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L De Acetis

Publications and source records attributed to L De Acetis.

12 recordsLinked to original sources

Limited changes in handedness and morphine reactivity in CD-1 mice after pre- and postnatal ozone exposure.

Outbred CD 1 mice were either not exposed (control group) or exposed to ozone (O3) (0.3, 0.6, or 0.9 ppm), during foetal and neonatal life until the time of weaning (postnatal day (PND) 26). On PND 70 the subjects were tested for handedness using a paw preference task assessing both the animals' capability to reach a food pellet in a feeding tube and the individual preference for the use of one of the other forepaw. O3 exposure did not affect the animals' capability to learn the task but caused changes in handedness. Specifically, females exposed to the intermediate O3 concentration showed a reduced preference for the right paw than both their same-sex controls and 0.6 ppm males. On PND 100, mice underwent a hot plate test after IP treatment by either saline or morphine HCl (10 mg/kg). The results were generally in the direction of reduced drug sensitivity after exposure to the highest concentration. The evidence for this effect was more robust in the case of an organised avoidance response (wall-rearing) than in the case of a reflexive response (limb withdrawal); in the case of the former, latency data showed an effect on both males and females while frequency data showed an effect only in females. Overall, the O3 effects are suggestive of subtle CNS changes affecting mouse behavioural responses.

Animals↗

Behavioral effects of peripheral interleukin-1 administration in adult CD-1 mice: specific inhibition of the offensive components of intermale agonistic behavior.

Peripheral administration of interleukin-1beta (IL-1beta) in rodents reduces exploratory behavior in a novel environment while decreasing social investigation of a juvenile conspecific. In this study we wanted to test the effects of peripherally administered IL-1beta on another aspect of the mouse social repertoire, namely intraspecific fighting towards an adult male intruder. In the first experiment, sickness behavior induced by IL-1beta (1 microg/mouse) in adult CD-1 mice was assessed by direct observation of behavioral changes following placement into a novel environment. Three hours after injection, subjects were individually introduced for 20 min in a cage with clean sawdust and a number of behavioral items recorded. Blood samples were collected at the end of the testing session. Body temperature was measured right before, 1 h and 3.5 h following injection. In IL-1beta treated mice, exploration (assessed by measuring duration and frequency of Wall Rearing and Rearing behaviors) was nearly totally suppressed, while duration and frequency of behaviors such as Grooming, Bar Holding, and Digging were also markedly reduced. Administration of IL-1beta significantly elevated CORT secretion above basal levels and, as previously reported for mice, induced hypothermia (about 2 degrees C). In the second experiment, we assessed mice receiving IL-1beta (0.25; 0.5 or 1 microg/mouse or saline solution) in a social context. Three hours after injection, subjects were placed into a neutral cage for 20 min with a non-injected adult male conspecific and aggressive behavior scored. Overall, IL-1beta administration affected the social repertoire of treated mice in a dose-dependent fashion. Specifically, agonistic components of aggressive behavior were nearly totally suppressed, while the defensive elements, such as Upright Defensive posture, Upright Submissive posture, Crouching, or Flee were not affected by IL-1beta. Overall these data support the notion that sickness behavior induced by IL-1beta administration represents an organized behavioral strategy and is not an aspecific response to an illness-type of condition.

Agonistic Behavior↗

Behavioural characterization of interleukin-6 overexpressing or deficient mice during agonistic encounters.

Interleukin-6 (IL-6) is a cytokine released by activated immune cells which has been shown to affect brain function. In this experiment aggressive and affiliative behaviour exhibited during agonistic encounters by transgenic male mice either not expressing (IL-6 -/-) or overexpressing (NSE-hIL-6) IL-6 in the central nervous system was investigated. All subjects were isolated for 24 days before the aggressive encounter and were 52 days old at the time of testing. Subjects were placed for 5 consecutive days in a neutral cage for 15 min with an opponent of the Balb/c strain that had been previously isolated for the same amount of time. The first and the last test sessions were videotaped to evaluate the first approach and the establishment of the social role, respectively. A number of behavioural categories were later scored. When compared with wild-type controls, IL-6 -/- mice showed a higher degree of aggressive behaviour as indicated by a higher frequency of Offensive Upright Posture, an effect more pronounced on the fifth encounter. On the contrary, NSE-hIL-6 subjects showed a tendency to be more involved in affiliative-type social interactions, displaying a higher frequency and duration of behaviours such as Anogenital, Nose or Body Sniff. IL-6 -/- mice showed a clear tendency to exhibit less affiliative interactions compared with their controls while dopamine levels were found to be modified in a number of brain regions in these mice. Overall, these data suggest that IL-6 affects both aggressive and affiliative-type interactions, although the behaviour of the NSE-hIL-6 subjects was less affected than that of the IL-6 -/- group. The effects of the genetic background of the animal in screening the outcome of gene manipulations on behaviour are also discussed.

3,4-Dihydroxyphenylacetic Acid↗

Postnatal NGF administration causes adult hyperalgesia and overreactivity to social stimuli but does not reverse capsaicin induced hypoalgesia.

The present longitudinal analysis was aimed at assessing (i) the effects of developmental capsaicin (CAPS) administration on nociceptive responsivity and on the response of adult mice to social stimuli; (ii) the action of NGF on the ontogeny of the same nociceptive response and social stimuli; (iii) whether capsaicin treatment could be reversed by subsequent treatment with NGF. CD-1 mouse pups were treated with either capsaicin (50 mg/kg, s.c.) or vehicle on postnatal days (PNDs) 5 and 8. Every other day from PND 9 to PND 21 the same pups received a daily injection of NGF (0.75 mg/kg, s.c.). During both the prepuberal stage (PNDs 14, 21, and 28) and adulthood, mice were repeatedly tested in a hot-plate apparatus (52 +/- 0.1 degrees C for 1 min). At adulthood they also underwent an aggressive behaviour test. NGF-treated mice showed a shorter latency to hindlimb licking response in the hot plate compared to both controls and NGF-CAPS groups. CAPS-treated subjects showed a long-lasting hypoalgesia at both prepuberal and adult stages that was not modified by subsequent NGF treatment. Finally, NGF-treated mice were more aggressive than both controls and CAPS-NGF animals.

Aggression↗

Removal of the submaxillary salivary glands first increases and then abolishes the agonistic response of male mice in repeated social encounters.

Adult male mice of the CD-1 strain were sialectomized (bilateral removal of submaxillary salivary glands) under IP Nembutal anesthesia and then individually housed for 5 weeks. Control mice were sham operated. The behaviors of sialectomized and control mice towards untreated, intact, matched opponents were videotaped during the first 10 min of a 20-min social encounter repeated for 10 consecutive days (isolation days 36-46). On the first session, sialectomized mice exhibited significant increases in elements of aggression (attack, bite, offensive sideways, offensive upright, and tail rattling). These behavioral changes significantly decreased over the remaining encounters, while defensive behaviors (defensive upright, oblique, parry, and defensive sideways) and elements of arrested flight increased progressively. The results suggest that sialectomy, perhaps by removing salivary NGF, interferes with the coping response of mice towards repeated agonist challenge from a conspecific.

Adaptation, Psychological↗

Neonatal capsaicin exposure affects isolation-induced aggressive behavior and hypothalamic substance P levels of adult male mice (Mus musculus).

Subcutaneous administration of capsaicin (50 mg/kg) at Postnatal Days 2 and 5 exerted long-term effects on isolation-induced aggressive behavior of adult mice (Mus musculus) of the CD-1 strain. Isolated capsaicin-treated mice (scored during a 10-min session) showed the highest frequency and the longest duration of total attacks, attacks, rattling, and offensive upright posture when compared with nonisolated capsaicin-treated subjects and both isolated and nonisolated vehicle control animals. Hypothalamic Substance P (SP) was assessed by radioimmunoassay. Capsaicin treatment significantly lowered hypothalamic SP content in both isolated and nonisolated mice. Moreover, individual scores of isolated capsaicin-treated subjects showed a significant correlation between SP depletion and expression of offensive upright posture. Isolation per se was revealed to play an important role in depleting SP from the hypothalamus.

Aggression↗

Capsaicin affects aggressive behavior, but not hot plate responding, of adult male mice.

Adult male mice of albino Swiss-derived CD-1 strain were used to assess the effects of capsaicin (a powerful agent that produces a marked depletion of the undecapeptide substance P) on both intraspecific aggressive behavior (induced by 8 weeks of individual housing) and pain sensitivity. Capsaicin was given SC, 48 h before behavioral testing. Aggressive behavior, scored during a 5-min session under red light, was significantly enhanced by capsaicin treatment (50 or 100 microliters of a 7.5 mg/ml solution). In fact, Total Aggressive Episodes, Attacks, and Upright Offensive Posture were significantly higher in the two capsaicin-treated groups, while Latency to the first Attack was decreased, when compared to both vehicle or unhandled controls. A concomitant decrease in Submissive Postures and Flee was also evident in capsaicin mice. Hot plate testing (55 +/- 0.1 degrees C, cutoff time 30 s), carried out on nonisolated mice, did not reveal any difference among the two capsaicin groups (same doses) and vehicle or unhandled controls.

Aggression↗

Scopolamine and acquisition of go-no go avoidance: a further analysis of the perseverative antimuscarinic deficit.

Rats treated with scopolamine (0.5 mg/kg SC daily) during the acquisition of a discrimination task with symmetrical negative reinforcement (light-go, noise/light-no go) showed a learning impairment, with both active and passive avoidance deficits. In the initial stage of such training, however, fewer passive avoidance errors and more active avoidance errors were made by treated animals if active avoidance pretraining had occurred in the no-drug state. A similar experiment using the same stimulus arrangement with asymmetrical reinforcement (no punishment of intertrial, and no go signal, responses) showed a scopolamine effect consisting mainly of increased responding to extinction signals and during intertrial intervals, with little or no active avoidance deficit. Furthermore, interactions due to changes in treatment conditions in successive stages of training were minimized in the latter task, suggesting that the effects of the shift-no shift factor on distribution of errors in the early stages of active-passive avoidance learning were unlikely to have been due to a genuine drug dissociation. Overall, these results and others obtained previously in the same and related tasks tend to rule out some unidimensional explanations of antimuscarinic effects, e.g., response disinhibition (an exclusively motor deficit) or impairment of stimulus sensitivity (an exclusively sensory deficit). The data rather confirm the notion of a sensorimotor drug bias leading to a shift in response prepotencies depending jointly on stimuli, responses, and response consequences. Prior learning history and behavioural compensation for adverse treatment consequences at the reinforcement level may interact with the sensorimotor bias so as to produce "set perseveration" (perseveration of response tendencies).

Animals↗

Behaviorally augmented tolerance during chronic cholinesterase reduction by paraoxon.

Repeated injection of paraoxon to pretrained rats 2 hr before avoidance sessions, at a dose causing considerable intoxication symptoms and reduction of brain acetylcholinesterase (0.125 mg/kg SC daily), induced marked performance depression followed by progressive development of tolerance. Additional groups treated either after each session (i.e., 23.5 hr before each subsequent session), or treated and not tested, showed a substantial depression when shifted to treatment 2 hr before sessions after achievement of tolerance by the animals tested from the beginning of the experiment at the time of maximal paraoxon effect. This indicates that chronic paraoxon tolerance cannot be ascribed entirely to metabolic and/or physiological changes occurring as a consequence of repeated treatment per se, but must be explained at least in part by postulating a behaviorally augmented (or "learned") component. In an additional experiment chronic paraoxon animals (0.1 mg/kg SC daily) were indistinguishable from control rats with respect to acquisition of light/go, noise-light/no go discrimination, i.e., of an active-passive avoidance task known to be highly sensitive to the disrupting (response-disinhibiting) effect of antimuscarinics. Therefore, the enhanced sensitivity to antimuscarinics in organophosphate tolerant rats, which is usually ascribed to cholinergic receptor changes, does not appear to be associated with a spontaneous "antimuscarinic-like" syndrome.

Animals↗