http://www.nature.com/cgi-taf/DynaPage.taf?file=/npp/journal/v29/n9/abs/1300469a.html

Neuropsychopharmacology (2004) 29, 1589-1596, advance online publication, 28 April 2004;
doi:10.1038/sj.npp.1300469

Synaptic Gating and ADHD: A Biological Theory of Comorbidity of ADHD and Anxiety

Florence Levy

School of Psychiatry, University of New South Wales, Prince of Wales Hospital, Randwick, Australia

Correspondence: F Levy, School of Psychiatry, University of New South Wales, Prince of Wales Hospital, Randwick NSW 2031, Australia. Tel: +61 2 93828213; Fax: +61 2 93828105; E-mail: f.levy@unsw.edu.au

Received: 13 January 2004
Revised: 18 March 2004
Accepted: 23 March 2004

ABSTRACT

To derive a biologically based theory of comorbidity in Attention Deficit Hyperactivity Disorder (ADHD). Theoretical concepts and empirical studies were reviewed to determine whether the behavioral inhibition concept provided an understanding of biological processes involved in comorbidity in ADHD. Empirical studies of ADHD have shown comorbidity of ADHD and anxiety, while studies of behavioral inhibition tend to suggest independent disruptive and anxiety traits. This paradox can be resolved by an understanding of the dynamics of mesolimbic dopamine (DA) systems, where reward and delay of reinforcement are determined by tonic/phasic DA relationships, resulting in impulsive 'fearless' responses when impaired. On the other hand, comorbid anxiety is related to impaired synaptic processes, which selectively gate fear (or aggressive) responses from the amygdala at the accumbens. Monosynaptic convergence between prefrontal, hippocampal, and amygdala projection neurons at the accumbens allows the operation of a synaptic gating mechanism between prefrontal cortex (PFC), hippocampus, and amygdala. Impairment of this mechanism by lowered PFC inhibition allows greater amygdala input, and anxiety-related processes more impact, over the accumbens. In conclusion, a dual theory incorporating long-term tonic/phasic mesolimbic DA relationships and secondly impairment of PFC and hippocampal inputs to synaptic gating of anxiety at the accumbens has implications for comorbidity in ADHD, as well as for possible pharmacological interventions, utilizing either stimulant or axiolytic interventions. The use of DA partial agonists may also be of interest.

Ok....

I may sound dumb but.....

Can someone translate this????? Maybe into Laymans terms. :p

-Anty

I'll try.....

"To derive a biologically based theory of comorbidity in Attention Deficit Hyperactivity Disorder (ADHD)." - To find a biological explaination as to why anxiety and ADHD are so often found together.

"Theoretical concepts and empirical studies were reviewed to determine whether the behavioral inhibition concept provided an understanding of biological processes involved in comorbidity in ADHD." - We looked though everything everyone else has published to see if any of their ideas on the "behavioral inhibition" theory of ADHD could explain what we hope to discover

"Empirical studies of ADHD have shown comorbidity of ADHD and anxiety, while studies of behavioral inhibition tend to suggest independent disruptive and anxiety traits." - Statistics show that ADHD and anxiety are often found together, but studies on behaviour inhibition indicate that anxiety isn't directly related to problems controling behaviour or paying attention.


"This paradox can be resolved by an understanding of the dynamics of mesolimbic dopamine (DA) systems, where reward and delay of reinforcement are determined by tonic/phasic DA relationships, resulting in impulsive 'fearless' responses when impaired." - We think this seeming "independance" is due to the cyclic nature of the "mesolimbic dopamine systems" (whatever specifically THAT is - dopamine is a neurotransmitter thought to have a great deal to do with ADHD) and that if it doesn't work right the person behaves in a impulsive fearless way - i.e. Dangerous!


"On the other hand, comorbid anxiety is related to impaired synaptic processes, which selectively gate fear (or aggressive) responses from the amygdala at the accumbens." - Anxiety is due to a different problem - the theory being that nerve cells that aren't working correctly allow only fearful or agressive signals get through from the amygdala (an area of the brain).


"Monosynaptic convergence between prefrontal, hippocampal, and amygdala projection neurons at the accumbens allows the operation of a synaptic gating mechanism between prefrontal cortex (PFC), hippocampus, and amygdala. Impairment of this mechanism by lowered PFC inhibition allows greater amygdala input, and anxiety-related processes more impact, over the accumbens." - This is over my head, but I think it means that if you have both systems not working correctly, bouncing signals from one part of the brain to another, you end result is ADHD and anxiety.

"In conclusion, a dual theory incorporating long-term tonic/phasic mesolimbic DA relationships and secondly impairment of PFC and hippocampal inputs to synaptic gating of anxiety at the accumbens has implications for comorbidity in ADHD, as well as for possible pharmacological interventions, utilizing either stimulant or axiolytic interventions. The use of DA partial agonists may also be of interest." - Our theory of a biological process behind the combination of ADHD and anxiety seems to work on paper and explains why we see ADHD and anxiety togther so often - this may be of help in developing drugs.

Was that any better?

Wow....Thanks Greg!!

You rock! :)

-Anty