Neuropsychological and behavioural disinhibition in adult ADHD compared to borderline personality disorder.

BACKGROUND: Although attention-deficit/hyperactivity disorder (ADHD) is thought to be an inhibitory disorder, the question remains of how specific the inhibitory deficit is in adults and whether it distinguishes ADHD from borderline personality disorder (BPD), with which it shares several clinical features, particularly impulsiveness. METHOD: The study assessed various motor and cognitive inhibitory functions (inhibition of prepotent, ongoing and interfering responses) in addition to working memory in adult ADHD patients with and without BPD, compared to subjects with BPD alone and controls. In addition, questionnaire data on various aspects of impulsiveness and anger regulation were assessed in all groups. RESULTS: ADHD patients performed worse than BPD individuals and controls in two inhibitory tasks: the stop signal task and the conflict module of the Attentional Network Task (ANT). In addition, they exhibited longer reaction times (RTs) and higher intra-individual variance in nearly all attentional tasks. The co-morbid group exhibited poor performance on the stop signal task but not on the conflict task. The BPD group barely differed from controls in neuropsychological performance but overlapped with ADHD in some behavioural problems, although they were less severe on the whole. CONCLUSIONS: Impaired inhibition is a core feature in adults with ADHD. In addition, slow RTs and high intra-individual variance in performance may reflect deficits in the regulation of activation and effort in ADHD patients. ADHD and BPD share some symptoms of behavioural dysregulation without common cognitive deficits, at least in the attentional realm.

Dopaminergic modulation of short-term synaptic plasticity in fast-spiking interneurons of primate dorsolateral prefrontal cortex.

Dopaminergic regulation of primate dorsolateral prefrontal cortex (PFC) activity is essential for cognitive functions such as working memory. However, the cellular mechanisms of dopamine neuromodulation in PFC are not well understood. We have studied the effects of dopamine receptor activation during persistent stimulation of excitatory inputs onto fast-spiking GABAergic interneurons in monkey PFC. Stimulation at 20 Hz induced short-term excitatory postsynaptic potential (EPSP) depression. The D1 receptor agonist SKF81297 (5 microM) significantly reduced the amplitude of the first EPSP but not of subsequent responses in EPSP trains, which still displayed significant depression. Dopamine (DA; 10 microM) effects were similar to those of SKF81297 and were abolished by the D1 antagonist SCH23390 (5 microM), indicating a D1 receptor-mediated effect. DA did not alter miniature excitatory postsynaptic currents, suggesting that its effects were activity dependent and presynaptic action potential dependent. In contrast to previous findings in pyramidal neurons, in fast-spiking cells, contribution of N-methyl-D-aspartate receptors to EPSPs at subthreshold potentials was not significant and fast-spiking cell depolarization decreased EPSP duration. In addition, DA had no significant effects on temporal summation. The selective decrease in the amplitude of the first EPSP in trains delivered every 10 s suggests that in fast-spiking neurons, DA reduces the amplitude of EPSPs evoked at low frequency but not of EPSPs evoked by repetitive stimulation. DA may therefore improve detection of EPSP bursts above background synaptic activity. EPSP bursts displaying short-term depression may transmit spike-timing-dependent temporal codes contained in presynaptic spike trains. Thus DA neuromodulation may increase the signal-to-noise ratio at fast-spiking cell inputs.