Final Exam Review Session Flashcards
(33 cards)
What system do indoleamines act on, and what drugs are indoleamines?
Indoleamines act on the serotonergic system and LSD and psilocybin are indoleamines
Why does LSD cause synesthesia?
↓ Thalamic-Association Cortical Connections = Decreased sensory integration
↑ Thalamic-Sensory Cortical Connections = Increased sensory processing
Sensory input is not filtered as effectively by the thalamus, leading to increased sensory connections while the normal perceptual integration is decreased.
To have an effect on the brain, Psilocybin has to be transformed into ___________ through ____________
Psilocin through dephosphorylation
What receptor is most responsible for the hallucinogenic effects of hallucinogens?
5-HT2A
What characteristic of hallucinogenic drugs is responsible for their therapeutic effects?
Psychoplastogenic or neural remodeling
Neuroplasticity
LSD has a half-life of 2-3 hours but its’ effects last for 6-15 hours. Why?
LSD binds to serotonin receptors and creates a lid, which prevents it from dissociating for a longer period than clearance from blood plasma
What Behavioral Procedure was used to show rodents experience Hallucinogens? Explain using the graph.
Drug discrimination
In class we discussed a study on Escitalopram and Psilocybin. Why did the authors only report the insignificant finding?
They ran multiple independent tests which increases the risk of Type 1 error (false positive)
They did not report the other results as significant
Monoamine Oxidase Inhibitors have problematic side effects. Name 2 different ways it causes these side effects.
Increases all monoamine levels leading to greater sympathetic nervous system activation - affects HR and BP
MAO in liver is also inhibited, leading to interactions with other drugs (cocaine & alcohol) and foods (cheese) - MAO breaks down tyramine and inhibition causes excess which can lead to high BP
Which of the following are hypothesis for depression?
a. Glutamate hypothesis
b. Monoamine hypothesis
c. Dopamine hypothesis
d. Gut-Brain-Axis hypothesis
e. Glucocorticoid hypothesis
f. Multiple-Hit model
b. Monoamine hypothesis
d. Gut-Brain-Axis hypothesis
e. Glucocorticoid hypothesis
Ketamine is an experimental, atypical antidepressant with long-lasting therapeutic effects. Which depression hypothesis best explains this and why?
- Glucocorticoid hypothesis
- Stress decreases BDNF release, which results in atrophy - ketamine increases BDNF instead of monoamines
What is an autoreceptor?
Receptor that regulates NT synthesis and release, located on presynaptic neurons
The HPA Axis as covered in class involves 3 discrete structures and 3 signaling chemicals. What are these, and how are they connected?
The Paraventricular Nucleus (PVN) of the Hypothalamus releases Corticotropin-Releasing Hormone (CRH)
The Anterior Pituitary releases Adrenocorticotropic Hormone (ACTH)
The Adrenal Cortex releases Cortisol a Glucocorticoid
What mechanism explains both the Glucocorticoid Hypothesis and the delayed onset of SSRI function?
Chronic negative feedback, leading to downregulation of receptors.
Glucocorticoid Hypothesis = ↓Glucocorticoid Receptors from chronic Cortisol activation
Chronic SSRI Use = ↓5-HT Autoreceptors from chronic 5-HT activation
SSRIs can improve depressive symptoms by:
A. Increased 5-HT Binding
B. Increased 5-HT Synthesis
C. Reduced CRF release
D. Increased Glucocorticoid Receptor Expression
E. Upregulation of 5-HT Receptors
F. Increased Glucocorticoid Binding Affinity
G. Increased BDNF expression
A. Increased 5-HT Binding
D. Increased Glucocorticoid Receptor Expression
F. Increased Glucocorticoid binding affinity
G. Increased BDNF expression
Why does the Dexamethasone Suppression Test work as a test for Depression?
Dexamethasone is a Glucocorticoid, which should activate the HPA Axis negative feedback loop and reduce circulating cortisol.
If this does not properly happen, it means the Glucocorticoid Receptors are not appropriately managing the system. This indicates Depression in the Glucocorticoid Hypothesis.
The _______ Nervous System in the gut connects to the brain through the _______ Nerve.
Enteric, Vagus
What are the three components of the Multiple-Hit Model?
- Genetic Predisposition
- Environmental Insults
- Exposure to Trauma
In Schizophrenia, which neurons have increased DA function and which have decreased DA?
Increased in Mesolimbic Neurons- Associated with positive psychotic symptoms.
Decreased in Mesocortical Neurons- Associated with negative cognitive symptoms.
How does the Glutamate Hypothesis connect to the Dopamine Hypothesis of Schizophrenia?
Glutamatergic neurons connect to the VTA, stimulating DA pathways. These glutamatergic neurons have reduced function in Schizophrenia.
Mesocortical pathways are directly stimulated by these neurons, so reducing their activity reduces Mesocortical DA.
Mesolimbic pathways are mediated by GABA, so reducing their activity increases Mesolimbic DA.
Why do atypical antipsychotics have reduced side effects compared to conventional antipsychotics?
Atypical antipsychotics are partial DA agonists or selective DA antagonists, which results in less unwanted inhibition of substantia nigra motor neurons.
Acetylcholinesterase has “near perfect” enzyme degradation in the synapse. What implication does this have for ACh reuptake?
Reuptake is not a mechanism for ACh clearance because it is fully cleared by enzymatic degradation. Instead, the product Choline is cleared through reuptake to synthesize more ACh.
AChE inhibitors: 2 good uses, 2 bad uses
Good: Treat myasthenia gravis and treats Alzheimer’s
Bad: Organophos Phosphorus compounds and chemical warfare (sarin gas)
True/false: mAChRs are inhibitory
Some are, some are excitatory
