Past studies have examined P3 amplitude as an index of cognitive function related to psychopathy with mixed results. Psychopathy is a heterogeneous set of dissociable traits, and no previous study has examined relationships between P3 and specific traits. A Two Process Theory (TPT) of psychopathy has recently been advanced predicting that P3 reductions are related to only one dimension. We evaluated the relationship between P3 and the two factors of the Psychopathic Personality Inventory (PPI) in 96 undergraduates who performed a visual task. One factor of the PPI, Self-Centered Impulsivity, is related to the dimension of the TPT predicted to underlie P3 reduction. Frontal amplitude reduction was uniquely and inversely related to this trait. The other PPI factor, Fearless Dominance, was associated with faster reaction times. Future work on psychopathic personality and P3 should evaluate whether relationships are unique to one personality dimension.
P300 amplitude predicts substance use or disorder by age 21. Earlier- versus later-onset substance disorders may reflect different levels of an externalizing psychopathology dimension. P300 in adolescence may not be as strongly related to later-onset substance problems as it is to earlier-onset ones. In the present study, visual P300 amplitude was measured at age 17 in a community-representative sample of young men. Substance and externalizing disorders were assessed at approximately ages 17, 20, and 24. Earlier-onset (by age 20) substance disorder was associated with higher rates of externalizing disorders than were later-onset problems. P300 amplitude was reduced in subjects with earlier-onset substance disorders, relative to later-onset and disorder-free subjects. Amplitude was also reduced in subjects with an externalizing disorder but no substance disorder. Earlier-onset subjects had reduced P300, even in the absence of an externalizing disorder. The results could not be attributed to a concurrent disorder or to recent substance use at the time of the P300 recording. The findings are consistent with P300 indexing an externalizing spectrum. Earlier-onset substance disorders are more strongly related to P300 and externalizing than are later-onset problems.
A variety of forms of drug misuse and diversion occurred among this population of adults who were prescribed anxiolytics or sedatives. Likelihood of engaging in misuse or diversion was associated with other substance use, substance use disorders, and personality characteristics. Despite the modest sample size and cross-sectional design, this study identified substantial heterogeneity in prescription anxiolytic and sedative misuse, suggesting that the use of clearly defined operational criteria will be essential in future efforts to further characterize this phenomenon.
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Superficial sarcoplasmic reticulum (SR) regulates smooth muscle force development directly by Ca(2+) release and removal to and from the cytoplasm (Somlyo and Somlyo. J Cardiovasc Pharmacol 8, Suppl 8: S42-S47, 1986) by buffering Ca(2+) influx and contributing to Ca(2+) extrusion (Mueller and van Breemen. Nature 281: 682-683, 1979) and indirectly by releasing Ca(2+) near Ca(2+)-activated K(+) channels (K(Ca)) to hyperpolarize the plasma membrane (Bolton and Imaizumi. Cell Calcium 20: 141-152, 1996 and Nelson et al. Science 270: 633-637, 1995). In the rabbit basilar artery, relative contributions of direct effects and those mediated through activation of K(Ca) were evaluated by measuring force and intracellular Ca(2+) concentration ([Ca(2+)](i)) in response to the SR-depleting agents thapsigargin and ryanodine and the large conductance K(Ca) (BK(Ca)) blockers iberiotoxin (IbTX) and tetraethylammonium ion (TEA). A large contraction was observed in response to K(Ca) blockade with either 3 mM TEA or 100 nM IbTX and also after addition of 10 microM ryanodine or 2 microM thapsigargin. When K(Ca) was blocked first with TEA or IbTX, subsequent addition of thapsigargin or ryanodine also increased force. Measurements of fura 2 fluorescence showed parallel increases in [Ca(2+)](i) in response to sequential blockade of sarco(endo)plasmic reticulum Ca(2+)-ATPase and K(Ca) regardless of the order of application. It appears that a significant fraction of K(Ca) remains activated in the absence of SR function and that SR contributes to relaxation after blockade of K(Ca). We found that depletion of SR before stimulating Ca(2+) influx through voltage-gated Ca(2+) channels markedly reduced force development rate and that thapsigargin abolished this effect. We conclude that the SR of rabbit cerebral arteries modulates constriction by direct and indirect mechanisms.
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