The validity of dopamine transfer deficit theory in ADHD SHR model. Essay

The validity of dopamine transfer deficit theory in ADHD SHR model. Essay

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The validity of dopamine transfer deficit theory in ADHD SHR model.
Introduction and Background
Attention deficit hyperactivity disorder (ADHD) is a disorder in which there is a persistent and developmentally abnormal level of overactivity, inattention and impulsivity. The physical cause or pathophysiology of this disease is currently unknown as the diagnosis is strictly based on relative or excessive increase in the symptoms such as overactivity, inattention or impulsivity which may otherwise also exist in normal individuals. The clinical symptoms considered for the detection of impulsivity in ADHD are often subjective or vague like ‘often blurts out answers before question have been completed’, ‘often has a difficulty awaiting turns’ and ‘often interrupts on others’ etc which is quite different from the basic science definition of impulsivity such as ‘an abnormally high preference of small, intermediate rewards over large delayed reward’ in a delay discounting task, ‘response during inter trial interval prior to the presentation of a cue associated with reward’ in a reaction time tasks. Till date no clear single gene has been successfully implicated exclusively in the aetiology of ADHD. However, significant associations of 4 different genes, D4 and D5 receptors and dopamine and serotonin transporters have been reported in several studies to play critical role in the aetiology. The list however is ever growing with some inclusions of inconclusive roles of DBH, HTR1B and SNAP-25 genes.
Developing animal models per se has not been easy for ADHD because of no clearly established pathological and etiological features and reliance upon heterogenous groups of symptoms found in variety of ADHD patients. This explains the existence of v...

... middle of paper ... clinical drug development in ADHD: lost in translation? British journal of pharmacology 164, 1107-1128.
Wickens, J.R., Macfarlane, J., Booker, C., and McNaughton, N. (2004). Dissociation of hypertension and fixed interval responding in two separate strains of genetically hypertensive rat. Behavioural brain research 152, 393-401.
Wickens, J.R., Tripp, G., and Gerhardt, G.A. (2007). Neurobiology of attention-deficit hyperactivity disorder (ADHD): from gene to therapy. Journal of neuroscience methods 166, 293.
Williams, J. (2008). Working toward a neurobiological account of ADHD: commentary on Gail Tripp and Jeff Wickens, dopamine transfer deficit. Journal of child psychology and psychiatry, and allied disciplines 49, 705-711; discussion 711.

Report Submitted by
Baburam Bhattarai
ID: 20138177
2nd semester, MS/PhD student, Department of Biological Sciences, KAIST

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