The prediction of somatic complaints using the Autonomic Nervous System Response Inventory (ANSRI) and the Daily Stress Inventory (DSI).

Understanding and prediction of veridical somatic complaints not caused by disease, dysfunction, trauma, or toxin, requires the assessment of at least two critical variables: predisposition to respond to stressors with peripheral physiological activation; and intensity/frequency/duration of stressors. The Autonomic Nervous System Response Inventory (ANSRI) and the Daily Stress Inventory (DSI) were used to assess these variables, and somatic complaints were recorded using the Wahler Physical Symptoms Inventory (WPSI). Subjects were 72 healthy undergraduates who completed the inventories and reported illness and medication usage over a 2 week period. Regression analyses showed that ANSRI, DSI, illness, and medication accounted for 35% of the variance in somatic complaints, though only ANSRI and DSI contributed significantly. Neuroticism (Eysenck Personality Questionnaire) did not add to R2, but did influence stressors' subjective impact. The correlation between regression equation-generated WPSI scores (derivation sample) and actual WPSI scores (holdout sample) was 0.59. A discriminant function analysis equation (derivation sample) applied to the holdout sample correctly classified 80% of the upper and lower third WPSI subjects. It was concluded that the ANSRI and DSI, and the variables they assess, are substantially related to the self-report of somatic complaints.

Further studies of the role of opioid receptors in the nigra in the morphine withdrawal syndrome.

Bilateral injection of naloxone (3.0-30.0 nmol) into the substantia nigra of morphine-dependent rats produced a withdrawal syndrome consisting of wet-dog shakes, teeth chattering, irritability to touch, diarrhea and hypothermia. Intense wet-dog shakes and grooming were observed after intranigral injection of the mu selective antagonist D-Phe-Cys-Try-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP, 3.0-30.0 nmol) in morphine-dependent animals. Body temperature after 30.0 nmol CTOP was significantly increased. A significant positive correlation between body temperature and wet-dog shakes was observed in morphine-dependent animals that received CTOP. Intranigral injection of beta-funaltrexamine (beta-FNA, 10.0 nmol), an irreversible mu antagonist, produced no signs of withdrawal in morphine-dependent animals. However, intranigral injection of beta-FNA (1.0-3.0 nmol) suppressed the antinociceptive effect of the mu-selective agonist, D-Ala2,N-Me-Phe4,Gly5-ol-enkephalin (DAGO, 1.0 nmol). The withdrawal syndrome produced by CTOP (10.0 nmol) was not suppressed by the administration of U50,488H (10.0 nmol), a kappa agonist, suggesting that the absence of an effect of beta-FNA was not due to its kappa agonist activity. Neither the delta-selective antagonist, naltrindole (NTI, 10.0 nmol) nor the kappa-selective antagonist, nor-binaltorphimine (nor-BNI, 10.0 nmol) produced withdrawal. Only wet-dog shakes were observed when CTOP, NTI and nor-BNI (5 nmol each) were administered together into the nigra. These studies suggest an involvement of mu receptors in the nigra in the wet-dog shakes and thermoregulatory dysfunction that occur during withdrawal of morphine. However, the subtypes of opioid receptors in the nigra, that mediate the other signs of morphine withdrawal remain obscure.