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S B Barton

Publications and source records attributed to S B Barton.

8 recordsLinked to original sources

Specificity of reference patterns in depressive thinking: agency and object roles in self-representation.

This study investigated A. T. Beck's (1970) negative cognitive triad as a model of depressive thinking. A mixed clinical sample (N = 126) completed the Sentence Completion Test for Depression (SCD) and self-report measures of depression and anxiety. Two reference patterns were tested: agency roles, people who are the source of thoughts, feelings, and actions (self and others); and object roles, points of reference location (self, other, world, future, and past). Cognitive effects were highly specific to depression. With self in agent role, significant correlations were observed with negative self, world, and future references but not with other people or the past. With others in agent role, only negative self references were correlated with depression (e.g., "Some people would not ... put me out if I was on fire"), suggesting an interpersonal extension to the negative cognitive triad.

Adolescent↗

A case study of anomaly detection: shallow semantic processing and cohesion establishment.

Although the establishment of a coherent mental representation depends on semantic analysis, such analysis is not necessarily complete. This is illustrated by failures to notice the anomaly in questions such as, "When an airplane crashes, where should the survivors be buried?" Four experiments were carried out to extend knowledge of what determines the incidental detection of the critical item. Detection is a function of the goodness of global fit of the item (Experiments 1 and 2) and the extent to which the scenario predicts the item (Experiment 3). Global good fit appears to result in shallow processing of details. In Experiment 4, it is shown that if satisfactory coherence can be established without detailed semantic analysis, through the recruitment of suitable information from a sentence, then processing is indeed shallow. The studies also show that a text is not understood by first producing a local semantic representation and then incorporating this into a global model, and that semantic processing is not strictly incremental.

Adult↗

Smoking and narcotics use among chronic pain patients.

Among 137 noncancer patients having pain for more than 6 mo. and being within 30 to 69 yr. of age, narcotics users were evenly distributed but tobacco smokers were significantly more likely than nonsmokers to use narcotics.

Adult↗

The calcium dependence of spontaneous and evoked quantal release at the frog neuromuscular junction.

1. The quantal output from stimulated nerve terminals in the frog sciatic nerve-sartorius muscle preparation in low-Ca(2+) Ringer solution was measured by the coefficient of variation and the failures methods. Adding sucrose to the Ringer to increase the tonicity or adding ethanol increased miniature end-plate potential (m.e.p.p.) frequency and also the end-plate potential (e.p.p.) amplitude. Earlier reports suggested that increases in tonicity did not increase evoked quantal release.2. Concanavalin A has been reported to block the increase in m.e.p.p. frequency caused by increasing the tonicity of the Ringer (Gorio & Mauro, 1979). This effect was confirmed. The lectin-treated preparations also failed to show an increase in evoked quantal release when the tonicity was increased.3. A model in which both spontaneous and evoked quantal releases depend on some power of the intracellular [Ca(2+)] is presented. The model predicts that rises in m.e.p.p. frequency will be accompanied by increased quantal output from stimulated nerve terminals. The maximum slope of the relationship between log (evoked quantal output) and log ([Ca(2+)](out)) will be less than the true power. A theoretical analysis shows that, as the true power approaches infinity, the maximum slope will be slightly above 4. The value for the slope usually found experimentally at the frog neuromuscular junction is also about 4.4. The model does not fit the experimental data. The observed increases in evoked quantal release are higher than those predicted for the observed increases in spontaneous release. There are several possible explanations for the discrepancy. Treatments that increase m.e.p.p. frequency may also increase Ca(2+) influx into the stimulated terminal. However, we prefer the explanation that there is a fraction of spontaneous release that is independent of the [Ca(2+)] in the terminal; if this is true the model might account for the data.5. The model can account for a variety of puzzling experimental observations, including: (a) the effect of hypertonic solutions and of diamine in decreasing the slope in the relation between log (evoked quantal output) and log ([Ca(2+)](out)); (b) the slope of near 1 observed at the crustacean neuromuscular junction; (c) the decrease in the slope produced by treatment with botulinum toxin.

Action Potentials↗

Facilitation and impulse propagation failure at the frog neuromuscular junction.

Exposure of frog neuromuscular junctions to solutions which contain a high concentration of calcium ions produces failure of neuromuscular transmission. This failure of transmission is abrupt and usually complete. However, some terminals produce small end-plate potentials even after the exposure to a high concentration of calcium ions. A second stimulus to the nerve can overcome the block of neuromuscular transmission if the interval between the stimuli is less than a critical value. The size of the end-plate potential is almost independent of the interstimulus interval if the latter is less than the critical value but more than the refractory period. The depth of this neuromuscular block is affected by temperature, potassium ions, osmotic pressure, cobalt ions, and prior high frequency stimulation of the nerve. Neuromuscular transmission failure coincides with failure of the nerve action potential (NAP) to invade the terminal. Prior to propagation failure, the second extracellularly recorded NAP is smaller, but is conducted faster than the first NAP. The relevance of these findings to the facilitation of transmitter release seen in solutions of normal divalent ion content is discussed.

Action Potentials↗

Bursts of miniature end-plate potentials can be released from localized regions of the frog motor nerve terminal.

We examined spontaneous transmitter release by simultaneously recording from end-plates with both an intracellular electrode and a focal extracellular electrode. In normal Ringer's solution the focal releases appear to be a near random portion of the pooled output. But in elevated [Sr2+]out bursts of miniature end-plate potentials (m.e.p.p.s.) occur, and these can be localized at a portion of the presynaptic terminal. The bursts are not artifacts caused by the focal recording technique. In some conditions, sections of the nerve terminal can exhibit an enhanced probability of quantal release that persists for seconds. We occasionally observe extracellular events that must be generated by m.e.p.p.s. in adjacent fibers.

Animals↗