Problem 3

Question 1

Why is the classic theory on genetics as a cause for psychiatric disorders not adequate?

Answer 1

Not everyone who has the genetic implications for a psychiatric disorder will develop one

Question 2

What is the Two-Hit hypothesis?

Answer 2

The two hit hypothesis states that the genetiv vulnerability for a disorder is only “the first hit”, this vulnerability develops into a disorder when more hits are sustained from stressors throughout life.

Question 3

Describe some types of neurodevelopmental disorders and the psychiatric disorders associated with it

Answer 3

Wrong migration: epilepsy, mental retardation, schizophrenia, & dyslexia
Abnormal synaptogenesis: mental retardation, autism, maybe schizophrenia

Question 4

What are 3 ways to theorethically ‘fix’ neurodegenerative diseases?

Answer 4

• stop abnormal gene production or block the unwanted actions of the gene products
• make neurotropic factors rescue degenerating neurons and halt the progression of the disorder
• transplantation of the new neurons, to compensate or replace the functions of the degenerating neurons

Question 5

What are Corticocortical loops?

Answer 5

A circuit between different (corical) areas where the information is sent downstream and the originating point receives feedback

Question 6

What kind of cells form the beginning and end of the CSTC loop?

Answer 6

Pyramidal cells

Question 7

Are pyramidal cells excitatory, inhibitory or both?

Answer 7

Excitatory

Question 8

How do pyramidal cells receive inhibiting input?

Answer 8

Nearby GABAergic neurons generate short distance inhibiting input, they inhibit the pyramidal cells indirectly.

Question 9

How is the CSTC loop being fine tuned?

Answer 9

Graded degrees of monoamines and other neurotransmitters can have inhibitory and excitatory input. With this input they signal with information to prioritize and which to ignore, this is called enhancing the signal to noise ratio.

Question 10

What is the Dopamine projection pathway?

Answer 10

HPBSN.
The projection originates from the brain stem, then it goes as follows:
Hypothalamus, Prefrontal cortex, Basal forebrain, Striatum, Nucleus accumbens
Dopamine is produced in the VTA and Substantia Nigra

Question 11

What is the Norepinephrine projection pathway?

Answer 11

HPBTS - originates in brainstem
Hypothalamus, Pfc, Basal forebrain, Thalamus, Spinal cord
Produced in the Locus Coerulus

Question 12

What is the serotonin projection pathway?

Answer 12

HPBTS - originates in the brain stem
Hypothalamus, Pfc, Basal forebrain, Thalamus, Spinal cord
Produced in the Raphe nuclei

Question 13

What is the Acetylcholine projection pathway that originates in the brainstem?

Answer 13

BHPBATH

Brainstem, Hypothalamus, Pfc, Basal forebrain, Amygdala, Thalamus, Hippocampus

Question 14

What is the Acetylcholine projection pathway that originates in the Basal forebrain?

Answer 14

BHAP

Basal forebrain, Hippocampus, Amygdala, Pfc

Question 15

What is stress sensitization?

Answer 15

When circuits are repeatedly stressed, the load becomes to much and the circuit becomes stress sensitized, this causes the circuit to work overtime even after the stressor is withdrawn, this does not cause symptoms immediately but it does cause loss of resilience

Question 16

What is diabolical learning?

Answer 16

When symptoms of disorders are left untreated, they can cause plastic changes. Recruiting more sick circuits, eliminating healthy compensating mechanisms, phosphorylating critical regulatory proteins and erecting better synaptic scaffolding in sick circuits to make them more efficient.

Question 17

What is a agonist?

Answer 17

An agonist is a ligand that has a normal effect on the receptor

Question 18

What is an antagonist?

Answer 18

An antagonist is a ligand that binds to the receptor but does not do any work, it doesnt activate it. But it blocks any agonists or inverse agonists from binding to it

Question 19

What is an inverse agonist?

Answer 19

The inverse agonist binds to the receptor and does the opposite of the agonist. It actively closes the channel (even disrupting the consitutive activity)

Question 20

What is affinity?

Answer 20

Affinity is the chemical attraction between the ligand and the receptor

Question 21

What is efficacy?

Answer 21

Efficacy is the tendency of a ligand to activate the receptor to which it is bound

Question 22

What is a partial agonist?

Answer 22

A agonist that only partially activates the receptor, always staying below the maximal capacity a full agonist would have.

Question 23

What is functional tolerance? (Up and down regulation)

Answer 23

Down regulation: repeated exposure to an agonist causes the target neurons to decrease the number of receptors it can bind to
Up regulation: repeated exposure to antagonists causes the number of receptors to go up to increase the probability of an agonist binding

Question 24

Why can a partial agonist be a net agonist or net antagonist?

Answer 24

The partial agonist can have both an agonistic and antagonistic effect because when there are no full agonists present they act as agonists, however when there are full agonists around the partial agonist causes a less effective response and thus having the same effect an antagonist would have.

Question 25

Explain Positive and negative allosteric modulation:

Answer 25

Positive: a neurotransmitter paired with a allosteric modulator maximize ionic condictance beyond what the nt can accomplish alone. Increases affinity and efficacy
Negative: leads to minimizing of the synaptic reuptake of neurotransmitters because the molecules that transport these nt’s have been blocked
Decreases affinity and efficacy

Question 26

Which is faster, G-protein-linked systems or ionotropic systems?

Answer 26

Ionotropic receptors are fast, while G-protein-linked ones are slower

Question 27

What is the differences between the two forms of the COMT gene?

Answer 27

The COMT gene has met- and val alleles. Subjects with the met-met variation show significantly more efficient processing in the DLPFC circuits during the n-back task. This is because the met-met gene have lower COMT activity, which means there is more dopamine available.

Question 28

What are the SERT genes?

Answer 28

The SERT gene has variations long and short. When processing fear, subjects with long-long variation have more efficient processing in the amygdala circuits. This is because SERT does the re uptake of serotoning, subjects with the long- long variation have more SERT activity, meaning less serotonin and better processing