PubMed · 1104213
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D H Cohen, P A Obrist. 1975. Interactions between behavior and the cardiovascular system.. https://doi.org/10.1161/01.res.37.6.693
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Play fighting is a frequent activity of juvenile rats and appears to show marked variability amongst individuals in that some rats play a great deal and others very little. This study attempted to identify some of the factors involved in producing this individual variability. The major influence over an individual's frequency of play as a juvenile was found to be the frequency of play by the partner. That is, play appears to be contagious, in that a high playing animal stimulates its partner to play frequently as well. In male juveniles, but seemingly not in female juveniles, the subsequent adult status of one partner as dominant influences the subordinate-to-be to initiate more playful contacts. In addition to these extrinsic influences, however, there appear to be intrinsic factors that influence whether an individual is a high or low playing animal. One intrinsic factor appears to be 'boldness', so that bolder animals tend to initiate more playful contacts. Higher players tend to be more susceptible to the stereotypy-inducing effects of the dopamine agonist, apomorphine, and tend to be more dependent upon the playful activity of the partner to maintain their own high levels of play. Both of these characteristics are consistent with other studies comparing bold and timid rats. Boldness, however, only seems to influence how much play a rat will exhibit, not how much play it is capable of exhibiting. Neonatal testosterone augmentation increases juvenile play fighting but not apomorphine susceptibility, suggesting that a high player need not be a bold animal. The total frequency of play an individual is capable of initiating appears to depend upon perinatal exposure to androgens. Boldness and the playfulness of the partner appear to modulate the expression of this hormonally set value.
Fully amygdala kindled rats were exposed to two different inter-male agonistic experiences in order to study the interaction between epilepsy and acute social stress. Victory experience did not influence the severity of seizure behaviour, whereas a single acute defeat modified both ictal and postictal seizure manifestations. Defeat resulted in less severe and shorter lasting motor seizures, and the accompanied postictal inhibition or behavioural depression was of shorter duration in comparison with pre-stress values. The ability of acute defeat to trigger anticonvulsant activity as implied by the weakened convulsive response is discussed.
The effects of discrete excitotoxic lesions of the basolateral (BL) and corticomedial (CM) amygdaloid areas on both male rat sexual behaviour and inter-male agonistic behaviour were investigated. The effects of the same lesions on the hormonal responses (luteinising hormone (LH) following sexual behaviour, corticosterone following aggressive interactions) which accompany these behavioural responses were measured. Basolateral lesions had no effect on male sexual behaviour but significantly reduced the level of aggressive inter-male behaviour. However, the increase in plasma corticosterone concentration which occurs after such an interaction was not affected by basolateral lesions. In contrast, corticomedial lesions did not affect inter-male offence but severely affected copulatory behaviour, including a significant decrease in the males' investigation of the receptive female. However, the increase in plasma LH concentrations induced by the presence of a receptive female was not affected by the CM lesion. These results demonstrate a dissociation between the two amygdaloid regions with respect to the contributions made to the two social behaviours under study. This anatomical division may reflect differential amygdaloid sensory control of these behaviours. A further dissociation between amygdaloid contribution to behavioural and hormonal responses was also revealed. Neither hormonal response showed a parallel decline with the relevant behavioural response, suggesting that neither the basolateral nor corticomedial amygdaloid complex is responsible for coordinating behavioural and endocrine responses to a specific stimulus.