Biomedical subjects

L C Schenberg

Publications and source records attributed to L C Schenberg.

24 records · Page 2Linked to original sources

PubMed1990

Logistic analysis of the defense reaction induced by electrical stimulation of the rat mesencephalic tectum.

Subliminal and threshold functions of behavioral output to electrical stimulation of the rat mesencephalic tectum were fitted using the logistic model. The results suggest the existence of isotopic albeit anisotropic freezing and flight mechanisms in the dorsal periaqueductal gray and deep layers of the superior colliculus. Moreover, the marked parallelism of immobility and running threshold functions indicates the probable coupling of these mechanisms through a kind of negative feedback. Finally, the good fitting to the model suggests that the behavioral output to electrical stimulation of these areas follows a logistic function of the logarithm of the stimulus intensity.

Aggression↗

PubMed1989

Cardiovascular change in response to prolonged defense area stimulation in freely moving rats.

The mean blood pressure and heart rate of freely moving rats were directly recorded over a 1-min period of electrical stimulation of the periaqueductal gray with intensities that induced freezing behavior, intense flight or no behavioral changes. Blood pressure and heart rate increased only when flight was induced and only during the first 15 s of stimulation. These cardiovascular changes suggest that homeostatic mechanisms act during the defense reaction and are markedly inhibited only at the beginning of the stimuli that induce the flight response, this inhibition quickly undergoing attenuation. These data do not suggest that activation of defense area, per se, contributes to the development of primary hypertension.

Animals↗

PubMed1983

GABA modulation of the defense reaction induced by brain electrical stimulation.

Earlier behavioral results led to the suggestion that GABA exerts a tonic inhibitory influence in the dorsal periaqueductal gray (DPAG) matter of the rat integrating defensive behavior. In the present experiments, the role of GABAergic mechanisms in the modulation of the autonomic component of the defense reaction was studied. Thus, the effects of intravenous (IV) injections of chlordiazepoxide as well as of intracerebral (IC) injections of midazolam in the dorsal midbrain, on the blood pressure (BP), heart rate (HR) and respiratory increases induced by electrical stimulation of the DPAG were measured in rats anesthetized with urethane. Chlordiazepoxide (10 mg/kg, IV) as well as midazolam (40 and 160 nmol, IC) attenuated the centrally-induced hypertension, without affecting basal BP. The tachycardia induced by aversive brain stimulation was similarly decreased by the benzodiazepines. In addition, the HR baseline was significantly raised by chlordiazepoxide and by the highest dose of midazolam. The tachypnea induced by brain electrical stimulation was also reduced by both benzodiazepines. Basal respiratory rate was slightly, but significantly decreased by chlordiazepoxide as well as by the two doses of midazolam used and to a lesser extent by the vehicle alone. Chlordiazepoxide attenuated the increase in respiratory depth caused by brain stimulation, while basal respiratory amplitude was not affected. The effects of midazolam on this parameter were unclear. Microinjection of bicuculline (5 and 10 nmol) or picrotoxin (0.3 and 1 nmol) into the DPAG increased the BP, HR and respiration, like the electrical stimulation. The latency and duration of bucuculline effects were shorter than those of picrotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

Neuroeffector mechanisms of the defense reaction in the rat.

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

Animals↗

PubMed1981

Depressant action of chlordiazepoxide on cardiovascular and respiratory changes induced by aversive electrical stimulation of the brain.

1. Electrical stimulation of the dorsal periaqueductal gray matter (DPAG), an aversive area of the rat brain, increased the mean blood pressure of awake rats as well as of animals anesthetized with urethane. 2. In the anesthetized rats, increases in heart rate and in breath rate were also induced by DPAG stimulation. 3. Chlordiazepoxide, a benzodiazepine, decreased the blood pressure rise caused by aversive stimulation of the brain in the awake rat. 4. Chlordiazepoxide elicited the same effect in urethane-anesthetized rats. In addition, the hyperpnea induced by electrical stimulation of the dorsal periaqueductal gray matter was also decreased by the drug. 5. The pressor response to intravenous noradrenaline was not affected by chlordiazepoxide. 6. These results suggest that benzodiazepines attenuate the neurovegetative changes accompanying emotion by depressing brain systems that integrate emotional behavior.

Animals↗

PubMed1978

Role of the periaqueductal gray substance in the antianxiety action of benzodiazepines.

In order to study the interactions between serotonergic mechanism and electrical stimulation of the mesencephalic central gray substance, rats were trained to lever-press for terminating aversive electric stimuli applied at the Periaqueductal gray and adjoining tectum of the mesencephalon. Experimental sessions consisted of 40 discrete escape trials of a maximum of 30 sec duration, separated by 30 sec intervals. Dose-effect curves of two tryptamine antagonists, cyproheptadine and methysergide, as well as of the benzodiazepine minor tranquilizer, chlordiazepoxide, on average escape latencies and on frequency distribution of individual latencies were determined. Doses of 3 to 10 mg/kg of cyproheptadine decreased average latencies of escape responding in six of eight rats studied. Doses of 10 and 30 mg/kg of methysergide also facilitated escape responding in one of three rats. In contrast, doses from 1 to 10 mg/kg of chlordiazepoxide, that cause little sedation or ataxia, produced dose-dependent increases in escape latencies. Furthermore, doses of 5.6 and 10 mg/kg of chlordiazepoxide partially blocked escape responding. The facilitatory effects of the tryptamine antagonists suggest that escape behavior is inhibited by brain tryptaminergic mechanisms, whereas the specific depressant effect of chlordiazepoxide on escape from Periaqueductal gray electrical stimulation suggest that this region may be involved in the antianxiety action of benzodiazepines.

Animals↗