1. ADHD Attention deficit hyperactivity disorder
4.1% American adults age 18 years and older in a given year.
9.0% of American children age 13 to 18 years.
Males are 4 times at risk than females

2. Drug Treatments Stimulant based
methylphenidate (Concerta, Metadate, Ritalin, others)
dextroamphetamine (Dexedrine)
dextroamphetamine-amphetamine (Adderall XR)
lisdexamfetamine (Vyvanse)
Non-stimulant
atomoxetine (Strattera)
bupropion (Wellbutrin, others)
desipramine (Norpramin).
clonidine (Catapres)
guanfacine (Intuniv, Tenex) 

3. Non-stimulant ADHD drugs do not have the same side effects as stimulant drugs because
They are given at lower doses
They act on a different pathway
They have the same side effects but side effects are not detectable
They have not been studied as long
Non-stimulant ADHD drugs do not have the same side effects as stimulant drugs because
They are given at lower doses
They act on a different pathway
They have the same side effects but side effects are not detectable
They have not been studied as long

4. Impulse control brain regions in ADHD frontal cortex basal ganglia
thalamus
Team Workshop 1. Go to and display the 3 brain regions. Link on course website

5. Stop-signal reaction time task (SSRTT)
Sound to single stop going to the light and return to get reward. BL is baseline

6. Loss of STS or inhibition improves impulse response
39, Xy+0
40, XY
Loss of STS or inhibition improves impulse response
COUMATE
DHEAS
intraperitoneal injection and per os (oral)

7. Why were 40, XY MIF mice used as the control for the SSRTT?
C57BL/6 mice were not available
C57BL/6 mice cant be used to perform SSRTT
To ensure that the mice had 40 chromosomes
The have the same genetic background as the 39, Xy+0 mice.
They have a mutant STS gene
Why were 40, XY MIF mice used as the control for the SSRTT?
C57BL/6 mice were not available
C57BL/6 mice cant be used to perform SSRTT
To ensure that the mice had 40 chromosomes
The have a similar genetic background as the 39, Xy+0 mice.
They have a mutant STS gene
39, Xy*0 mice have X and Y endjoined that deltes the STS gene. Wildtype 40,XY MF1 mice (Harlan, UK, aged 3–4 months
at start of testing) were used in initial work validating the
SSRTT; this was necessary as our previous work used
C57BL/6 strain mice (Humby et al, 2013). This group of
mice were also used for the drug studies. For the genetic
study, 39,XY*O and 40,XY mice on a predominantly MF1 is outbred.

8. Workshop 2: Discuss the reaction steroid sulfatase (STS) catalyzes and how this might be important in ADHD?
Testoterone (L) and Estradiol (right)

9. Workshop 3: Provide a molecular explanation of why coumate is an inhibitor of STS?

10. Workshop 4: Discuss the following aspects of mouse models and neurological disease.
Why are they useful?
Why are they problematic?

11. Remember Before 12 PM of the next class day:
go to b.socrative.com/student/login and complete the quiz