Key Neurotransmitters
Monoamines
Dopamine
Acetylcholine
Amino Acids
GABA
Norepinephrine
Catecholamines
Glutamate
Drives reward, motivation, motor functions
Think:
Drive
psychOsis
Parkinsonism
Attention
Motor
Inhibition (prolactin)
Narcotics
Extrapyramidal
Mesolimbic pathway (reward/motivation)
Too little: depression, negative symptoms of schizophrenia, thought to be involved in ADHD symptoms (executive function)
Too much: psychosis symptoms, symptoms of drug intoxication
Nigrostriatal pathway (stop/go or motor)
Too Little
Involved in Arousal, attention, anxiety
Located in Locus Ceruleus (Cerebrus --> Ceruleus)
Fight or flight reaction (autonomic reactivity including sweating, chills, nausea, palpitations, dyspnea)
Serotonin
Low
Too much: anxiety
Too Little: Anxiety
Too much
Low activity of post-synaptic receptors
Anxiety
Treatment
Benzodiazepines (second line) enhance inhibitory effects of GABA
TCAs
depletion of serotonin
Depression (unipolar and bipolar)
too little: depression, ADHD
Alterations
Too little release
ADHD
Decreased activity: Alzheimer's disease, dementia
Found in Motor Neurons
Involved in ANS at both parasympathetic and sympathetic systems
ACh-EI (ACh enzyme inhibitors) i.e. Aricept
Stimulants (methylphenidates, amphetamine preparations)
Nonstimulants: norepinephrine uptake inhibitor
Alpha agonists (Guanfacine, clonidine)
Works on post-synaptic Alpha 2 (inhibitory norepinephrine) receptors in prefrontal cortex, thus enhancing norepinephrine action
blocks norepinephrine reuptake pumps, which increases norepinephrine transmission. Also allows additional dopamine transmission due to the action of norepinephrine pumps in degradation of dopamine in the frontal cortex
increases norepinephrine and dopamine in the frontal cortex by blocking reuptake
Amphetamine preparations also facilitate release of dopamine and norepinephrine and therefore may contribute to side-effects of stimulants
Methylphenidates do not facilitate additional release of dopamine and norepinephrine and work only at the reuptake sites
Too much
Key excitatory neurotransmitter, known as the "master switch" due to ability to turn "on" other neurotransmitters
Hypofunction of NMDA substrate in the frontal cortex thought to play a role in Alzheimers, Schizophrenia
Think: Autonomic, Contraction, Hippocamus
Autonomic: parasympathetic (bradycardia, GI motility)
Contraction (muscle, motor)
Hippocampus (Learning, memory, alert/wake, attention)
Found in brain, brainstem
Pineal gland, Pons
Important to limbic system (emotion, mood, hunger, sex, instincts, sleep)
Think: Head, Red Fed (Dead)
Head: satisfaction, sociality, migraines, anxiety, impulsivity, sex drive
Red: Platelets, bleeding
Fed: GI motility, nausea / Dead: (serotonin syndrome) 2-12% mortality
Final product of Sympathetic neurons of ANS
A1, B1: excitatory receptors
A2, B2: Inhibitory receoptors
Inhibitory actions at Gaba A (Calcium channel) and Gaba B (cAMP decrease and increased activity at Potassium channels)
Universal Inhibitor (think opposite of Glutamate)
Abuse/Addiction behaviors
General Receptor concepts
Full agonist: Mimics the neurotransmitter
Partial Agonist: weakly mimics the neurotransitter
Neutral antagonist: opposes the neurotransmitter
Inverse antagonist: inverse effect
SNRIs
Too Much: Huntington's symptoms, Tics (Tourettes), Tardive dyskinesia
Parkinsons
Schizophrenia
Antipsychotics
SSRIs
increases serotogenergic and noradgrenergic transmission.
May increase dopamine dopamine neurotransmission
Regulates amount of norepinephrine (down) and serotonin (up)
boosts noradrenergic neurotransmission, including dopamine, higher doses may boost serotonergic transmission
increases serotogenergic transmission
inhibits AChE making more ACh available, compensating in part for the symptoms of dementia in memory
Schizophrenia
Lamotrigine is an example of medication that works on glutamate; blocks voltage-sensitive sensitive sodium channels, which inhibits glutamate. Off-lable use as adjunct for psychosis and schizophrenia
increase circulating serotonin by blocking reuptake
High
Serotonin syndrome
agitation/restlessness, insomnia, confusion, loss of muscle coordination, diarrhea, HA, seizure
Mania in Bipolar disorder
Tics (Tourettes)
Generates somnolence/decreased alertness, decreases anxiety and muscle tension, decreases memory
Aripiprazole: partial Dopamine agonist, thought to decrease dopamine concentrations when high, and increase when concentrations are low
Dopamine antagonist, reducing positive symptoms of schizophrenia. some antagonist action at serotonin receptors thought to improve negative symptoms
Dopamine Agonists: pramipexole, rotigotine work to mimic action of dopamine
Carbidopa-levidopa: converted to dopamine by striatal enzymes in the brain (levidopa) and prevents degradation of degradation of dopamine/levidopa (carbidopa)