[Effectivity of intraventricularly administered Na-orotate on a conditioned flight reaction of the rat].
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Two studies were conducted. In the first study, four strains of male rats--Long-Evans (LE), Sprague-Dawley (SD), Wistar, Fisher 344--were immersed in fresh water or water soiled by a rat of the same strain which presumably contains an alarm substance. LE rats were less immobile than SD, Wistar, and Fisher rats in fresh water. All strains were significantly less immobile in soiled water; however, relative to immobility times in fresh water, the decrease in immobility in soiled water was greatest for SD rats and least for Wistar rats. A second study tested SD and Wistar rats in water soiled by animals of the same strain compared to water soiled by animals of the other strain. This study indicated that Wistar rats produce less alarm substance or less potent substance and are also less reactive to it than SD rats. The results of these two studies indicate that some strains are more affected by alarm substance than others and the differential response is due both to decreased production/potency and reaction to the substance.
Rats were injected with naloxone hydrochloride (3 mg/kg) or saline and subjected to preshock or no preshock prior to receiving a test shock that elicited defensive burying. Preshock was administered in a context different from, or the same as, that in which the test shock was delivered. The combination of naloxone and preshock led to more defensive burying than did saline and preshock. This was the case regardless of preshock context, a result suggesting that fear and/or analgesia may not always be critical ingredients in the preshock-naloxone interaction. Interpretative matters notwithstanding, the pattern of results for defensive burying was in basic agreement with that of other research on naloxone and defensive behavior and represents an extension of the literature to a new species-specific defense reaction.
In order to localize groups of neurons commanding the defense reaction, microinjections of L-glutamate (GLU, 5 nmol in 0.2 microliter, during 20 s) were made inside the dorsal midbrain of unanesthetized rats provided with an intra-arterial cannula for blood pressure (BP) recording. In 9 rats, GLU microinjection induced freezing behavior or flight, accompanied by a 30.1 +/- 4.8 mmHg increase in BP. The latency of the GLU effect was 16 +/- 2 s and its duration 89 +/- 8 s, as measured from the BP recordings. In 9 other rats, GLU microinjection did not evoke defensive behavior and the BP increase was 6.0 +/- 0.9 mmHg, significantly lower (P less than 0.001) than in the former group. Control injections of artificial cerebrospinal fluid (CSF) did not cause behavioral changes and increased BP by less than 3 mmHg. Histology revealed that in all rats in which GLU induced a defense reaction the injection sites were inside the dorsal periaqueductal gray (PAG). Sites in which GLU injection was ineffective were localized in the midbrain tegmentum, outside the borders of the PAG (8 rats), or inside the ventral PAG (1 rat). Since GLU stimulates neuron cell bodies and their dendritic processes but not passing axons, these results strongly suggest that the dorsal PAG of the rat contains a group of neurons that controls behavioral and autonomic manifestations of the defense reaction.
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The effects of spinal lesions on reactions of rats to nociceptive electrocutaneous stimulation (ES) were evaluated by measuring the speed of operant escape responses, the magnitude of hindlimb flexion reflexes and the amplitude of reflex vocalizations. ES intensities ranging from 0.1 to 0.8mA were delivered to either hindpaw of rats that were trained to terminate stimulation (perform an escape response) with one forelimb. Unilateral thoracic lesions within the lateral column were produced by surgically transecting axons, with or without insertion of blood-soaked Gelfoam into the lesion cavity. The latter procedure was intended to standardize and maximize hemotoxic damage to the gray matter at the lesion site. The speed of conscious escape responses to all intensities was reduced contralaterally and to comparable extents following each type of lesion. Involvement of mid-lateral axons was an important determinant of contralateral deficits in escape responding. Escape speed for ipsilateral stimulation was not affected by the lesion without intentional insertion of blood but was reliably increased by addition of blood to the lesion site. Flexion reflexes were substantially decreased contralaterally and slightly decreased ipsilaterally, in accordance with previous investigations of anterolateral lesion effects in monkeys. Early (reflex) vocalizations were essentially eliminated for stimulation contralateral to the lesions, but vocalizations following ipsilateral stimulation were little affected. Postoperative variations in behavioral responsivity over time were not accounted for by pre- and post-estrous stages of the estrous cycle. The principal finding of this study is that hemotoxic accompaniments of a spinal lesion produce hyperalgesia for nociceptive stimulation applied ipsilaterally to segments well caudal to the lesion. This finding indicates that hemotoxic injury of the gray matter near an anterolateral spinal lesion enhances the excitation of certain rostral structures that receive nociceptive information.
Experimental study of behavior of Lymnaea truncatula in the presence of terrestrial or aquatic predators. The presence of predators disturbes the daily rhythm connected with amphibious conditions of non-infested snails. In half-immersed habitats, Zonitoides nitidus, terrestrial predator, produces a progressive immersion of surviving snails; but the latter run away to dry zones in drying habitats or with aquatic predators. The infested snails (phasis E 1) present the same reactions of behaviour in presence of predators, but the reactions are more limited.
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Tadpoles of the western toad (Bufo boreas) and of the Cascades frog (Rana cascadae) show an alarm reaction to an extract containing chemical cues from damaged conspecifics. The mean time spent by individual B. boreas tadpoles in the half of the test tank to which the extract solution was added was significantly lower than expected by chance. Activity was also significantly greater in Bufo extract tests than in control tests. Tadpoles did not avoid an extract of another tadpole species (Hyla regilla). Rana cascadae tadpoles did not avoid areas containing Rana extract but did significantly increase their level of activity in response to the extract. These results suggest that the R. cascadae tadpole alarm reaction exists but differs from the B. boreas reaction.
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