This study investigates the role of extrinsic and intrinsic predictors in the perception of affect in mostly unfamiliar musical chords from the Bohlen-Pierce microtonal tuning system. Extrinsic predictors are derived, in part, from long-term statistical regularities in music; for example, the prevalence of a chord in a corpus of music that is relevant to a participant. Conversely, intrinsic predictors make no use of long-term statistical regularities in music; for example, psychoacoustic features inherent in the music, such as roughness. Two types of affect were measured for each chord: pleasantness/unpleasantness and happiness/sadness. We modelled the data with a number of novel and well-established intrinsic predictors, namely roughness , harmonicity , spectral entropy and average pitch height ; and a single extrinsic predictor, 12-TET Dissimilarity , which was estimated by the chord’s smallest distance to any 12-tone equally tempered chord. Musical sophistication was modelled as a potential moderator of the above predictors. Two experiments were conducted, each using slightly different tunings of the Bohlen-Pierce musical system: a just intonation version and an equal-tempered version. It was found that, across both tunings and across both affective responses, all the tested intrinsic features and 12-TET Dissimilarity have consistent influences in the expected direction. These results contrast with much current music perception research, which tends to assume the dominance of extrinsic over intrinsic predictors. This study highlights the importance of both intrinsic characteristics of the acoustic signal itself, as well as extrinsic factors, such as 12-TET Dissimilarity, on perception of affect in music.

This study has confirmed that interruptions are frequent and result in clinical errors and procedural failures, compromising patient safety. These interruptions contribute a substantial additional workload to medication tasks. Various interventions should be implemented to reduce non-patient-related interruptions. Medication systems and procedures are advocated, that reduce the need for joint double-checking of medications, indirectly avoiding interruptions.

Four experiments studied the role of opioid receptors in the midbrain periaqueductal gray matter (PAG), an important structure eliciting conditioned fear responses, in the extinction of Pavlovian fear. Rats received pairings of an auditory conditioned stimulus (CS) with a foot shock unconditioned stimulus (US). The freezing conditioned response (CR) elicited by the CS was then extinguished via nonreinforced presentations of the CS. Microinjection of the opioid receptor antagonist naloxone into the ventrolateral PAG (vlPAG) before nonreinforced CS presentations impaired development of extinction, but such microinjections at the end of extinction did not reinstate an already extinguished freezing CR. This role for opioid receptors in fear extinction was specific to the vlPAG because infusions of naloxone into the dorsal PAG did not impair fear extinction. Finally, the impairment of fear extinction produced by vlPAG infusions of naloxone was dose-dependent. These results show for the first time that the midbrain PAG contributes to fear extinction and specifically identify a role for vlPAG opioid receptors in the acquisition but not the expression of such extinction. Taken together with our previous findings, we suggest that, during fear conditioning, activation of vlPAG opioid receptors contributes to detection of the discrepancy between the actual and expected outcome of the conditioning trial. vlPAG opioid receptors regulate the learning that accrues to the CS and other stimuli present on a trial because they instantiate an associative error correction process influencing US information reaching the site of CS-US convergence in the amygdala. During nonreinforcement, this vlPAG opioid receptor contribution signals extinction.

Injection of the opioid receptor antagonist naloxone facilitated acquisition of fear to contextual and auditory conditioned stimuli (CSs) in Experiments 1A and 1B. Experiment 2 showed that prior conditioning to a distinctive context blocked conditioning to an auditory CS. Blocking of CS fear was prevented by administrations of naloxone or increases in footshock intensity. Blocking of CS fear was facilitated by decreases in footshock intensity in a naloxone-reversible manner. Experiment 3 showed that compound conditioning of two CSs, each previously and separately paired with shock, produced overexpectation of fear that was reversed by naloxone. These results are consistent with a role for opioid receptors controlling Pavlovian association formation by regulating the discrepancy ( Ϫ ⌺V) described by R. A. Rescorla and A. R. Wagner (1972).

A laboratory model was developed to study human avoidance learning. Participants could avoid an electric shock signalled by a 5-s conditioned stimulus (CS) by pressing one of a set of response buttons. Self-reported shock expectancy and skin conductance were recorded during a subsequent 10-s interval before shock. Shock expectancy declined when the correct avoidance response was learned and returned when the response was unavailable. Learning transferred to another shock CS. Parallel effects were observed on skin conductance once performance anxiety was controlled by requiring responding on all trials. Learning was faster when the Pavlovian contingencies were trained before introduction of the instrumental response. The results support a cognitive model of anxiety in which performance of an avoidance response reduces expectancy of an aversive outcome and thereby reduces anxiety.

The likelihood, size, and speed of eyelid movements are thought to covary during the acquisition and expression of conditioning in rabbits (Oryctolagus cuniculus) and are generally accepted as interchangeable measures of the associative strength activated by the conditioned stimulus (CS). To test this assumption, the authors examined the patterns of covariation in these eyelid movement measures in acquisition and stimulus generalization in the upper eyelid and nictitating membrane. Rather than the expected covariation among these measures, eyelid movement magnitudes during the CS were distributed in approximately a bimodal manner. That is, eyelid activity consisted largely of a mixture of very small (< 0.125 mm) baseline measurements and larger (> 1 mm) movements. The results are discussed with respect to their implications for real-time models of eyelid conditioning.

Neal, Charles R., Jr., Gabrielle Weidemann, Mohamed Kabbaj, and Delia M. Vázquez. Effect of neonatal dexamethasone exposure on growth and neurological development in the adult rat. Am J Physiol Regul Integr Comp Physiol 287: R375-R385, 2004. First published April 29, 2004; 10.1152/ajpregu.00012.2004.-Until recently, the synthetic glucocorticoid dexamethasone was commonly used to lessen the morbidity of chronic lung disease in premature infants. This practice diminished as dexamethasone use was linked to an increased incidence of cerebral palsy and short-term neurodevelopmental delay. Of more concern is the fact that we know little regarding dexamethasone effects on long-term neurodevelopment. To study the effects of neonatal dexamethasone exposure on long-term neurodevelopment, we have developed a rat model where newborn pups are exposed to tapering doses of dexamethasone at time points corresponding to the neurodevelopmental age when human infants are traditionally exposed to this drug in the neonatal intensive care unit. Using a within-litter design, pups were assigned to one of three groups on postnatal day 2 (P2): handled controls, saline-injected controls, and animals receiving intramuscular dexamethasone between P3 and P6. Somatic growth was decreased in dexamethasone-treated animals. Dexamethasone-treated animals demonstrated slight delays in indexes of neurodevelopment and physical maturation at P7 and P14, but not P20. In adolescence (P45), there was no difference between groups in an open field test. However, as adult dexamethasone-treated animals were less active in the open field and spent more time in closed arms of the elevated plus maze. The serum corticosterone response to crowding stress in dexamethasone-treated animals was no different from controls, but they demonstrate a delay in return of corticosterone levels to baseline. These differences in behavior and hormonal stress responsiveness suggest that neonatal dexamethasone exposure may permanently alter function of the neuroendocrine stress axis. steroids; prematurity; brain; corticosterone; limbic-hypothalamicpituitary-adrenal axis SEVERE RESPIRATORY DISTRESS syndrome is commonly experienced in extremely low birth weight (ELBW) infants, resulting in various degrees of ventilator and/or oxygen dependency and subsequent onset of chronic lung disease (CLD). Until recently, administration of a prolonged course of postnatal dexamethasone to ELBW infants was frequently practiced in an attempt to lessen the progression of CLD. Although clinical trials using dexamethasone in this fashion failed to consistently demonstrate improvement in mortality or length of hospitalization, exposures of up to 42 days were commonly used in many neonatal units (4,8,17,55,56). A recent study examining the outcome of ELBW infants (birth weight between 500 and 750 g) found that 43% of those infants born from 1990 to 1992 received dexamethasone compared with 84% of ELBW infants born between 1993 and 1995 (40). Routine use of dexamethasone continued until Yeh and colleag...

No abstract