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)