Evidence For Cross-sensitization Research Articles

Reciprocal effects of single or repeated exposure to methylphenidate or sex in adult male rats

Exposure to rewards can alter behavioral reactivity to them. For example, stimulants sensitize locomotor activation, whereas sexual experience sensitizes copulatory behaviors. Moreover, rewards can cross-sensitize one another. Although stimulants are known to cross-sensitize locomotor effects, the evidence for cross-sensitization between stimulants and sex is less clear. This study determined the effects of single and repeated pre-exposure to methylphenidate (MPH) or sex on one another in adult male rats. Cross-sensitization between MPH (5mg/kg) and sex (30min with sexually experienced female) was examined. Adult male rats were pre-exposed to 0, 1, or 10 trials of either sex or MPH before being exposed to the other reward. Locomotor chambers were used in MPH trials. Bilevel chambers were used in sexual trials, and sexual behaviors were video scored. The amount of prior sexual experience differentially influenced the ceiling of MPH-dependent sensitization; in the last drug trial, locomotion was highest in males given 1 previous sexual trial compared with 0 or 10. Compared with MPH-naive males, pre-exposure to MPH (1 and 10 trials) reduced the number of ejaculations without impacting sexual performance (intromission/mount latency and frequency). These findings indicate that the degree of pre-exposure to a reward can differentially affect reactivity to novel rewards. The results showed that previous findings of cross-sensitization between amphetamine and sex do not extend to MPH. However, exposure to MPH prior to sexual experience can increase the amount of sexual stimulation needed to achieve ejaculation.

Bivalent effects of MK-801 on ethanol-induced sensitization do not parallel its effects on ethanol-induced tolerance.

The relationship between the effects of the N-methyl-D-aspartate (NMDA) antagonist MK-801 on acute responses to ethanol and its ability to block ethanol sensitization and tolerance was examined in DBA/2J mice. Cross-sensitization between these drugs was also studied. Repeated administration of 0.1 mg/kg MK-801 with ethanol potentiated, whereas 0.25 mg/kg attenuated, sensitization to ethanol's locomotor stimulant effects; rearing was similarly affected. There was evidence for cross-sensitization between ethanol and 0.25 mg/kg MK-801. MK-801 potentiated ethanol's ataxic effects in the grid test, but had no effect on tolerance to this effect. MK-801's effects on ethanol sensitization appeared to be related to its own behavioral effects, rather than NMDA receptor blockade per se. Further, these studies demonstrate dissociation between ethanol sensitization and tolerance.

Pharmacological specificity of enhanced sensitivity to naltrexone in rats

Rats treated weekly with cumulative doses (1-100 mg/kg, IP) of naltrexone develop an enhanced sensitivity to the operant response-rate decreasing effect of naltrexone. In the present experiment the pharmacological specificity of that enhanced sensitivity was determined by testing a variety of drugs for cross-sensitivity to naltrexone. Cross-sensitivity was evaluated with two procedures. In one, dose-effect functions were determined for each of the test compounds before and after the development of enhanced sensitivity to naltrexone in a single group of rats. In the second procedure, one group of rats was made sensitive to naltrexone, while a second was not. Test compounds were then evaluated in both groups. For both procedures, a shift to the left in the dose-effect functions similar to naltrexone was considered evidence of cross-sensitivity. Of the opioid antagonists tested, only naloxone showed clear cross-sensitivity to naltrexone, although MR 2266 and diprenorphine also showed evidence of cross-sensitivity. The opioid antagonist quadazocine did not show cross-sensitivity to naltrexone on the day of testing, although some evidence of cross-sensitivity was evident 24 h later. In addition, the dose-effect function for d-amphetamine was significantly changed following naltrexone treatment. No evidence of cross-sensitivity was observed for the optical isomer of naloxone, d-naloxone, or for naloxone's quaternary derivative, naloxone methiodide. None of the opioid agonists or agonist-antagonists tested showed cross-sensitivity to naltrexone (i.e. morphine, U-50, 488H, ethylketocyclazocine, N-allylnormetazocine and pentazocine). The non-opioid drugs chlordiazepoxide and phencyclidine also failed to show evidence of cross-sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Implications of behavioral sensitization and kindling for stress-induced behavioral change.

Psychomotor stimulant-induced behavioral sensitization and electrophysiological kindling are not animal models of stress with obvious face validity; however, we discuss them here as they may guide us to new principles concerning changes in long-term responsivity in behavior that may be relevant to some stress situations. Moreover, there is an extensive literature indicating that there are important interactions between psychomotor stimulant-induced behavioral sensitization and stress-induced behavioral alterations. Stimulants such as amphetamine and cocaine are thought to exert many of their actions by potentiating noradrenergic and dopaminergic neurotransmission. Stresses, in many instances, are also capable of acting on these catecholamine and related neurochemical substrates. Thus, it is not surprising that under some conditions, stresses may facilitate subsequent reactivity to psychomotor stimulants and, vice-versa, that psychomotor stimulant pretreatment may enhance stress responsivity. Seymour Antelman and colleagues have reviewed elsewhere (1,2) evidence for cross-sensitization between stress and stimulants. It is not the point of this paper to argue that this is a universal principle; we and others have observed in some instances that stresses may decrease subsequent stimulant-induced behavior. What we are suggesting is that, in many instances, stimulant-induced effects on short- and long-term alterations in behavior may be mediated by the same neurochemical systems that are relevant to the consideration of stress-induced changes in behavior.KeywordsPanic AttackBehavioral SensitizationRapid CyclingCocaine SensitizationBehavioral PathologyThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Ninety-eight fixed drug eruptions with provocation tests.

Ninety-eight patients having fixed drug eruptions were subjected to provocation tests. Cutaneous involvement was seen in 43, mucous membrane in 33 patients, while cutaneous and mucous membrane involvement was seen in 22 patients. The causative drugs were found to be trimethoprim-sulphamethoxazole (45), acetylsalicylic acid (24), hyoscine butylbromide (Buscopan) (8), ibuprofen (Brufen) (6), oxyphenbutazone (6), tetracycline hydrochloride (2), phenolphthalein (1) and phenobarbitone (1). There was evidence of cross-sensitivity between oxyphenbutazone and phenylbutazone.

Drugs causing fixed eruptions.

ABSTRACTSeventy one patients having fixed drug eruptions were subjected to provocation tests. The greatest number of cases were due to acetylsalicylic acid (18). Other drugs responsible were hyposcine butylbromide (15), oxyphenbutazone (14), sulphadiazine (7), tetracycline hydrochloride (6), metamizole (5) and ibuprofen (3). Other drugs were less frequent. There was evidence of cross sensitivity between various tetracyclines and sulphonamides and also between oxyphenbutazone and phenylbutazone. One patient had two groups of lesions, each reacting to a different, chemically unrelated drug.

Drugs causing fixed eruptions

Forty patients having fixed drug eruptions were subjected to provocation tests. Twelve patients failed to complete the provocation tests while in the remaining, the causative drugs were shown to be tetracyclines (6), analgin (metamizole) (6), oxyphenbutazone (5), phenobarbitone (4), sulphadiazine (3), sulphaphenazole (2), penicillin (1), suphadimethoxone (1), Saridon (1), sulphadimidine (1) and sulphamethoxypryridazine (1). There was evidence of cross-sensitivity between tetracycline and demethylchlortetracycline and also between exyphenbutazone and phenylbutazone, but not between different sulphonamides, In 2 cases, the minimum dose of the drug capable of reactivating the lesions was 100 mg of sulphadiazine and 50 mg of Saridon respectively.

Attenuation of Contact Sensitization in Man

Attenuation of Contact Sensitization in Man