Patho of ADHD and Pharmocology of Stimulants - Li

Key areas for neural circuits attention

PFC, parietal cortex, thalamus, and brainstem

Pathophys of ADHD

Majorly genetic, male more than female, dopamine transporter affected

What neurotransmitter is affected in ADHD

dopamine transporter

What part of the brain may be functioning correctly in adhd?

Medial prefrontal cortex

MOA of methylxanthines - like coffee!

Antagonizes adenosine receptors, inhibits phosphodiesterase, increases activity of ryanodine receptors

What do the presynaptic A1 receptors do

decrease Ca influx which inhibits endocytosis which inhibits the release of glutamate and dopamine

What do the postsynaptic A1 receptors do

Open K+ channels which inhibits through hyperpolarization

Primary effect of A2A

excitatory

What do presynaptic A2A do?

Increase neurotransmitter release

What do the postsynaptic A2A receptors do

increase excitablity

Pharmacology of Methylxanthines

Increase alertness, decreased fatigue

What does the brain reward pathway do when taking stimulants?

release dopamine

What transmitters do stimulants inhibit?

DA, NE, serotonin

How is dopamine released when it comes to stimulants?

PFC sends projections to VTA which releases dopamine. It also receives feedback from NAc

MOA of amphetamines

Acts on DAT, NET, and VMAT2 which increases the release of neurotransmitters and increases hyperexcitability

What amphetamine is the exception when it comes to the targets of neurotransmitters and what is it more selective for?

MDMA is more selective for 5-HT

Non stimulants for ADHD

Atomoxetine: NET inhibitor, TCAs, Buproprion, Clonidine/Guanfacine, and modafinil which is approved for narcolepsy not ADHD