Sex,strain, and housing: Variables influencing the effects of prior shock exposure on shock-induced aggression

A series of experiments was conducted to investigate sex, housing conditions, and strain as possible factors influencing the interference effect of prior exposure to shock on shock-induced aggression. In albino subjects, female rats and rats housed in community cages evidenced the greatest suppression in aggression following prior exposure to shock. In addition, ten sessions of prior exposure to shock produced a greater suppression in shock-induced fighting than 20 sessions of prior exposure to shock. The prior shock effect was not obtained with hooded subjects. Responsivity to shock was also investigated to determine whether the prior exposure to shock attenuation of shock-induced fighting was a consequence of reduced activity in response to shock. Responsivity to shock measured with an isometric platform accounted for less than 4% of the variance in shock-induced fighting in the single experiment that obtained a correlation between responsivity and shock-induced aggression.     

An objective technique for recording shock-induced aggression in unrestrained pairs of rats

Pairs of rats received grid shock in a conical enclosure. Each shock elicited the stereotyped fighting posture. An omnidirectional pole, which was always between the rats, was accidentally operated whenever the rats fought. The number of pole hits, and the number of observed fight bouts, increased with current intensity. The number of pole hits served as a reliable and objective measure of shock-induced fighting in rats.     

Effects of post-trial administration of naloxone and beta-endorphin on shock-induced fighting in rats

To study the involvement of endogenous opioid peptides in the development of shock-induced fighting, naloxone (2 mg/kg) or beta-endorphin (10 micrograms/kg) was administered subcutaneously immediately after the session and during nine consecutive daily sessions to rats repeatedly exposed to electric shocks. beta-Endorphin blocked the development of shock-induced fighting while naloxone facilitated it but only when shock-induced fighting occurred at a low rate. The effects of beta-endorphin were time dependent since when beta-endorphin was injected 90 min after the shock session instead of immediately after, its impairing effect disappeared. In addition, naloxone blocked the impairment produced by beta-endorphin. Differential postsession treatment of each member of pairs of rats with naloxone and beta-endorphin resulted in a higher probability of rats treated with naloxone to be dominant over rats treated with beta-endorphin in the test situation. These results are discussed in relation with the possible involvement of endogenous opioids in the modulation of the physiological consequences of defensive behavioral responses to shock.     

Shock-induced aggression as a function of prior experience with avoidance, fighting, or unavoidable shock

Rats were trained in shock-induced aggression, free operant avoidance, or were presented with unavoidable shocks. Fighting in response to shock was subsequently measured by intermatching individual animals that had received the three training procedures. The fighting probabilities of animals with histories of avoidance and dominant animals with histories of fighting were higher than the fighting probabilities of non-dominant fighting rats or rats with a history of unavoidable shocks. Animals with higher fighting probabilities disrupted avoidance baselines more than animals with lower fighting probabilities. Control experiments suggested that fighting decrements produced by administration of prior grid-shock were due to the acquisition of behaviors incompatible with aggression.     

Behavioral studies in spontaneously hypertensive rats

In the present study we examined some behavioral patterns in spontaneously hypertensive (SHR) male rats as compared with Wistar (W) rats. The following methods were employed: open field test, two-way active avoidance, passive avoidance, shock-induced fighting, shock-induced suppression of drinking (conflict test), and dominant-subordinate behavior in rats competing for water. Spontaneously hypertensive rats showed higher level of locomotor activity, lower emotionality, lower anxiety level, increased acquisition of avoidance tasks, and enhanced dominance behavior. In addition, hypertensive rats were less aggressive in shock-induced fighting test. It is concluded, that spontaneously hypertensive rats seem to be hyperactive in terms of locomotor activity while their emotionality appears to be paradoxically reduced.     

Punishment of irritable aggression

In a series of three experiments using a restrained target procedure the influence of shock punishment of shock-induced aggression in rats was assessed. Regardless of prior experience with shock-induced aggression, punishment resulted in a suppression of the frequency and total duration of the fighting behavior. In addition, possible alternative explanations that have clouded studies of punishment of irritable aggression were ruled out by demonstrating that the suppression was not a consequence of altered parameters of shock frequency and duration.     

Spontaneously hypertensive Wistar-derived male rats are more aggressive than those of their normotensive progenitor strain

We compared a group of spontaneously hypertensive rats (SHRs) to a group of Wistar-Kyoto (WKY) rats on each of the three most commonly studied forms of aggressive behavior in rats: muricide, intraspecific aggression, and shock-induced fighting (SIF). A significantly higher proportion of SHRs were muricidal; they also fought more at the lowest shock level. A trend for a higher incidence of intraspecific offense behaviors by SHRs was not significant. SHR flinch and jump thresholds were lower than the respective WKY thresholds. Although there were no significant correlations between shock thresholds and any aspects of SIF, the possibility that strain differences in shock sensitivity may contribute to differences in SIF cannot be ruled out. Within strains, there were no correlations among the different forms of aggression. Several different inherited characteristics may be associated with the accentuation of different forms of aggression in SHRs.     

Effects of previous housing conditions on shock-induced aggression.

This study investigated shock-induced aggression as a function of housing rats in single or communal cages for varying periods of time before testing. Rates of fighting were unaffected by housing conditions when rats spent seven or 14 days in either of these settings before testing. Placing rats in these settings for 21 or 28 days before testing, however, did affect rates of fighting. Communal caging of subjects for 28 days before testing was particularly deleterious to shock-induced aggression. How rats are housed outside the experimental chamber is a variable affecting shock-induced aggression and should be considered both in designing future studies and as a topic for future investigation.     

Alterations in shock-induced fighting and locomotor activity following intracerebroventricular injection of hydrocortisone in the rat

Three experiments were conducted in an attempt to clarify the facilitatory influence of hydrocortisone on shock-induced fighting in rats. Results of the first experiment indicated a biphasic, dose-dependent action of intraventricularly-administered hydrocortisone. Low (25 μg) and intermediate (50 μg) doses both facilitated fighting whilst the high (100 μg) dose exerted a potent suppressant effect. Two control tests were performed to determine whether alterations in pain reactivity or locomotor activity could have accounted for the observed changes in fighting behaviour. None of the treatments altered shock thresholds (Experiment 2) but whilst neither low nor intermediate doses affected activity measures, the high dose preferentially reduced vertical activity (Experiment 3).     

Ethanol effects on shock-induced fighting and muricide by rats

Ethanol (0.25-1 gm/kg body weight; IP) did not significantly alter shock-induced fighting, regardless of whether it was administered to both rats or to only one rat of the pair. Higher doses tended to decrease shock-induced fighting. Ethanol (0.25-2 gm/kg body weight; IP) also did not induce “nonkiller” rats to kill mice and only high doses (1.5 and 2 gm/kg body weight) decreased the incidence of muricide in “killer” rats. The depressant effects of ethanol on both shock-induced fighting and muricide appeared to result from drug-induced ataxia rather than from a direct effect of ethanol on aggressive behavior.     

Interaction between reflexive fighting and cooperative escape

Subjects separated by a Plexiglas partition were trained to follow a cooperative escape procedure which produced behavior like the escape responding of individual subjects. Removal of the partition produced fighting and less efficient escape. Efficient escape behavior was restored and fighting disappeared when the partition was replaced. Neither increased space nor a moving toy affected escape behavior. The results indicate that switching animals from an isolated to a social situation produced a change in the effect of shock upon escape which was related to shock-induced fighting.     

Amygdaloid function in the central cholinergic mediation of shock-induced aggression in the rat

A series of experiments was designed to examine the role of central cholinergic mechanisms in shock-induced aggression. Cholinergic blockade in the basolateral amygdala, ventral hippocampus, or dorsal hippocampus resulted in greatly reduced levels of fighting in response to footshock. However, while pain sensitivity remained unaltered in the amygdala group, both of the hippocampal groups exhibited decreased shock sensitivity. Further investigation of the amygdala revealed (1) increased fighting in response to increased cholinergic levels, (2) neuroanatomical specificity to the basolateral division of this complex, (3) that an intact basolateral amygdala is essential to the normal manifestation of shock-induced aggression, and (4) that social attraction remains unaltered by cholinergic blockade of the basolateral amygdala. Motor coordination and motor activity were not significantly affected in any treatment condition.     

Effects of long-term shock and associated stimuli on aggressive and manual responses

Squirrel monkeys were exposed to response-independent, fixed-frequency shock that produced biting attack upon a pneumatic hose. Attacks decreased within and across sessions at low intensities and high frequencies of shock, but increased within and across sessions at higher intensities and lower shock frequencies. Stimuli paired with shock, when presented alone, came to produce biting, and stimuli correlated with shock parameters that produced increases in responding within sessions produced similar increases when presented alone. Further experiments showed that continuing exposure to shock also produced lever pressing or chain pulling, with longer shock exposure again producing higher response rates. Whereas biting generally decreased throughout the intershock interval, manual responding generally increased as shock time approached, but immediately before shock was often suppressed. Following shock, biting attack predominated over manual behavior. The results suggest a possible explanation for the extreme resistance of avoidance behavior to extinction, and may also partially explain the persistence of responding during schedules of response-produced shock. Relationships of the present findings to naturalistic observations of relations between fleeing, freezing, and fighting performances are discussed.     

Choice for signalled over unsignalled shock as a function of shock intensity

Choice between a signalled shock schedule and an unsignalled one was examined at various shock intensities. Three rats were given the opportunity to change from the unsignalled schedule to the signalled one at intensity values between 0.15 mA and 1.0 mA. Steps were usually 0.15 mA and both ascending and descending series were given. For two other rats, shock intensity increased from 0.20 mA to 1.0 mA in 0.20-mA increments; for two additional rats, shock intensity was first 3.0 mA and was then reduced to 1.0 mA. Subjects tended to remain in the unsignalled schedule at the lower shock intensities, but spent most of each session under the signalled schedule at the higher intensities (1.0 mA and 3.0 mA). In addition, the time spent in the signalled schedule tended to vary systematically with shock intensity over at least part of the range of intensity values. It was concluded that the relationship between shock intensity and choice behavior is similar to the relationship between intensity and behavior in procedures involving avoidance, escape, and punishment.     

Reflexive fighting in response to aversive stimulation

Reflexive fighting was elicited between paired rats as a reflex reaction to electric shock prior to any specific conditioning. Such fighting was fairly stereotyped and easily differentiated from the rats' usual behavior. The strength of this reflex was not attributable to any apparent operant reinforcement. Elicitation of fighting was a direct function of the enclosed floor area and a nonmonotonic function of the shock intensity.

Failure to scramble the polarity of the electrified grid produced inconsistent fighting. Under optimal conditions fighting was consistently elicited by shock regardless of the rat's sex, strain, previous familiarity with each other, or the number present during shock. Repeated shock presentations did not produce an appreciable decrease in fighting until signs of physical debility appeared. Although shock did not cause a rat to attack inanimate objects, it did produce attack movements toward other small animals. Failure of guinea pigs to defend themselves revealed that the elicitation of fighting from the rat does not require reciprocal attack. Paired hamsters showed fighting reactions similar to those of the rats, whereas guinea pigs failed to fight. Electrode shock and a heated floor elicited fighting between the rats, but intense noise and a cooled floor did not.

     

Aggressive behavior inhibition by serotonin and quipazine injected into the amygdala in the rat

The effects on aggressive behavior, open-field activity, and pain threshold of bilateral microinjections of serotonin (20 micrograms) and quipazine (20 micrograms), the direct serotonergic receptor agonist, into the cortico-medial amygdala were investigated in Wistar rats. Both drugs significantly prolonged the attack latency in isolated killer rats (predatory aggression model), and suppressed the incidence of aggressive postures/attacks in shock-induced fighting test (affective aggression). The only difference in the open-field behavior was the lower number of central square entries in drug-treated compared to saline-injected rats. None of the substances produced any significant change in jump threshold. It is concluded that stimulation of serotonin receptors within the amygdala produces inhibition of affective and muricidal behavior in isolated rats. The effect does not seem to be dependent on changes in general activity and pain sensitivity.     

The role of norepinephrine and acetylcholine in mediating escape deficits produced by inescapable shocks

This study examined the role of neurochemical changes produced by inescapable shock, specifically the depletion of norepinephrine (NE) and enhancement of acetylcholine (ACh), in mediating subsequent inescapable shock-induced deficits in escape acquisition in rats. Enhancement of these neurochemical changes by injections of the NE synthesis inhibitor, FLA-63 (10 mg/kg), or the anticholinesterase, eserine sulphate (3 X 0.5 mg/kg), during the inescapable shock enhanced the subsequent escape deficits observed 3 days later. In contrast, these drugs had no effect on the subsequent escape behavior of rats that were not exposed to inescapable shock. Since these effects could not be attributed to carry-over or state-dependent effects of the drugs, these data suggest that the magnitude of the escape deficit produced by prior inescapable shock is dependent on the magnitude of the initial inescapable shock-induced changes in NE and ACh.     

Escalation of irritable aggression: Control by consequences and antecedents

Two experiments demonstrated that rats could be trained in a negative reinforcement paradigm to display a shock-induced aggressive response on the first shock presented. Later, rats that had been submitted to the negative reinforcement training procedure displayed more shock-induced aggression than did control groups during a test session that was situationally different from the one used during training. A third experiment demonstrated that noxious antecedent events, if presented with sufficient rapidity, can combine to increase the probability of aggressive behavior. The three experiments together suggest that aversive antecedents and reinforcement contingencies could be involved in the escalation of irritable aggression.     

The effect of shock intensity upon responding under a multiple-avoidance schedule

The effect of two shock intensities (1.00 and 2.00 mA) were studied in the acquisition, maintenance, and extinction of unsignalled avoidance by albino rats. Single and multiple avoidance schedules were employed, with shock intensity being the principal condition that differed between schedule components. The higher shock intensity was generally more effective in producing avoidance. Higher response rates and lower shock rates were observed under high-intensity shock when performance stabilized. When the multiple schedule was introduced, the six rats trained under a single shock intensity all showed poorer performance under the new shock intensity, whether it was higher or lower than the training intensity. Performance under the original shock intensity did not change substantially with the introduction of a different shock intensity in the other multiple schedule component. Performance under the new shock intensity showed gradual improvement with continued exposure to it. All of the rats showed persistent “warm-up”, receiving approximately 40% of the total session shocks in the first one-sixth of the session. The degree of warm-up was unrelated to avoidance shock intensity.     

Immobility as an avoidance response, and its disruption by drugs

Much of the available literature on avoidance behavior is based on responses which require the animal to run, lever-press, or to make some active response to avoid noxious stimulation. The purpose of Experiment I reported in this paper was to determine whether animals can learn to sit or stand motionless in order to escape or avoid electric shock. Five experimental rats were given escape-avoidance training, while five yoked control animals received electric shocks without any response-related contingency. It was shown that an immobility avoidance response, as distinct from the unconditioned “freezing” response to shock, can be trained. The results of Experiment II (30 rats) revealed that this response is more readily acquired at higher shock intensities than at lower ones, provided escape by jumping is prevented at the high shock intensities. The effects of six doses of each of three drugs on the immobility avoidance response were studied in Experiment III (13 rats). Methylphenidate, chlorpromazine, and imipramine all produced a decrement in the immobility response, but the pattern and amount of the effects of the three drugs were quite different, one from the other. The implications of these findings for a general theory of avoidance behavior and for drug screening are discussed.