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Scott A Oakman

Publications and source records attributed to Scott A Oakman.

2 recordsLinked to original sources

Calcyon transcript expression in macaque brain.

The anatomical distribution of the transcript encoding calcyon, a 24 kDa membrane protein associated with coupling D1-like dopamine receptor activation to potentiated intracellular calcium release, was examined using in situ hybridization in the macaque brain. Calcyon mRNA is found to be abundantly distributed throughout the primate brain. In neocortex, moderately dense, diffuse signal is found in all areas, with increased intensity present in a superficial isodense band corresponding generally to cortical layers II and III. Increased intensity of signal is also seen in the pyramidal cell layers of medial prefrontal and anterior cingulate cortex. Calcyon mRNA is present abundantly in subcortical limbic areas such as the nucleus accumbens, septum, hypothalamus, amygdala, and hippocampus. Moderate calcyon transcript expression is seen in caudate and putamen, with lower levels in globus pallidus. Thalamic nuclei, including the reticular nucleus, express low to moderate levels. Very dense expression is noted in the substantia nigra pars compacta. Numerous brainstem regions express this transcript, notably monoaminergic nuclei including the locus coeruleus and dorsal raphe. The cerebellum has detectable levels of expression in both cortex and deep nuclei. Although calcyon is hypothesized as a means for D1-like receptors to modulate "cross-talk" with other neurotransmitter receptor systems, it is notable that abundant calcyon transcript is detected in brain regions not associated with D1-like neurotransmission, particularly the substantia nigra pars compacta and other dopamine-synthesizing cell groups. A substantial proportion of this may relate to the reported association of calcyon with the D5 receptor, or in addition, may suggest that calcyon has a wider role as a regulator of intracellular signal transduction.

Animals↗

Effect of ondansetron, a 5-HT3 receptor antagonist, on the dynamic association between bulimic behaviors and pain thresholds.

Thresholds for detection of both pressure and thermal pain are elevated in patients with bulimia nervosa. The present study was aimed at determining (1) if pressure pain detection thresholds (PDT) varied dynamically with the primary disease symptoms of binge eating and vomiting and (2) if the elevation in PDT was effected by treatment with ondansetron (ONDAN), a 5-HT3 receptor antagonist. PDT was defined as the mean of the minimal amount of pressure (measured in g) perceived as painful when exerted by a 1 mm2 blunted point onto the center of the ventral surface of the ungual phalanx of digits 2-5 of the non-dominant hand. Fourteen female patients with severe bulimia nervosa (currently >seven binge/vomit episodes per week; > 2 years illness duration) served as participants. PDT were evaluated at weekly intervals during the course of ongoing treatment studies (double-blind and 'open' label) investigating the therapeutic effects of ONDAN. Data were analyzed by random regression analyses, allowing for the repeated-measures and non-orthogonal design. Data collected from 14 patients under the no-drug condition indicated that PDT increased over the interval between binge/vomit episodes, with significant elevations occurring at times when patients had naturally exceeded their average inter-binge interval. Eleven of these 14 patients underwent 4 weeks of ONDAN treatment. Under this drug condition, the time since the last binge/vomit episode was no longer a significant predictor of PDT. These patients also experienced a significant reduction in the frequency of bulimic behaviors, a finding reported in detail elsewhere. The above finding from untreated patients support the involvement of a common underlying mechanism driving both the increase in pain detection thresholds and the occurrence of the next bulimic episode. This possibility is further supported by the findings that ONDAN treatment is associated with a significant moderation of both variables. The effect of ONDAN may be mediated by blockade of afferent vagal neurotransmission, although other mechanisms must be considered.

Adult↗