Inhibitory control failures and blunted cortisol response to psychosocial stress in amphetamine consumers after 6 months of abstinence

Amphetamine abuse has been conceived as an addictive illness where stress regulation and inhibitory control may be crucial factors determining chronicity and relapse. Since amphetamine consumption may disrupt the cerebral systems regulating inhibition and stress behaviors, deregulation on these systems may be expected even after long-term abstinence periods. The present study aimed to evaluate the ability of abstinent amphetamine consumers to regulate stress parameters and to inhibit cognitive patterns under the acute trier social stress test (TSST) paradigm. Materials and Methods, a cohort study was conducted in a sample of 44 young individuals (average age: 24.6 years). The sample included 22 amphetamine consumers recruited from an addiction treatment center and 22 healthy nonconsumers belonging to the same sociodemographic conditions. Both groups were exposed to the TSST once the consumers completed 6 months in abstinence. To evaluate stress reactivity, we collected five saliva samples distributed before, during, and after stress exposure. Inhibitory capacity was also assessed before and after stress using the Stroop and d2 cancellation tests. Results, under stress conditions, cortisol measures were significantly lower in amphetamine consumers (1105.34 ± 756.958) than in healthy nonconsumers (1771.86 ± 1174.248) P = 0.022. Without stress, amphetamine consumers also showed lower cortisol values (1027.61 ± 709.8) than nonconsumers (1844.21 ± 1099.15) P = 0.016. Regarding inhibitory capacity, stress also was associated to consumer's lower scores on the Stroop (5.17 ± 8.34 vs. 10.58 ± 7.83) P = 0.032 and d2 tests (190.27 ± 29.47 vs. 218.00 ± 38.08) P = 0.010. Conclusion: We concluded that both the stress regulatory system and executive function system (attentional/inhibitory control) represent key vulnerability conditions to the long-term effect of compulsive amphetamine consumption

Chronic exposure of juvenile rats to environmental noise impairs hippocampal cell proliferation in adulthood

Increasing evidence indicates that chronic exposure to environmental noise may permanently affect the central nervous system. The aim of this study was to evaluate the long-term effects of early exposure to environmental noise on the hippocampal cell proliferation of the adult male rat. Early-weaned Wistar rats were exposed for 15 days to a rats′ audiogram-fitted adaptation to a noisy environment. Two months later, the rats were injected with the cellular proliferation marker 5΄bromodeoxiuridine (BrdU), and their brains were processed for immunohistochemical analysis. Coronal sections were immunolabeled with anti-BrdU antibodies to identify new-born cells in dentate gyrus (DG), cornu amonis areas CA1 and CA3. In addition, blood samples were obtained to evaluate corticosterone serum levels after noise exposure. All data are expressed as mean΁standard deviation. For mean comparisons between groups, we used the Student t test. We found an increase in corticosterone serum levels after environmental noise exposure. Interestingly, noise-exposed rats showed a long-term reduction of proliferating cells in the hippocampal formation, as compared to controls. These findings indicate that chronic environmental noise exposure at young ages produces persistent non-auditory impairment that modifies cell proliferation in the hippocampal formation

Combined approach for experimental Oto-neurosurgical procedures

Background: Experimental procedures will continue to be a key element while going through the learning curve in the use of the endoscope and minimally invasive procedures. We describe the technical procedure of an experimental approach to middle ear in New Zealand rabbits through external auditory canal and its relevance as an ideal model to study graft materials and serve as a training tool for potential applications in otoneurology. Methods: A group of 28 adult New Zealand rabbits were subjected to an experimental myringoplasty, combining the transmeatal and retroauricular approach with endoscopic assistance and microsurgical technique. The different anatomical steps and systematization of the complete experimental procedure are described. Results: An experimental approach to middle ear live model and basic anatomic description was successfully used, standardizing the ideal technique. The eardrum could regenerate with no complications and with functional preservation in all the myringoplasty cases. This strategy involves a safe combined approach to the tympanic membrane and others neurosurgical as transcochlear and translaberyntic approaches and is useful as a test of other experimental procedures to evaluate biomaterials to repair the eardrum currently studied. This experimental myringoplasty model also facilitates functional tests such as impedanciometry and the endoscopic follow-up of the whole process. Conclusions: The method described to perform an experimental myringoplasty (type I tympanoplasty) in a New Zealand rabbit is an option to be used as a basic model to study the behavior of the graft in the tympanic membrane. Also, basic concepts for the use of combined instrumentation are established in the treatment of eardrum lesions, as a refinement of the technical training application in microsurgery and assisted endoscopy in the transcochlear and translaberintic approaches and otoneurology areas. Copyright © 2012 Macías-Reyes. H

Early-life exposure to noise reduces mPFC astrocyte numbers and T-maze alternation/discrimination task performance in adult male rats

In this experiment, we evaluated the long-term effects of noise by assessing both astrocyte changes in medial prefrontal cortex (mPFC) and mPFC-related alternation/discrimination tasks. Twenty-one-day-old male rats were exposed during a period of 15 days to a standardized rats′ audiogram-fitted adaptation of a human noisy environment. We measured serum corticosterone (CORT) levels at the end of the exposure and periodically registered body weight gain. In order to evaluate the long-term effects of this exposure, we assessed the rats′ performance on the T-maze apparatus 3 months later. Astrocyte numbers and proliferative changes in mPFC were also evaluated at this stage. We found that environmental noise (EN) exposure significantly increased serum CORT levels and negatively affected the body weight gain curve. Accordingly, enduring effects of noise were demonstrated on mPFC. The ability to solve alternation/discrimination tasks was reduced, as well as the number of astroglial cells. We also found reduced cytogenesis among the mPFC areas evaluated. Our results support the idea that early exposure to environmental stressors may have long-lasting consequences affecting complex cognitive processes. These results also suggest that glial changes may become an important element behind the cognitive and morphological alterations accompanying the PFC changes seen in some stress-related pathologies