Biomedical subjects
Publications and source records attributed to R Adamec.
Synaptic responses in hippocampal granule cells to stimulation of their afferent fibers from the entorhinal cortex fluctuate with a 24-hour period. The phase of this cycle for rats and monkeys depends on whether the animal is naturally nocturnal or diurnal. In a rat blinded by enucleation, the rhythm persists but drifts out of phase with the rhythm of sighted controls.
This report presents studies which relate limbic epileptic excitability to behavioral measures of defensive suppression of predatory attack in cats. Correlated with heightened defensiveness to environmental stimuli among non-killer cats is a heightened amygdaloid epileptic excitability, as well as a heightened conduction of amygdaloid epileptic activity to thalamic and hypothalamic substrates of predatory response in the amygdala to the complex visual stimuli presented by rat prey. These neurosensory responses correlate well with measures of epileptic excitability. Brain and behavior measures appear related since enhancement of excitability in the amygdala and of projection of epileptic activity by repeated electrical stimulation of predatory attacks. Furthermore, the ventral hippocampus seems capable of antagonizing the behaviorally suppressive effects of heightened amygdaloid excitability perhaps at points of convergence of amygdaloid and hippocampal output.
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The effects of kindling of the right anterior medial amygdala of Wistar rats was studied. Kindling lastingly increased anxiety (decreased open-arm exploration) in the elevated plus-maze 1 week after the last kindled seizure, replicating previous findings. Changes in anxiety were independent of changes in exploration or activity in either the plus-maze or hole board. A new finding is the dependence on baseline behavior of kindling induced behavioral changes. Using a novel-retest paradigm, it was possible to retest rats in the plus-maze without changes in their open arm explorations. This permitted pretesting rats to determine their baseline levels of plus-maze anxiety. Controls proved to be stable in their plus-maze behavior over a retest interval of 3 weeks. Rats below the median level of Test 1 open-arm exploration were unaffected by kindling. Those above the Test 1 median level of open-arm exploration showed reduced exploration following kindling. Kindling did not affect closed-arm entries in the plus-maze in this analysis. However, it was discovered that rats with arm entries below a critical level on Test 1 showed an increase in closed-arm entries following kindling. These findings point out how baseline behaviors can interact with kindling to influence behavioral outcome. Risk assessment was unchanged by kindling in this study, unlike previous reports. Subtle changes in focus location within the medial amygdala may have altered the effects of kindling on risk assessment. The electrodes in this study were in a slightly but significantly different location in the medial amygdala than in previous studies. As in previous studies, risk assessment was measured as frequency and duration of stretch attend postures toward the open arm of the plus maze when the hind quarters were in the closed arms. Risk assessment was taken as a ratio of time spent in the closed arms of the maze. This study, along with others reviewed elsewhere, suggest that a complex set of factors contributes to the effects of kindling on behavior. The fact that previous studies have not taken them into account perhaps explains inconsistencies in the reported behavioral effects of kindling on behavior in rodents.
We studied lasting behavioral effects of kindling of three parts of the central nucleus of the amygdala and the anterior nucleus basalis in the right hemisphere of male Wistar rats. Kindling lastingly changed two measures of anxiety in the elevated plus-maze. The nature of the change depended on the location of the kindled focus. Kindling of the posterior central nucleus decreased both open-arm exploration and frequency of risk assessment in the elevated plus-maze 1 week after the fourth stage 5 seizure. Kindling of the middle parts of the central nucleus was without behavioral effects. Kindling of the anterior central nucleus and the anterior nucleus basalis increased risk assessment, which was interpreted as an anxiolytic effect. Changes in risk assessment produced by kindling of the central nucleus were dependent on open-arm avoidance, whereas the effects of nucleus basalis kindling were independent of open-arm avoidance. Analysis of covariance and factor analysis support the view that control of risk assessment is by circuitry, which is independent of that which controls open-arm avoidance. Moreover, part of this circuitry appears to involve the anterior nucleus basalis. Changes in plus-maze behavior were independent of changes in exploration or activity in either the plus-maze or hole board. These findings add to a growing body of evidence that suggests that subtle differences in location of a kindled focus within the rat amygdala lead to different behavioral outcomes.
We determine the value of the programmed ventricular stimulation (PVS) and of clinical, angiographic and electrophysiologic variables in assessing the long-term risk of arrhythmia recurrence in a group of coronary artery diseased patients presenting with a first episode of monomorphic sustained ventricular tachycardia (VT) treated with amiodarone. Mortality and arrhythmia recurrence rates were retrospectively assessed in 55 consecutive patients with previous myocardial infarction presenting with a first VT episode. Results of left heart catheterization, echocardiography and time-domain signal-averaging were collected. Patients underwent PVS after amiodarone oral loading and were classified according to inducibility before being all discharged on amiodarone (200 mg daily). The mean follow-up was 42+/-31 months. Total and cardiac mortality rates were 29% (16 patients) and 23% (13 patients) respectively. Sudden death (SD) occurred in nine patients (16%). VT recurred in 13 patients (23%). Sustained monomorphic VT was inducible in 40 patients (72%) after amiodarone loading. Neither total mortality (10/40 vs. 6/15) nor cardiac mortality (3/40 vs. 1/15) were significantly different between inducible and non-inducible patients. Recurrent VT rate was 27% (11/40 patients) for the inducible group and 13% (2/15 patients) for the non-inducible group (NS). SD occurred in 6/40 inducible patients (15%) and in 2/15 non-inducible patients (13%) (NS). Arrhythmic events occurred in 42% (17/40) inducible patients vs. 26% (4/15) non-inducible patients (P=0.07). Parameters correlated with outcome were ejection fraction (EF) (5 SD/11 patients with EF <0.3 vs. 4/44 with EF >0.3, P=0.003), mitral insufficiency (MI) (4 SD/10 patients with MI vs. 4/44 patients without MI, P=0.004) and age (65+/-9 years for patients with VT recurrence vs. 58+/-9, P=0.02). Although the risk stratification can be improved, reliable and safe long-term prediction of recurrence of malignant ventricular arrhythmia in individual patients cannot be made. Consequently, the systematic implantation of a cardioverter-defibrillator in case of a first episode of sustained VT occurring in coronary artery disease patients should be further debated.
The effects of kindling and inverse benzodiazepine receptor agonist beta-carbolines on animal models of anxiety are briefly reviewed in relation to affective disorder associated with chemical exposure. Recent experimental results are described. In the present study, cats were given the inverse benzodiazepine receptor agonist, FG-7142, a powerful anxiogenic compound in humans and animals. Neural transmission in pathways involved in defensive behavior in the cat was monitored using evoked potential techniques. Change in these pathways was related to behavioral changes induced by the drug. It was found that a single dose of FG-7142 lastingly increased defensive response to rodents for at least 40 days after drug administration. Behavioral change was specific to defensive response, since approach-attack behavior remained unchanged, replicating previous studies. The benzodiazepine receptor antagonist, Flumazenil, reversed the increase in defensiveness in a drug-dependent manner, replicating previous findings. Increased defensiveness was paralleled by a delayed onset potentiation of neural transmission between the amygdala and the medial hypothalamus of the left hemisphere. Potentiation in the left hemisphere was transient, decaying between 6 and 12 days after the drug. There was a longer lasting potentiation (LTP) of activity evoked in the left and right amygdalo-periacqueductal gray pathways and in the right amygdalo-medial hypothalamic pathway. Potentiation in these pathways appeared at the time of behavioral change. Potentiation of the right amygdalo-periacqueductal gray and right amygdalo-medial hypothalamic pathways persisted until the end of the experiment. In contrast, potentiation of the left amygdalo-periacqueductal gray pathway faded by 40 days after the drug. Flumazenil decreased potentiation ony in the right amygdalo-periacqueductal gray pathway. These data strongly suggest that lasting affective change is mediated by lasting changes in particular efferents of the amygdala of the right hemisphere. Behavioral and physiological effects of FG-7142 were blocked by the N-methyl-D-Aspartate (NMDA) receptor blocker, AP7. The data suggest that failure of neural inhibition induced by FG-7142 engages NMDA receptor processes to produce lasting potentiation of transmission in neural circuits that mediate defensive response with behavioral consequences. Since FG-7142 interferes with GABA mediated neural inhibition and is proconvulsant, its action might mimic the action of other environmental chemicals with similar properties, such as chlorinated hydrocarbon insecticides. The relationship of the present data to the literature on the neural and behavioral effects of insecticide exposure is discussed. The significance of these findings for multiple chemical sensitivity disorder is also briefly discussed.