetically malfunctioning circuit, 4) Consider the portfolio of neurotransmitters that theoretically regulate each circuit, 5) Select a treatment that targets the neurotransmitter regulating the hypothetically malfunctioning circuit, 6) Add or switch to another treatment if the symptom is not relieved, 7) Repeat this process for each symptom until the patient is asymptomatic or in remission whenever possible.

Frequently, symptoms do not remit. In that case, the strategy is to change the treatment or add to the existing treatment by targeting a different neurotransmitter in the hypothetically malfunctioning circuit.