Phonological priming of spoken words refers to improved recognition of targets preceded by primes that share at least one of their constituent phonemes (e.g., BULL-BEER). Phonetic priming refers to reduced recognition of targets preceded by primes that share no phonemes with targets but are phonetically similar to targets (e.g., BULL-VEER). Five experiments were conducted to investigate the role of bias in phonological priming. Performance was compared across conditions of phonological and phonetic priming under a variety of procedural manipulations. Ss in phonological priming conditions systematically modified their responses on unrelated priming trials in perceptual identification, and they were slower and more errorful on unrelated trials in lexical decision than were Ss in phonetic priming conditions. Phonetic and phonological priming effects display different time courses and also different interactions with changes in proportion of related priming trials. Phonological priming involves bias; phonetic priming appears to reflect basic properties of activation and competition in spoken word recognition.
We used spike-triggered averaging of rectified electromyographic activity to determine whether corticomotoneuronal (CM) cells produce postspike effects in muscles of both proximal and distal forelimb joints in monkeys performing a reach and prehension task. Two monkeys were trained to perform a self-paced task in which they reached forward from a starting position to retrieve a food reward from a small cylindrical well. We compiled spike-triggered averages from 22 to 24 separate forelimb muscles at both proximal (shoulder, elbow) and distal (wrist, digits, intrinsic hand) joints. Of 174 cells examined, 112 produced postspike effects in at least one of the target muscles. Of those cells, 45.5% produced postspike effects in both proximal and distal forelimb muscles. A nearly equal number (44.7%) produced postspike effects in distal muscles only, whereas a clear minority (9.8%) produced postspike effects in only proximal muscles. The majority of CM cells (71.4%) produced effects in two or more muscles, with an average muscle field of 3.1 +/- 2.1 (mean +/- SD) for facilitation plus suppression. Of 345 postspike effects identified, 70.7% were facilitation effects and 29.3% were suppression effects. The large majority of effects (72.2%) were in distal muscles. When averaged by joint, the latency and peak magnitude of postspike facilitation showed a stepwise increase from proximal to distal joints. The results of this study show that the majority of CM cells engaged in coordinated forelimb reaching movements facilitate and/or suppress muscles at multiple joints, including muscles at both proximal and distal joints. The results also show that CM cells make more frequent and more potent terminations in motoneuron pools of distal compared with proximal muscles.
Morphine is known to prevent the development of cell-mediated immune (CMI) responses and enhance expression of the CCR5 receptor in monocyte macrophages. We undertook a study to determine the effect of morphine on the neuropathogenesis and immunopathogenesis of simian immunodeficiency virus (SIV) infection in Indian Rhesus Macaques. Hypothetically, the effect of morphine would be to prevent the development of CMI responses to SIV and to enhance the infection in macrophages. Sixteen Rhesus Macaques were divided into three experimental groups: M (morphine only, n = 5), VM (morphine + SIV, n = 6), and V (SIV only, n = 5). Animals in groups M and VM were given 2.5 mg/kg of morphine sulfate, four times daily, for up to 59 weeks. Groups VM and V were inoculated with SIVmacR71/17E 26 weeks after the beginning of morphine administration. Morphine prevented the development of enzyme-linked immunosorbent spot-forming cell CMI responses in contrast to virus control animals, all of which developed CMI. Whereas morphine treatment had no effect on viremia, cerebrospinal fluid viral titers or survival over the time course of the study, the drug was associated with a tendency for greater build-up of virus in the brains of infected animals. Histopathological changes in the brains of animals that developed disease were of a demyelinating type in the VM animals compared to an encephalitic type in the V animals. This difference may have been associated with the immunosuppressive effect of the drug in inhibiting CMI responses.
The presence of postspike facilitation (PSpF) in spike-triggered averages of electromyographic (EMG) activity provides a useful means of identifying cortical neurons with excitatory synaptic linkages to motoneurons. Similarly the presence of postspike suppression (PSpS) suggests the presence of underlying inhibitory synaptic linkages. The question we have addressed in this study concerns the extent to which the presence and strength of PSpF and PSpS from corticomotoneuronal (CM) cells correlates with the magnitude of covariation in activity of the CM cell and its target muscles. For this purpose, we have isolated cells during a reach and prehension task during which the activity of 24 individual proximal and distal forelimb muscles was recorded. These muscles show broad coactivation but with a highly fractionated and muscle specific fine structure of peaks and valleys. Covariation was assessed by computing long-term (2 s) cross-correlations between CM cells and forelimb muscles. The magnitude of cross-correlations was greater for muscles with facilitation effects than muscles lacking effects in spike-triggered averages. The results also demonstrate a significant relationship between the sign of the postspike effect (facilitation or suppression) and the presence of a peak or trough in the cross-correlation. Of all the target muscles with facilitation effects in spike-triggered averages (PSpF, PSpF with synchrony, or synchrony facilitation alone), 89.5% were associated with significant cross-correlation peaks, indicating positively covarying muscle and CM cell activity. Seven percent of facilitation effects were not associated with a significant effect in the cross-correlation, whereas only 3.4% of effects were associated with correlation troughs. In contrast, of all the muscles with suppression effects in spike-triggered averages, 38.9% were associated with significant troughs in the cross-correlation, indicating an inverse relation between CM cell and muscle activity consistent with the presence of suppression. Fifty-five percent of suppression effects was associated with correlation peaks, whereas 5.6% was not associated with a significant effect in the cross-correlation. Limiting the analysis to moderate and strong facilitation effects, the magnitude of PSpF was correlated weakly with the magnitude of the cell-muscle cross-correlation peak. Nevertheless, the results show that although many CM cell-target muscle pairs covary during the reach and prehension task in a way consistent with the sign and strength of the CM cell's synaptic effects on target motoneurons, many exceptions exist. The results are compatible with a model in which control of particular motoneuron pools reflects not only the summation of signals from many CM cells but also signals from additional descending, sensory afferent, and intrinsic spinal cord neurons. Any one neuron will make only a small contribution to the overall activity of the motoneuron pool. In view of this, it is not surprising that relationships between postspike effects and ...
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