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  Table of Contents    
Year : 2011  |  Volume : 13  |  Issue : 53  |  Page : 286-291
Chronic exposure of juvenile rats to environmental noise impairs hippocampal cell proliferation in adulthood

1 Department of Neurosciences, Health sciences University Center, University of Guadalajara; Biomedic Research University Center (CUIB), University of Colima, Mexico
2 Department of Neurosciences, Health sciences University Center, University of Guadalajara; Neurosciences Division, CIBO, Mexican Social Security Institute, Guadalajara, Mexico
3 Department of Neurosciences, Health sciences University Center, University of Guadalajara, Mexico
4 Biomedic Research University Center (CUIB), University of Colima, Mexico
5 Cellular neurobiology Lab, CUCBA, University of Guadalajara, Mexico
6 Neuroscience Lab, School of Psychology, University of Colima, Mexico

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Date of Web Publication14-Jul-2011

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.

Keywords: Dentate gyrus, environmental noise, hippocampus, neurogenesis

How to cite this article:
Jáuregui-Huerta F, García-Estrada J, Ruvalcaba-Delgadillo Y, Trujillo X, Huerta M, Feria-Velasco A, Gonzalez-Perez O, Luquín S. Chronic exposure of juvenile rats to environmental noise impairs hippocampal cell proliferation in adulthood. Noise Health 2011;13:286-91

How to cite this URL:
Jáuregui-Huerta F, García-Estrada J, Ruvalcaba-Delgadillo Y, Trujillo X, Huerta M, Feria-Velasco A, Gonzalez-Perez O, Luquín S. Chronic exposure of juvenile rats to environmental noise impairs hippocampal cell proliferation in adulthood. Noise Health [serial online] 2011 [cited 2021 Jan 25];13:286-91. Available from: https://www.noiseandhealth.org/text.asp?2011/13/53/286/82961

  Introduction Top

Environmental noise can disrupt the physiological function of both auditory and non-auditory systems. Deleterious effects of noise on the central nervous system (CNS) may be produced by over-stimulation of audition-related structures and by increasing the activity of non-auditory structures. Classical auditory structures commonly affected by noise include the cochlear nucleus, [1] inferior colliculus [2],[3] and auditory cortex. [4],[5] The hippocampal formation, on the other hand, has been proposed to be a potential extra-auditory target for the deleterious effects of noise. It has been shown that chronic or intense exposure to noise impairs hippocampus-dependent memory, [6] reduces the number of hippocampal neurons and their ramifications, [7] enhances cell death of granule and pyramidal neurons, [8] and produces an increase in the firing frequency of hippocampus place cells. [9] The hippocampus is a limbic structure crucial for the formation of explicit memory in humans [10] and spatial memory in rodents, [11] which has been also recognized as a key target for environmental factors. [7],[9],[12] Particularly, hippocampal neurogenesis in the adult brain has been studied in relation to environmental conditions. (For review, see [13] .)

It has been long recognized that early environmental stimuli play a critical role during brain development. [14] Adverse experience can modify permanently the brain structure when such experience is undergone in the early stages of life. In the rat, the maturation process of hippocampus occurs few weeks after birth. [15] Thus prenatal chronic or intense exposure to noxious events affects hippocampal development, [16] and it has been suggested that such effects persist in later stages of life. [17] The hippocampal vulnerability to the effects of noise exposure at early-weaned stages is unknown and it is also unclear whether these deleterious effects persist in later stages. Since hippocampal cell proliferation is a potential target for detrimental effects of environmental noise, we tested the hypothesis that chronic exposure to environmental noise during early life modifies hippocampal cell proliferation in the adult stages. The aim of the study was then to evaluate the long-term effects of early exposure to environmental noise on the hippocampal cell proliferation of the adult male rat. Our findings indicated that chronic environmental noise exposure at young ages reduces the cell proliferation in the dentate gyrus and the CA3 region in the adult hippocampus.

  Methods Top


The subjects were 30 Swiss Wistar male rats randomly obtained from an in-house breeding facility at the Centro de Investigacion Biomedica de Occidente, Guadalajara, Mexico. The rats were weaned on postnatal day 21 (PND 21), housed in standard polycarbonate cages and maintained on a 12-hour light-dark cycle, with lights on at 07:00. Standard Purina; rat chow pellets and tap water were provided ad libitum. Experimental procedures were approved by the institutional ethics commission and were in accordance to the US National Institute of Health Guide for the Care and Use of Laboratory Animals. Body weight was measured routinely on PNDs 21, 24, 28, 32, 36 and 40; and thereafter, weekly, until PND 90.

Environmental exposure to noise (PNDs 21-35)

For chronic environmental exposure to noise, the rats' audiogram-fitted adaptation of a noisy environment (kindly provided by Dr. A. Rabat) was employed. [18] [Figure 1] illustrates the general procedure followed in these experiments. Briefly, urban audio files containing unpredictable noise events with a duration ranging from 18 to 39 seconds and spaced by silent intervals ranging from 20 to 165 seconds were randomly presented to rats during the dark phase (19:00 to 07:00) throughout the 15 days post-weaning (i.e., PNDs 21-35). Animals were housed in a special sound-isolated acoustic stress chamber provided with professional tweeters (Steren; 80-1088) suspended 60 cm above the solid grid cages and connected to an amplifier (Mackie M1400; freq. 20 Hz-70 kHz; 300 W-8 Ω) equipment with mixer software that delivered the acoustic signal at levels ranging from 70 dB for the background noise to 85-103 dB for the noisy events. To make sure that the sound intensity was homogeneous at all places in the cage, noise intensity was measured by placing a sound-level meter (Radio Shack; , Mexico).
Figure 1: General procedure followed in our experiment. Experimental procedures are chronologically depicted above the line. Postnatal age is written below the line

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Corticosterone assays

Immediately after the noise procedure, a subgroup of rats was decapitated and their trunk blood was collected in heparinized tubes. Blood samples were obtained immediately after the noise was ended at PND 36, and in the morning of PND 90 (always between 07:00 and 08:00, in order to avoid circadian variation). Plasma corticosterone levels were measured using an enzyme immunoassay kit (Correlate-EIA from Assay Designs Inc., USA).

Bromodeoxiuridine (BrdU) protocols

Bromodeoxiuridine administration

label newly born cells, the thymidine analog Bromodeoxiuridine (BrdU) (Sigma-Aldrich, St. Louis, Missouri) was used. At PND 77, all animals received 3 intra-peritoneum (i.p.) injections of BrdU (50 mg/kg, dissolved in 0.9% NaCl) starting at 0700 and every 6 hours until 1900. The rats were killed 14 days after BrdU injections [Figure 1].

BrdU immunohistochemistry

After transcardiac perfusion with phosphate-buffered saline followed by 4% paraformaldehyde, brains were post-fixed in the same fixative and cut in the coronal plane into 40- μm-thick sections using a vibratome (Leica VT1000E; Leica Microsystems, Wetzlar, Germany). To visualize BrdU-positive cells, free-floating sections were first pre-treated to denature DNA. Sections were incubated in 2 N HCl for 30 minutes at 37°C and rinsed with 0.1 M borate buffer (pH, 8.5). Subsequently, sections were washed with PBS and incubated with blocking solution (10% normal goat serum in 0.1 M PBS) for 60 minutes at room temperature, and then for 12 hours at 4°C with the monoclonal antibody against BrdU (rat anti-BrdU; Accurate Scientific, OBT003; dilution, 1:1000). After rinsing in PBS, sections were incubated with the secondary antibody (Alexa fluor 488 goat anti-rat IgG, Molecular Probes; dilution, 1:500) for 2 hours at room temperature. Sections were finally mounted on slides and cover-slipped using fluorescent mounting media (Vectashield Vector Labs, Burlingame, CA).

BrdU counting

Series of systematically selected brain sections (200-μm apart each) starting at bregma -2.1 and ending at bregma -4.5 were used for counting of BrdU-positive cells in both control and environmental noise-exposed rats. All slides were coded, and the experimenter was blinded to group assignment prior to examination. All BrdU-positive cells within the DG, CA3 and CA1 areas were manually counted using a "Χ400" magnification. All data are expressed as mean±standard deviation. For mean comparisons between groups, we used the Student t test. In all cases, a value of P<.05 was chosen to establish significant differences.

  Results Top

Effect of environmental noise on body weight gain

Body weight was recorded from PND 21 to PND 90. Body weight gain was lesser in rats exposed to environmental noise as compared to the control group [Figure 2]. We found statistically significant differences at PND 28 [F(1,17)=6.992, P<.05), and such reduction persisted until PND 35 [F(1,17)=5.687, P<.05). Once the noise was suspended, noise-exposed rats recovered body weight that was lost, and no significant differences between the two groups were found from PND 70 to PND 90.
Figure 2: The rat's body weight gain from PND 21 to PND 70 is expressed in grams. The noise-exposed rats gained lesser weight as compared to the control rats (statistically significant only on PNDs 28 and 32). *P<.05. Bars represent the mean±standard error mean S.E.M. of the values obtained

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Effect of environmental noise on serum corticosterone levels

Serum corticosterone (CORT) levels were assessed at PND 36 and PND 90 in controls and the stressed group [Figure 3]. Serum CORT levels at 36 PND (immediately after noise exposure) were 2-fold higher in the noise-exposed group as compared to controls (P<0.05; Student t test). However, we did not find statistically significant differences in CORT levels between the groups at PND 90 (~2 months after noise exposure).
Figure 3: Mean±S.E.M. plasma levels of corticosterone obtained after exposure to environmental noise (left panel, PND 36) and after an undisturbed period (right panel, PND 90). Increased CORT levels were found only immediately after exposure to noise (*P<.05). Bars represent the mean±standard deviation mean S.D.M.

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Effect of environmental noise on BrdU-labeled cells

To determine whether noise modifies the hippocampal cell proliferation, we quantified the number of BrdU immunopositive cells per microscopic area (0.739 mm 2 ) in DG, CA3 and CA1 regions. In the DG area, the BrdU cell population was reduced in 47.9% of the rats in the noise-exposed group (10.33±1.72) as compared to controls (21.5±3.08) (P<.05) [Figure 4]. In CA3 hippocampus [Figure 4], the number of BrdU+ cells in noise-exposed rats (0.49±0.06) showed a statistically significant reduction as compared to the control group (1.32±0.22) (P<.05) [Figure 5]. No differences between the groups were found in the CA1 region.
Figure 4: Pictures show BrdU-positive cells in dentate gyrus in controls and the noise-exposed group. The quantification of the BrdU-positive cells is shown in the histogram. Bars represent the mean±standard deviation. Asterisk indicates statistically significant difference (P<.05; Student t test)

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Figure 5: Pictures show BrdU-positive cells in CA3 hippocampus in controls and the noise-exposed group. The quantification of the BrdU-positive cells is shown in the histogram. Bars represent the mean±standard deviation. Asterisk indicates statistically significant difference (P<.05; Student t test)

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  Discussion Top

Environmental noise has deleterious effects on health as a consequence of progressive hearing deficit due to CNS injury. In the present study, the effect of noise on the CNS was analyzed in terms of its capability to induce long-term changes in the rat hippocampus. Our results show that chronic exposure to environmental noise in the early stages of life produces a long-lasting reduction in cell proliferation at hippocampus in neurogenic and non-neurogenic hippocampal regions. This non-auditory effect of noise may be related to the capacity of environmental noise to increase the activity of the hypothalamic-pituitary-adrenal (HPA) system.

The hippocampal formation is an important target in the CNS for the deleterious effects of environmental stressors. Extra-auditory effects of noise and their potential role as an environmental stressor have attracted attention of researchers trying to assess the effect of noise-induced stress on hippocampal formation. [7],[9] Besides the obvious importance of preceding experiments, it is important to consider that almost all of the studies about the effects of noise on hippocampal formation have been done using artificial models of noise (e.g., white noise, broadband noise, etc.), which are not necessarily representative of the human noisy environment. [6] With this in mind, we included in our experiment a validated model developed by Rabat and co-workers in which a human noisy environment was adapted to rats' audition. [18] As pointed out above, our results demonstrated a noticeable reduction in hippocampal cell proliferation in the exposed rats.

The mechanism that leads environmental noise to impair hippocampal cell proliferation is poorly understood. On the basis of the raised levels of CORT and lesser body weight gain among the noise-exposed rats in our experiment, we believe that some stress-related mechanism may affect proliferation. Recent evidence proposes that psychosocial stress decreases proliferation via activation of the HPA axis. [19] Glucocorticoids regulate cell proliferation [20] and cell survival [21] through either GR (glucocorticoid receptor) or MR (mineralocorticoid receptor). High levels of these two types of receptors are present in the hippocampus and have been found in neural progenitors, mature neurons and glial cells. [21],[22],[23] Activation of GR, as a consequence of high glucocorticoid (GC) levels or synthetic agonists, suppresses hippocampal cell proliferation. [24] Furthermore, environmental noise may act as a chronic stressor for rats; consequently, it can down-regulate the cell proliferation and the survival of the new-born hippocampal cells. [21] Experimental evidence indicates that even one acute episode of social stress produces long-lasting effects on the incorporation of new hippocampal neurons by reducing their survival rate. [25] Other stress experiments have demonstrated that early exposure to threatening conditions may exert long-term effects via changes in HPA axis activity. [26],[27] The HPA system is susceptible to programming during development [28] ; so early-life stress can permanently change the activity of the HPA mediators, [29] affecting the hippocampal plasticity. A support for this hypothesis comes from experiments showing that early-life stress decreases production of new granule neurons in adulthood through a corticosteroid-dependent mechanism. [16]

The first few weeks of postnatal development represent a critical period for the maturation of both a rat's central auditory system [30] and hippocampal formation. [31] Evidence indicates that nonclassical auditory pathways may provide a link to limbic structures through the dorsal-medial thalamic auditory nucleus. [32] Neuroimaging studies have shown that these nonclassical pathways, normally inactive, may become activated in individuals with tinnitus and in children. [33],[34] Although there are no connections linking directly the classical auditory system to hippocampus, evidence indicates that a brief exposure to high-intensity noise increases the firing frequency patterns of hippocampus place cells. [13] Therefore, it is possible that a down-regulation of proliferation may be triggered directly by noise, which produces neuronal hyperactivity as occurs in temporal lobe epilepsy. [35] Acute exposure to noise causes a long-lasting suppression of hippocampal neurogenesis in adult rats, [12] which supports the notion that effects of noise on CNS are more persistent than peripheral auditory effects. [36] Behavioral studies show that exploratory behavior in a water maze is impaired by noise exposure during the critical period of postnatal hearing development (PND 12 to 30). [36] Thus the long-term effects of noise on hippocampal neurogenesis may be related to auditory mechanisms. Taken together, our results and the previous findings strongly suggest that besides its classical auditory effects, the environmental noise may affect the cell organization of the brain. Due to the high incidence of noise pollution and hippocampus-dependent pathologies in modern societies, further studies are needed to elucidate the precise mechanism of hippocampal dysfunction after a long-term noise exposure.

  References Top

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Correspondence Address:
Joaquín García-Estrada
Centro de Investigacion Biomedica de Occte. del IMSS. Sierra Mojada 800. Centro Medico. Col. Independencia Ote. Guadalajara Jalisco Mexico. CP 44340
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Source of Support: This work was supported by research grants: CONACyT-Jalisco Government 2008-05-99060 and CONACyT-UdeG repatriation grant to Fernando Jauregui, Conflict of Interest: None

DOI: 10.4103/1463-1741.82961

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