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37 Cards in this Set

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  • Back
What are the 5 main monoamine neurotransmitters?
How are the catecholamines synthesized? which is the rate-limiting step?
1.Tyrosine is hydroxylated to L-DOPA. This is the rate-limiting step
2.L-DOPA is decarboxylated to dopamine
3.Dopamine is hydroxylated to norepinephrine
4.Norepinephrine is methylated to epinephrine
How is serotonin synthesized?
1.Trytophan is hydroxylated to 5-HTP
2.5-HTP is decarboxylated to serotonin
How is histamine synthesized?
Histadine is decarboxylated to histamine.
How are monoamines released from the pre-synaptic terminal?
They are stored in secretory vesicles which are released in a Ca++ mediated fashion.
Describe the monoamine receptors on the postsynaptic terminal. Are they inhibitory of excitatory?
The receptors are metabotropic and coupled to a G-protein. The effects of binding may be excitatory or inhibitory depending on the specific receptor.
How are monoamines removed from the synaptic cleft?
*catecholamines may be degraded by CoMT
*they may be taken back up by the pre-synaptic terminal via DAT, NET, or SERT
What happens to monoamines that are taken back up by the pre-synaptic terminal?
*they may be degraded by MAO
*they may be reloaded into secretory vesicles by VMAT
What are autoreceptors?
They are receptors found on the pre-synaptic membrane that downregulate synthesis and release of neurotransmitter when activated.
Monoaminergic neurons are among the most important in the brain and make up a large proportion of the total cell population.
False: monoaminergic neurons are very important, but they only make up a small fraction of the total number of neurons.
Where does the nigrostriatal pathway originate from? Where does it project?
*originates in the substantia nigra
*projects to the striatum (caudate and putamen)
What effects are seen with loss of neurons in the nigrastriatal pathway?
Parkinson's symptoms
Where does the mesolimbic pathway originate from? Where does it project? What neurotransmitter is carried on this path?
*originates at the midbrain tegmentum
*projects to the limbic system, especially the nucleus accumbens
What is the function of the mesolimbic pathway?
It is part of the "reward" circuit of the brain.
Where does the mesocortical pathway originate from? Where does it project? What disease is said to involve malfunction in this pathway?
*originates from the midbrain tegmentum
*projects to the cerebral cortex
What are the three dopaminergic pathways in the brain?
Where does the noradrenergic pathway originate? Where does this path project?
*locus coeruleus
*projects through the MFB to the rest of the cerebrum
*also projects to the cerebellum and spinal cord
What is the function of the noradrenergic pathway?
This pathway is thought to be involved in arousal, attention, and feeding.
Which of the monoaminergic pathways pass through the MFB?
Where does the serotoninergic pathway originate from? Where does it project to?
*originates at the raphe nuclei of the midbrain
*projects through the MFB to the cerebrum
*also projects to the spinal cord to interact with descending pain control pathways
Where does the histamine pathway originate? What is the function of this pathway?
*originates at the tuberomammillary nuclei of the hypothalamus
*involved in arousal and wakefulness
What is the effect of inhibition of the H1 receptor? What drug is known to do this?
*blocking this histamine receptor results in sedation
Tolerance is largely a psychological phenomenom.
False: tolerance is a physiological adaptation.
Which monoaminergic pathway has been implicated in substance abuse?
The mesolimbic dopaminergic pathway - the "reward" circuit of the brain.
What is the mode of action of cocaine and amphetamine?
They block pre-synaptic uptake of dopamine and norepinephrine, thus prolonging the time these neurotransmitters are in the synaptic cleft.
Why are MAO inhibitors seldom used for treatment of depression?
They have serious side effects related to accumulation of tyramine, which is also broken down by MAO.
What is the mode of action of the tricyclic antidepressants?
By inhibiting DAT, NET, and SERT they block the re-uptake of these neurotransmitters.
What is the mode of action of the SSRIs?
By inhibiting the action of SERT, it blocks the reuptake of serotonin.
What has been shown to be the most effective treatment for depression?
ECT, with a success rate of 85%.
How is lithium thought to work in the treatment of bipolar disorder?
It is thought to inhibit second messenger pathways in the post-synaptic terminal.
What are some "positive" symptoms of schizophrenia? What are some negative symptoms?
*hallucinations (auditory and visual), delusions, paranoia, disorganized thought
*poverty of thought, emotion and motivation; catatonia
What kinds of anatomical changes are seen in the brains of schizophrenia patients?
Atrophy with widening of sulci and ventricular enlargement, with emphasis at the vermis, hippocampus, prefrontal cortex, and thalamus.
What are two pieces of evidence that support the dopamine hypothesis of schizophrenia?
1.Drugs which block dopaminergic transmission alleviate symptoms
2.Drugs that induce dopaminergic transmission cause psychosis
What is the mode of the first generation neuroleptics? What side effects are associated with their use?
They are specific D2 antagonists which prevent dopaminergic transmission. Side effects include Parkinsonism and problems of excessive movement: acute dystonia and tardive dyskinesia.
Do second generation neuroleptics have a more or less specific mode action as compared to first generation drugs?
Second generation neuroleptics have a broader mode of action and inhibit serotoninergic as well as dopaminergic transmission.
What is the mode of action of the third generation neuroleptics?
They are mixed agonist/antagonists of dopaminergic transmission that allow partial activation of receptors.
What are two pieces of evidence AGAINST the dopamine hypothesis of schizophrenia?
1.Antipsychotic drugs are not specific to dopaminergic transmission.
2.Psychosis may be produced by activation of other receptors.
3.Drugs block dopamine receptors right away, but symptoms may not disappear for days or weeks.