This finding is consistent with previous reports of deficits in the phase advances of mice lacking PACAP signaling [2], [3], [4].
There is also scope for over reporting of deficits to make the case for future additional resourcing of HPSR + A units.
Another observation that supports this hypothesis is that several reports of deficits in glia in the cerebral cortex depended upon laminar analysis, with the greatest effects in layers III, V, and VI (Cotter et al. 2001a, 2002; Rajkowska et al. 1999, 2001; Uranova et al. 2004; Vostrikov et al. 2007).
A study by Johnson et al. tested children with HFA and ADHD on a Sustained Attention to Response Task (SART) and report of clear deficits in response inhibition and sustained attention in the ADHD group.
For attentional disengagement, the best-known prior report of a deficit in ASD (Landry & Bryson, 2004) found an attentional disengagement cost of about 2 s.
Data from the literature report the existence of deficits in the three facets of impulsivity in ADHD subjects [ 27].
Similarly EEG Event-related potential (ERP) studies report a myriad of deficits during attentional tasks during polar mood states, such as reduced P300 amplitude and latency [ 10, 11].
Given previous reports of learning deficits after DA depletion in striatum [32], it seems unexpected that raclopride injected into striatum had no effect on learning.
There are several reports of neural deficits in CDGIIc patients, including severe mental retardation, microcephaly, cortical atrophy, seizures, psychomotor retardation and hypotonia [2], [4], [51].
A limitation of these studies is their reliance on self-report of cognitive deficits rather than objective examination.
