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.2024 Aug 25;14(9):855.
doi: 10.3390/brainsci14090855.

Nicotine's Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters

Affiliations

Nicotine's Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters

Ana Carolina Dutra-Tavares et al. Brain Sci..

Abstract

Tobacco consumption in schizophrenia (SCHZ) patients is highly prevalent. Data support the occurrence of sequential events during comorbidity establishment, and both smoking first, SCHZ second and SCHZ first, smoking second sequences have been proposed. To investigate whether these two possibilities lead to distinct outcomes of comorbidity, we used a phencyclidine-induced SCHZ model and nicotine exposure as a surrogate of smoking. C57Bl/6 mice were submitted to a protocol that either began with 4 days of phencyclidine exposure or 4 days of nicotine exposure. This period was followed by 5 days of combined phencyclidine + nicotine exposure. Locomotor sensitization and pre-pulse inhibition (PPI) were assessed due to their well-known associations with SCHZ as opposed to rearing, an unrelated behavior. Nicotine priming potentiated phencyclidine-evoked sensitization. However, nicotine exposure after SCHZ modeling did not interfere with phencyclidine's effects. In the PPI test, nicotine after SCHZ modeling worsened the phencyclidine-evoked deficiency in males. In contrast, nicotine priming had no effects. Regarding rearing, nicotine priming failed to interfere with phencyclidine-mediated inhibition. Similarly, phencyclidine priming did not modify nicotine-mediated inhibition. The present results indicate that the sequence, either SCHZ-first or nicotine-first, differentially impacts comorbidity outcomes, a finding that is relevant for the identification of mechanisms of nicotine interference in the neurobiology of SCHZ.

Keywords: E-cigarette; NMDA receptor antagonism; comorbidity; positive symptoms; pre-pulse inhibition; psychosis; smoking; tobacco.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 2
Figure 2
Distance traveled as a measure of locomotor activity in the open field during Acquisition (ACQ) phase 1 of Experiment 1 (a) and Experiment 2 (b). Each session (ACQ1, ACQ2, ACQ3, and ACQ4) lasted 40 min, which was divided into 2 intervals (Int1 and Int2) of 20 min each. The mice from Experiment 1 were either exposed daily to phencyclidine (PCP group) or received saline injections (VEH group). As for Experiment 2, the mice either received nicotine (NIC group) or saline (VEH group) before the tests. Values are means ± S.E.M. *p < 0.05, ***p < 0.001 vs. NIC group within a given interval.
Figure 3
Figure 3
Distance traveled as a measure of locomotor activity in the open field during Acquisition (ACQ) phase 2 of Experiment 1 (a) and Experiment 2 (b). Each session (ACQ5, ACQ6, ACQ7, and ACQ8) lasted 40 min and was divided into 2 intervals (Int1 and Int2) of 20 min each. Data are shown separately for 4 experimental groups. The vehicle (VEH) group received saline injections throughout the experimental protocol. In Experiment 1, half of the mice that received saline injections in ACQ phase 1 received nicotine from ACQ5 to ACQ8 (VEH/NIC group). As for the mice that received phencyclidine during ACQ phase 1, half received 4 additional days of phencyclidine injections (PCP/PCP group), while the other half, in addition to phencyclidine, were exposed to nicotine (PCP/PCPNIC group). In Experiment 2, half of the mice that received saline injections in ACQ phase 1 received phencyclidine from ACQ5 to ACQ8 (VEH/PCP group). As for the mice that received nicotine during ACQ phase 1, half received 4 additional days of nicotine injections (NIC/NIC group), while the other half received both phencyclidine and nicotine (NIC/PCPNIC group). Values are means ± S.E.M.††† p < 0.001: for Experiment 1 (a), VEH and VEH/NIC vs. PCP/PCP PCP/PCPNIC, and for Experiment 2 (b), VEH and NIC/NIC vs. VEH/PCP and NIC/PCPNIC. *p < 0.05, **p < 0.01 and ***p < 0.001 for comparisons between groups as indicated in the graphs or between intervals (boxes);&p < 0.05, and&&&p < 0.001 vs. PCP/PCP or VEH/PCP, while### p < 0.001 vs. NIC/PCPNIC and$ p < 0.05 and$$ p < 0.01 sex differences within a given group; different colors indicate the groups that were compared.
Figure 4
Figure 4
Number of rearings in the open field during Acquisition (ACQ) phases 1 (A and B) and 2 (C and D). The first and last 10 min (Int1 and Int2) of ACQ1, ACQ4, ACQ5, and ACQ8 were analyzed. During ACQ phase 1 of Experiment 1 (a), the mice were either exposed daily to phencyclidine (PCP group) or received saline injections (VEH group) from ACQ1 to ACQ4. As for ACQ phase 1 of Experiment 2 (b), the mice either received nicotine (NIC group) or saline (VEH group). During ACQ phase 2 of Experiment 1 (c), half of the mice that received saline injections in ACQ phase 1 received additional saline injections (VEH group), while the other half received nicotine from ACQ5 to ACQ8 (VEH/NIC group). As for the mice that received phencyclidine during ACQ phase 1, half received 4 additional days of phencyclidine injections (PCP/PCP group), while the other half, in addition to phencyclidine, were exposed to nicotine (PCP/PCPNIC group). During ACQ phase 2 of Experiment 2 (d), half of the mice that received saline injections in ACQ phase 1 received additional daily saline injections (VEH group), while the other half received phencyclidine (VEH/PCP group). As for the mice that received nicotine during ACQ phase 1, half received 4 additional days of nicotine injections (NIC/NIC group), while the other half received both phencyclidine and nicotine (NIC/PCPNIC group). Values are means ± S.E.M. *p < 0.05, **p < 0.01 and ***p < 0.001 VEH vs. all other groups or for comparisons between intervals (boxes).### p < 0.001 PCP/PCP vs. all other groups.
Figure 1
Figure 1
Timeline of experiments 1 and 2.
Figure 5
Figure 5
Percentage of pre-pulse inhibition (%PPI) at 70, 75, and 80 dB in males and females. For both Experiment 1 (a) and Experiment 2 (b), data are shown separately for 4 experimental groups. In the Experiment 1 indent, data from 80 dB pP are exhibited separately for males and females to show the interference of nicotine in phencyclidine-evoked deficits. The vehicle (VEH) group received saline injections throughout the experimental protocol. In Experiment 1 (a), half of the mice that received saline injections in ACQ phase 1 received nicotine from ACQ5 to PPI (VEH/NIC group). As for the mice that received phencyclidine during ACQ phase 1, half received 5 additional days of phencyclidine injections (PCP/PCP group), while the other half, in addition to phencyclidine, was exposed to nicotine (PCP/PCPNIC group). In Experiment 2 (b), half of the mice that received saline injections in ACQ phase 1 received phencyclidine from ACQ5 to PPI (VEH/PCP group). As for mice that received nicotine during ACQ phase 1, half received 5 additional days of nicotine injections (NIC/NIC group), while the other half received both phencyclidine and nicotine (NIC/PCPNIC group). In a separate experiment (c), the mice were tested immediately after acute exposures to phencyclidine and nicotine. VEHacute = vehicle group; PCPacute = acutely exposed to phencyclidine; PCPNIC = acutely exposed to phencyclidine and nicotine.† p < 0.05,†† p< 0.01, and††† p < 0.001 for Experiment 1 (a), VEH and VEH/NIC vs. PCP/PCP PCP/PCPNIC, and for Experiment 2 (b), VEH and NIC/NIC vs.VEH/PCP and NIC/PCPNIC;&p < 0.05 vs. PCP/PCP, and### p < 0.001 vs. PCP/PCPNIC. *p < 0.05, **p < 0.01.
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