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neurotransmitters
psychopharmacology
Question | Answer |
---|---|
Communication between neurons are through | neurotransmitters and the receptors. |
Parts of the neuron | body is the soma, axon terminal, axon, dendrites, schwann cells (make myelin sheath), nucleus, node of ranvier |
Hormones now act as | neurotransmitters (histamines) |
Acetylcholine (ACh) is involved in both | learning and memory and muscle movement |
Dopmaine impacts our | arousal and mood states, thought processes, and physical movement |
Serotonin and norepinephrine are neurotransmitters involved in levels of | arousal and mood, and play a major role in mood disorders such as depression |
GABA is the main inhibitory neurotransmitter in the nervous system | calms; low levels make people anxious. Antianxiety medications increase levels of GABA to inhibit excitation/calm people down |
Glutamate is the main | excitatory neurotransmitter |
Acetylcholine- (where synthesized) cells in | pedunculopontine complex project to midbrain, thalamus. Peripheral- motor neurons. |
Electrical versus chemical impulses | chemical is longer- like meds which take time |
Dopamine's synthetic precursor is | 3,4-dihydroxyphenylalanine (L-DOPA) – (useful for treatment of Parkinson's dz which presents with low dopamine. Schizophrenia on the other hand is thought to be predominantly due to excess dopamine). |
Synthesis of Dopamine is synthesized in cell groups in the midbrain's | substantia nigrae and ventral tegmental areas (VTA) - note well. |
Serotonin is also synthesized in | the gut- may cause the s/e of nausea- encourage the pt to continue to take |
Acetylcholine is r/t | dementia and alzheimers |
The four pathways relevant to the pharmacology of antipsychotics in the treatment of schizophrenia are | 1) mesolimbic pathway (+ symptoms), 2) mesocortical pathway (- symptoms) 3) nigrostriatal pathway (EPS and tardive dyskinesia) 4) tuberoinfundibular pathway (hyperprolactinemia) |
Dopaminergic pathways | mesolimbic, mesocortical, tuberoinfundibular and nigrostriatal pathway |
Nigrostriatal pathway | Associated with movement. Depletion of dopamine in the nigrostriatal pathway causes Parkinson's disease. |
Mesolimbic pathway | Axons of a subset of neurons in the ventral tegmental areas (VTA) and terminate in the nucleus accumbens (also part of the corpus striata complex). |
Mesocortical Pathway | The axons of a second subset of neurons in the VTA and continue on to innervate the frontal cortex. |
Negative s/s | withdrawal, anhedonia, flat affect |
Positive s/s | hallucinations, delusions… |
Tuberoinfundibular pathway | Axons from these neurons project to an anatomically specific area of the pituitary gland called the infundibulum- connects the hypothalamus with the pituitary gland. |
Hyperactivation(high levels of dopamine) from the ventral tegmental area (VTA) to limbic areas might be related to | positive symptoms of schizophrenia. |
Hypofunction(low levels of dopamine) of the mesocortical pathway might in part explain | cognitive and negative symptoms of schizophrenia. |
D2 blockade(excessive restriction of dopamine) of the nigrostriatal pathway can cause | EPS. |
D2 blockade(excessive restriction of dopamine) of the tuberoinfundibular pathway increases | prolactin blood levels. |
Low levels dopamine are associated with | Parkinson’s disease, and excessively high levels are associated with schizophrenia |
L-Dopa is an agonist that increases production | of dopamine |
Anti-psychotic drugs are antagonists that block the receptor sites for | dopamine |
Amphetamine acts as an agonist by stimulating the release of | dopamine from axon terminals(explains why addicts may present with psychotic symptoms – positive sxs) |
Cocaine is an agonist that blocks the re-uptake of | dopamine(may explain why users exhibit psychotic sxs) |
Tryptophan serves as the precursor for the synthesis of | serotonin and melatonin |
Synthesis of serotonin | the neurons of the raphe nuclei are the principal source of serotonin release(note well). |
Highest concentration of serotonin | found in the platelets and in cells in the gastrointestinal tract, where it is used to regulate intestinal movements (explains why GI side effect is common with most antidepressants). |
Epinephrine is synthesized in the | adrenal glands and released into the bloodstream when dangerous circumstances occur |
Epinephrine rapidly prepares the body for action and boosts the supply of | oxygen and glucose to the brain and muscles while suppressing other non-emergency bodily processes (digestion in particular). |
Norepinephrine synthesis | Neurons in the loci coerulei, a pair of structures located within the pons of the brain stem, synthesize norepinephrine. |
norepinephrine prepares the brain to encounter and respond to | stimuli from the environment, thereby facilitating vigilance. So in both roles, norepinephrine mediates arousal. |
Glutamate, is GABA's excitatory | counterpart, in that Glutamate is the primary excitatory neurotransmitter in the central nervous system- Important role in learning and memory. |
GABA (gamma-aminobutyric acid) is the primary | inhibitory neurotransmitter in the central nervous system. |
Lack of GABA may contribute to | epilepsy, a brain disorder resulting in uncontrolled movement and convulsions |
Anti-anxiety drugs are agonists for | GABA |
Four histamine receptors have been identified, all of which are | G protein-coupled receptors. |
Histamine effects | Wakefulness, cognitive ability and food consumption.***Antihistamines may then cause sleepiness, and cognitive impairment or dulling |
Glutamate is r/t | GABA- synthesized before GABA- for learning and memory |
Gaba is derived from | glutamate gaba is used for neuropathy |
H3 | central system effect- for children we give Vistaril |
Inverse agonist | Drugs that bind to different area of the receptor and works to fully antagonize function- ie: parkinson’s med |
Ventral tegmental area | where dopamine originates- our friend |
Locus coeruleus | where norepinephrine originate |
Raphe nuclei | where serotonin originates |