Fig. 1. Modifications by a previous exposure to hot plate of the latencies of avoidance reactions at the second exposure, performed at various times after the first one. At various times (3 h, 24 h, 8 days, 16 days and 24 days) after the first exposure to the hot plate, the avoidance latencies were measured at a second exposure. The percentage of mice which lick their paws in the second exposure are indicated vertically between parentheses. M ± SEM of 50 (for the first exposure) and 10 mice per group. No symbol P > 0.05; ***P < 0.001 as compared to first exposure values by using one way ANOVA followed by Newman–Keuls test (for latency) and χ² test (for % of responding mice). The SEM of mean of licking latencies was not calculated since most of mice preexposed to the hot plate did not lick their paws.

Fig. 2. Effect of an electroconvulsive shock (ECS) applied immediately after the first hot plate exposure, on the avoidance reaction latencies measured, at the second exposure, 2 days later. An ECS (9 mA, 1 s) was applied by bi-auricular electrodes to mice, immediately after their jump from the hot plate. They were tested 2 days later on the hot plate. The percentage of mice which lick their paws in the second exposure are indicated vertically between parentheses. M ± SEM of 10 mice per group. No symbol P > 0.05; **P < 0.01; ***P < 0.001, as compared to respective group not previously exposed to the hot plate by using Newman–Keuls test (for latency) and χ² test (for % of responding mice). A two-way ANOVA failed to reveal significant interactions between ECS effect and exposure: F(1,36) = 2.07; P = 0.16. The SEM of mean of licking latencies was not calculated since most of mice preexposed to the hot plate did not lick their paws.

Fig. 3. Effect of an ether anesthesia delivered immediately after the first hot plate exposure on the latencies of avoidance reaction at the second exposure 2 days later. An ether anesthesia was delivered to mice immediately after the jump from the hot plate; they were tested 48 h later on the hot plate. The percentage of mice which lick their paws in the second exposure are indicated between parentheses. M ± SEM of 10 mice per group. No symbol P > 0.05; ***P < 0.001 as compared to respective group previously submitted or not to ether anesthesia by using Newman–Keuls test (for latency) and χ test (for % of responding mice). A two-way ANOVA failed to reveal significant interactions between ether anesthesia treatment and exposure: F(1,36) = 0.46; P = 0.50. The SEM of mean of licking latencies was not calculated since most of mice preexposed to the hot plate did not lick their paws.

Fig. 4. Effect of a pretreatment by diazepam on the modifications in latencies of avoidance reaction of mice exposed 2 days before to the hot plate. Saline or diazepam (1 mg/kg) was injected i.p. 20 min before the first exposure to the hot plate; 2 days later, they were exposed a second time to the hot plate, and their latencies of avoidance reactions were measured. The percentage of mice which lick their paws in the second exposure are indicated vertically between parentheses. M ± SEM of 10 mice per group. No symbol P > 0.05; *P < 0.05; **P < 0.01; ***P < 0.001 as compared to their respective first exposure groups by using Newman–Keuls test (for latency) and χ² test (for % of responding mice). a: P < 0.05; b: P < 0.01 as compared to their respective control groups. A two-way ANOVA failed to reveal significant interactions between diazepam treatment and exposure: F(1,36) = 1.83; P = 0.19. The SEM of mean of licking latencies was not calculated since most of mice preexposed to the hot plate did not lick their paws.

Modifications by a first exposure to the hot plate either at 35 °C or 55 °C of the avoidance reaction of latencies at a second exposure, performed 48 h later, at 55 °C

Mice of groups A and C were exposed, respectively, first time to the hot plate 55 °C and 35 °C. The second exposure to the hot plate (55 °C) of A and C groups occurred 48 h after the first exposure, simultaneously as the first exposure of the animals of the B group (control). M ± SEM of 10 mice per group. No symbol P > 0.05; **P < 0.01; ***P < 0.001 as compared to respective first exposure values by using one way ANOVA followed by the Newman–Keuls test (for latency) and χ² test (for % of responding mice).

Modifications of the avoidance reaction latencies measured 48 h after a first exposure to the hot plate in mice treated with morphine either before or immediately after the first exposure

Saline or morphine (5 mg/kg) was injected s.c. to mice, either 30 min before (groups E and F) or immediately after (groups A and B) the first exposure to the hot plate. Two days later, they were exposed a second time to the hot plate, simultaneously as the first exposure of the animals of control groups C and D, and their latencies of avoidance reactions were measured. Since mice injected with morphine before the exposure to the hot plate neither licked their paws nor jumped, we decided a cut off time of 60 s in the same order that the jumping time of saline-injected mice. M ± SEM of 10 mice per group. No symbol P > 0.05; **P < 0.01; ***P < 0.001 as compared to their respective values at the first exposure (groups A and B) or to groups only previously injected with saline (group C) or morphine (group D) but not exposed to the hot plate by using one and two way ANOVA followed by Newman–Keuls test (for latency) and χ² test (for % of responding mice). A two-way ANOVA failed to reveal significant interactions between morphine (treatment after first exposure) treatment and exposure: F(1,36) = 0.0006; P = 0.981.

Effect of a pretreatment by increasing doses of scopolamine on the modifications in avoidance reaction latencies of mice exposed 2 days before to the hot plate

Saline or scopolamine (0.75, 1.5 or 3 mg/kg) was injected s.c. 20 min before the first exposure to the hot plate. Two days later, they were exposed a second time to the hot plate, and their avoidance reaction latencies were measured. M ± SEM of 10 mice per group. No symbol P > 0.05; **P < 0.01; ***P < 0.001 as compared to their respective 1st exposure groups by using Newman–Keuls test (for latency) and χ² test (for % of responding mice). c: P < 0.001 as compared to their respective control groups. A two-way ANOVA failed to reveal significant interactions between scopolamine treatment and exposure: F(3,72) = 0.32; P = 0.82.

Modifications of the avoidance reaction latencies measured 48 h after a first exposure to the hot plate in mice treated with haloperidol

Saline or haloperidol (50, 100 and 200 μg/kg) was injected i.p. to mice, 20 min before the first exposure (A–D) or immediately after the first exposure (E, F) to the hot plate. Two days later, they were exposed a second time to the hot plate, simultaneously as the first exposure of the animals of controls group (G, H), and their latencies of avoidance reactions were measured. M ± SEM of 10 mice per group. No symbol P > 0.05; *P < 0.05; **P < 0.01 as compared to their respective 1st exposure groups, by using Newman–Keuls test (for latency) and χ² test (for % of responding mice). b: P < 0.01; c: P < 0.001 as compared to their respective control groups. A two-way ANOVA reveals a significant interaction between haloperidol treatment and exposure: F(3,72) = 3.17; P < 0.05 (for group treated before the first exposure) and F(1,36) = 5.38; P < 0.05 (for group treated after the first exposure).