Prepubertal and adult male rats differ in the degree and pattern of stress reactive neurons in brain regions that project to the paraventricular nucleus of the hypothalamus.

The hormonal stress response, mediated by the hypothalamic-pituitary-adrenal (HPA) axis, shows greater responsiveness to various stressors in prepubertal compared to adult animals. Though the implications of this age-related change are unclear, this heightened reactivity might contribute to the increase in stress-related dysfunctions observed during adolescence. Interestingly, prepubertal animals show greater stress-induced neural activation compared to adults in the paraventricular nucleus of the hypothalamus (PVN), the area responsible for initiating the hormonal stress response. Thus, it is possible that direct afferents to the PVN, such as the anterior bed nucleus of the stria terminalis (aBST), nucleus of the solitary tract (NTS), posterior BST (pBST), medial preoptic area (MPOA), and dorsomedial nucleus (DMN), contribute to this age-dependent change in reactivity. To investigate these possibilities, two separate experiments were conducted in prepubertal (30 days old) and adult (70 days old) male rats using the retrograde tracer, Fluoro-Gold (FG), and FOS immunohistochemistry to study neural connectivity and activation, respectively. Though there was no difference in the number or size of FG-positive cells in the PVN afferents we examined, we found a significantly greater number of stress-induced FOS-like-positive cells in the aBST and significantly fewer in the DMN in prepubertal compared to adult animals. Together these data suggest that functional, instead of structural, changes in nuclei that project to the PVN may lead to the greater PVN stress responsiveness observed prior to adolescence. Furthermore, these data indicate that nuclei known to directly modulate HPA stress responsiveness show differential activation patterns before and after adolescent development.

Sterile Gelatin Film Reduces Cortical Injury Associated With Brain Tumor Re-Resection.

BACKGROUND: Recurrent intracranial tumors frequently require re-resection. Dural adhesions to the cortex increase the morbidity and duration of these revision craniotomies. OBJECTIVE: To describe the use of commercially available sterile gelatin film to prevent meningocerebral adhesions and decrease the rate of surgically induced ischemia from revision craniotomy. METHODS: This retrospective cohort study examined patients with recurrent glioma, meningioma, and metastasis who underwent re-resection at least 30 d following their initial tumor resection. Cortical surface tissue ischemia after re-resection on diffusion-weighted magnetic resonance imaging was compared for patients with (gelatin film group) and without (nongelatin film group) a history of gelatin film placement at the conclusion of their initial tumor resection. RESULTS: A total of 84 patients in the gelatin film group were compared to 86 patients in the nongelatin film group. Patient age, sex, tumor pathology, tumor volume, tumor eloquence, laterality of surgical approach, history of radiotherapy, and time interval between resections did not differ between groups. Radiographic evidence of cortical ischemia following reoperation was less prevalent in the gelatin film group (13.1% vs 32.6%; P < .01). In multivariate logistic regression analysis, no gelatin film (P < .01) and larger tumor size (P = .02) predicted cortical surface ischemia following revision craniotomy. Postoperative complications in the gelatin film and nongelatin film group otherwise did not differ. CONCLUSION: Routine placement of commercially available sterile gelatin film on the cortex prior to dural closure is associated with decreased surgically induced tissue ischemia at the time of revision tumor craniotomy.

Surgical morbidity of transsylvian versus transcortical approaches to insular gliomas.

OBJECTIVE: The choice of transsylvian versus transcortical corridors for resection of insular gliomas remains controversial. Functional pathway compromise from transcortical transgression and vascular injury during transsylvian dissection are the primary concerns. In this study, data from a single-center experience with both approaches were compared to determine whether one approach was associated with a higher rate of morbidity than the other. METHODS: The authors identified 100 consecutive patients who underwent resection of pure insular gliomas at the Barrow Neurological Institute. Volumetric analysis was performed using FLAIR and contrast-enhanced T1-weighted MRI for low- and high-grade gliomas, respectively, for extent of resection (EOR) and diffusion-weighted sequences were used to detect for postoperative ischemia. Step-wise logistic regression analysis was performed to identify predictors of neurological morbidity. RESULTS: Data from 100 patients with low-grade or high-grade insular gliomas were analyzed. Fifty-two patients (52%) underwent a transsylvian approach, and 48 patients (48%) underwent a transcortical approach. The mean (± SD) EOR was 91.6% ± 12.4% in the transsylvian group and 88.6% ± 14.2% in the transcortical group (p = 0.26). Clinical outcome metrics for the 2 groups were similar. Overall, 13 patients (25%) in the transsylvian group and 10 patients (21%) in the transcortical group had evidence of ischemia on postoperative MR images. For both approaches, high-grade histology was associated with permanent morbidity (p = 0.01). For patients with gliomas located within the superior-posterior quadrant of the insula, development of postoperative ischemia was associated with only the transsylvian approach (46% vs 0%, p = 0.02). CONCLUSIONS: Areas of restricted diffusion are common on postoperative MRI following resection of insular gliomas, but only a minority of these patients develop permanent neurological deficits. Insular glioma patients with high-grade histology may be at particular risk for developing symptomatic postoperative ischemia. Both the transcortical and transsylvian corridors are associated with reasonable morbidity profiles, although gliomas situated within the superior-posterior quadrant of the insula are more safely accessed with a transcortical approach.

Adolescence and the ontogeny of the hormonal stress response in male and female rats and mice.

Adolescent development is marked by many changes in neuroendocrine function, resulting in both immediate and long-term influences on an individual's physiology and behavior. Stress-induced hormonal responses are one such change, with adolescent animals often showing different patterns of hormonal reactivity following a stressor compared with adults. This review will describe the unique ways in which adolescent animals respond to a variety of stressors and how these adolescent-related changes in hormonal responsiveness can be further modified by the sex and previous experience of the individual. Potential central and peripheral mechanisms that contribute to these developmental shifts in stress reactivity are also discussed. Finally, the short- and long-term programming effects of chronic stress exposure during adolescence on later adult hormonal responsiveness are also examined. Though far from a clear understanding of the neurobehavioral consequences of these adolescent-related shifts in stress reactivity, continued study of developmental changes in stress-induced hormonal responses may shed light on the increased vulnerability to physical and psychological dysfunctions that often accompany a stressful adolescence.

Stress-induced oxytocin release and oxytocin cell number and size in prepubertal and adult male and female rats.

Studies indicate that adolescent exposure to stress is a potent environmental factor that contributes to psychological and physiological disorders, though the mechanisms that mediate these dysfunctions are not well understood. Periadolescent animals display greater stress-induced hypothalamic-pituitary-adrenal (HPA) axis responses than adults, which may contribute to these vulnerabilities. In addition to the HPA axis, the hypothalamo-neurohypophyseal tract (HNT) is also activated in response to stress. In adults, stress activates this system resulting in secretion of oxytocin from neurons in the supraoptic (SON) and paraventricular (PVN) nuclei. However, it is currently unknown whether a similar or different response occurs in prepubertal animals. Given the influence of these hormones on a variety of emotional behaviors and physiological systems known to change as an animal transitions into adulthood, we investigated stress-induced HPA and HNT hormonal responses before and after stress, as well as the number and size of oxytocin-containing cells in the SON and PVN of prepubertal (30d) and adult (70d) male and female rats. Though we found the well-established protracted adrenocorticotropic hormone and corticosterone response in prepubertal males and females, only adult males and prepubertal females showed a significant stress-induced increase in plasma oxytocin levels. Moreover, though we found no pubertal changes in the number of oxytocin cells, we did find a pubertal-related increase in oxytocin somal size in both the SON and PVN of males and females. Taken together, these data indicate that neuroendocrine systems can show different patterns of stress reactivity before and after adolescent development and that these responses can be further modified by sex. Given the impact of these hormones on a variety of systems, it will be imperative to further explore these changes in hormonal stress reactivity and their role in adolescent health.