Cage Control Group Research Articles

Long-term serotonin abnormalities in the brain of immature rats subjected to febrile seizures.

Febrile seizures (FS) are the most common neurological disorder at a young age in humans. Animal models of hyperthermia-induced seizures provide a tool to investigate the underlying mechanisms of FS related to epilepsy development and its co-morbidities. The present study investigates the alterations in monoamine neurotransmitters in two brain areas: the cortex and the hippo-campus in animals subjected to prolonged FS at their immature age. Experimental animals were divided into three groups: cage-control group (NHT-NFS), positive hyperthermic control group (HT-NFS), and the hyperthermia-induced febrile seizure group (HT-FS). Each group was further subdivided into young (Y) and adult (A) groups. There were significant changes in the cortical and hippocampal serotonin neurotransmitters that were persistent until adulthood. However, the changes in the two other neurotransmitters, norepinephrine and dopamine, were transient and have been recovered in adulthood. The present study sheds more light on the importance of monoamine neurotransmitters in epileptogenesis following FS.

Enhancement of the RhoA/Rho kinase pathway is associated with stress-related erectile dysfunction in a restraint water immersion stress model.

Stress is a risk factor for erectile dysfunction (ED); however, the pathology of stress‐induced ED remains unclear. Accordingly, in this study, we investigated the mechanisms of stress‐induced ED using a rat model. Ten‐week‐old male Wistar/ST rats were maintained in a cage filled with water to a height of 2 cm (stress group) or a normal cage (control group). We found that water immersion stress significantly enhanced the contractile response to noradrenaline in the corpus cavernosum (CC) (p < 0.05). Moreover, stress significantly decreased erectile function, as assessed by changes in intracavernous pressure (p < 0.01). In addition, Rho kinase‐1 (ROCK‐1) protein expression was significantly upregulated under stress conditions (p < 0.05), and phosphorylated myosin light chain (phospho‐MLC) levels, contribute to smooth muscle contraction, were also upregulated (p < 0.01). Treatment with fasudil hydrochloride, a Rho kinase inhibitor, for 5 days significantly improved erectile function (p < 0.01) and normalized ROCK‐1 and phospho‐MLC levels (p < 0.01). Thus, the RhoA/Rho kinase pathway may be associated with stress‐induced ED via contraction of CC. Stress also decreased the smooth muscle/collagen ratio of CC (p < 0.01), and fasudil treatment did not alleviate these effects (p = 0.50). These findings suggested that penile fibrosis gradually progressed under stress conditions and that fibrosis may be independent of the RhoA/Rho kinase pathway, implying that longer exposure to stress may promote ED. We conclude that stress‐induced ED was caused by contraction of CC mediated by the RhoA/Rho kinase pathway.

Apical intercalated cell cluster: A distinct sensory regulator in the amygdala.

GABAergic neurons regulate different aspects of information processing in the amygdala. Among these are clusters of intercalated cells (ITCs), which have been implicated in fear-related behaviors. Although a few of the ITC clusters have been studied, the functional role of apical ITCs (apITCs) is unknown. Here, we combine monosynaptic rabies tracing with optogenetics and demonstrate that apITCs receive synaptic input from medial geniculate nucleus (MGm), posterior intralaminar nucleus (PIN), and medial dorsal nucleus of the thalamus and from a diverse range of cortical areas including temporal association, entorhinal, insular, piriform, and somatosensory cortex. Upon fear learning, PIN/MGm inputs are strengthened, indicative of their involvement in fear behaviors. 3-D reconstruction of apITCs reveals local arborization and innervation of the dorsal striatum and lateral amygdala. We further show that apITCs provide sensory feedforward inhibition to LA principal cells, a putative mechanism for controlling plasticity during fear learning.

Effect of long-term confinement on metabolic and physiological parameters in mice

Long-term and mild confinement or isolation in an enclosed environment can occur in situations such as disasters, specific political, economic or social events, nuclear shelters, seabed exploration, polar expeditions, and space travel. To investigate the effects of stress caused by long-term confinement in an enclosed environment in mammals, we divided 8-week-old C57BL/6J mice into four groups that were housed in a closed environment with a narrow metabolic cage (stress group), normal metabolic cage (control group), conventional cage (conventional group) or conventional cage with wire mesh floor (wire mesh group). The phenotypes of the mice were examined for four weeks, followed by behavioral tests. Weight gain suppression was observed in the stress group. Continuous analysis of these mice every two minutes for four weeks using an implanted measuring device showed a significantly decreased amount of spontaneous activity and subcutaneous temperature in the stress group. After housing in each environment for four weeks, the behavioral tests of mice in the stress group also revealed a shorter latency to fall off in the rotarod test and shorter stride length and interstep distance in the footprint test. Interestingly, the lower spontaneous activity of mice in the stress group was rescued by housing in conventional cages. These results suggest a temporary effect of long-term confinement in an enclosed environment as a chronic and mild stress on homeostasis in mammals.

58. Benefits of macroscale topography features on and within interbody cages

BACKGROUND CONTEXT Implant design, material, surfaces, graft and surgical techniques play important roles in the success of interbody fusions and the ability to radiographically assess. PEEK's positive attributes of mechanical properties and radiolucency are maintained using a molecularly bonded submicron deposition of titanium to improve bone on-growth. Novel macroscale topography features on the endplate surfaces and inside the aperture were hypothesized to allow early bone integration and mechanical stability. PURPOSE To evaluate the effect of macroscale topography on a PEEK/Titanium composite cage in a large animal model of interbody fusion. STUDY DESIGN/SETTING Preclinical large animal model. PATIENT SAMPLE Not applicable. OUTCOME MEASURES Not applicable METHODS Lateral L45 interbody fusions were performed in 4-5-year-old ewes using a PEEK/titanium composite cage (Control group) compared to the same cage with macro 3D features on the endplate and inside the aperture (Test group). Iliac crest autograft was placed in the aperture and bilateral pedicle screws and rods for posterior stabilisation. Fusion assessment at 6 and 12 weeks (n=10 per group) included manual palpation, X-rays, mCT, tensile testing and pmMA histology. RESULTS The Test group's manual palpation was 9/10 and 10/10 at 6 and 12 weeks while the control was 4/10 and 7/10 at 6 and 12 weeks. Radiographs and mCT confirmed new bone formation in the aperture of the Control group cages with time while some areas of aperture radiolucency were present. Radiographs and mCT of the Test group cages revealed new bone formation and integration within the topography features on the endplates and inside the aperture which progressed with time. Histology confirmed the radiographic findings in the control group and integration with the host endplates and remodeled bone within the apertures in the Test group. Tensile testing demonstrated nearly a 3-fold statistically significant increase in mechanical properties at both time points for the Test group vs the control group. CONCLUSIONS The macroscale features in the Test group provided multiple opportunities for bone integration between the host endplates and graft within the aperture. Early bony integration translated to a statistically significant increase in mechanical strength compared to the control cage which did not include the same geometric features. Promising data in this clinically relevant animal model warrants further study in humans. FDA DEVICE/DRUG STATUS Shoreline RT (Approved for this indication).

Effect of Withania Somnifera on the antioxidant and neurotransmitter status in sleep deprivation induced Wistar rats.

Sleep is normally a period of relaxation and repair, important for the maintenance of physiological homeostasis and psychological balance. "Globally, millions of people experiences sleep deprivation daily". Sleep deprivation (SD) impairs cognitive functions, decreases anti-oxidative defense and induces neuronal changes. Withania somnifera (WS), commonly known as an "Indian Ginseng" has broad therapeutic applications, including anti-inflammatory activities, actions on immune system, circulatory system, central nervous system etc., The study is aimed to assess effect of Withania somnifera on antioxidant status and neurotransmitter level in sleep deprivation induced male Wistar albino rats. The study was done in the Department of Physiology, Meenakshi Medical College and Hospital, Enathur, Kanchipuram. 24 male adult Wistar rats weighing 120-150g were used for the study. They were divided into 4 groups with 6 animals in each group. (Group I - cage control, Group II - large platform control, Group III - sleep deprived group and Group IV – WS treated SD group). Animals were deprived sleep for one week using a modified multiple platform method. Oxidative stress parameters and antioxidant enzymes were measured using spectrophotometry. Neurotransmitters such as dopamine and serotonin concentration in the serum were measured by ELISA method. There was a marked (by one-way ANOVA test) decrease observed in the antioxidants enzymes in the cortex of both large platform control and sleep deprivation induced group. The group treated with W. somnifera root extract significantly reduced the free radical production and lipid peroxidation with simultaneous increase in the level of antioxidant enzymes compared to the untreated group. Also in our study the concentration of dopamine and serotonin was found to be significantly reduced (p < 0.05) in sleep deprived (SD) and large platform control group when compared to cage control group. Whereas the group treated with W. somnifera (400mg/kg b.wt) increased the neurotransmitter levels significantly. Withania somnifera proved to be an effective therapeutic agent by maintaining the antioxidant status and neurotransmitter levels.

NO-Dependent Mechanisms of Myosin Heavy Chain Transcription Regulation in Rat Soleus Muscle After 7-Days Hindlimb Unloading.

It is known that nitric oxide (NO) may affect myosin heavy chain (MyHC) isoform mRNA transcription in skeletal muscles. The content of NO in soleus muscles decreases during rat hindlimb unloading as well as slow MyHC mRNA transcription. We aimed to detect which signaling pathways are involved in NO-dependent prevention of hindlimb-suspension (HS)-induced changes in MyHCs’ expression pattern. Male Wistar rats were divided into four groups: cage control group (C), hindlimb suspended for 7 days (7HS), hindlimb suspended for 7 days with L-arginine administration (7HS+A) (500 mg/kg body mass), and hindlimb suspended for 7 days with both L-arginine (500 mg/kg) and NO-synthase inhibitor L-NAME administration (50 mg/kg) (7HS+A+N). L-arginine treatment during 7 days of rat HS prevented HS-induced NO content decrease and slow MyHC mRNA transcription decrease and attenuated fast MyHC IIb mRNA transcription increase; it also prevented NFATc1 nuclear content decrease, calsarcin-2 expression increase, and GSK-3β Ser 9 phosphorylation decrease. Moreover, L-arginine administration prevented the HS-induced myh7b and PGC1α mRNAs content decreases and slow-type genes repressor SOX6 mRNA transcription increase. All these slow fiber-type protective effects of L-arginine were blocked in HS+A+N group, indicating that these effects were NO-dependent. Thus, NO decrease prevention during HS restores calcineurin/NFATc1 and myh7b/SOX6 signaling.

Effects of chronic sleep deprivation on upper respiratory tract mucosal histology and mucociliary clearance on rats.

In this study, we aimed to investigate the effects of chronic sleep deprivation on mucociliary clearance, which is the primary defence mechanism of the upper airway tract and nasal mucosal histology. Forty-two Wistar Albino rats (250-300g), 8 or 12 weeks old, were randomly assigned into three groups as follows. The first sleep-deprivation group consisted of 14 rats (A), another 14 of them were assigned to platform group (B), and the remaining 14 were included to the home cage control group (C). For the two deprivation groups (A and B), the modified multiple platform method (MMPM) was used to induce sleep deprivation for 21days. Tc-99m MAA rhinoscintigraphy was performed to assess mucociliary clearance and the nasal histopathological changes of the sacrificed rats were also examined. Mucociliary clearance was significantly higher in sleep deprivation (A) and deprivation control (B) groups than the control group (C) (p=.037). The ratio of columnar ciliary was significantly higher in group A and B than in the control group (p=.003). The transitional epithelial ratio in groups A and B was also significantly increased compared with group C (p=.04). The control group's squamous epithelial ratio was increased compared to the sleep-deprived groups (p=.003). There was a significantly increased inflammatory response in the ciliated columnar epithelium in groups A and B compared to group C (p=.02). For the first time in the literature, we demonstrated that chronic sleep deprivation has caused a significant increase in mucociliary clearance speed and in the number of ciliary cells.

Voluntary Wheel Running Attenuates Salt-Induced Vascular Stiffness Independent of Blood Pressure.

Excess dietary salt can lead to the development of arterial stiffness and high blood pressure (BP). Regular physical activity can protect against arterial stiffening and lower BP. Less is known regarding the role of exercise on the vasculature independent of BP under high salt (HS) conditions. The aim of the study was to determine whether wheel running protects against the development of dietary salt-induced arterial stiffness independent of BP. Rats were maintained on either normal salt (NS; 0.49% NaCl) or HS (4.0% NaCl) diet for 6 weeks and further divided into a voluntary wheel running (NS-VWR, HS-VWR) or cage control group (NS, HS). Carotid-femoral pulse wave velocity (PWV) was measured using applanation tonometry at baseline (BSL) and 6 weeks. BP was measured weekly and remained unchanged among groups throughout the 6 weeks (P > 0.05). PWV was elevated at 6 weeks in HS compared to baseline (HS-BSL, 3.27 ± 0.17 vs. HS-6 week, 4.13 ± 0.26 m/s; P < 0.05) and was lower at 6 weeks in both VWR groups (NS-VWR, 2.98 ± 0.29, HS-VWR, 3.11 ± 0.23 m/s) when compared to HS at 6 weeks (P < 0.05). This was supported by a significant increase in aortic collagen I in the HS group alone and transforming growth factor beta (TGF-β) was greater in the HS group compared to both NS groups (P < 0.05). Wheel running resulted in a greater aortic phosphorylated eNOS and SOD-2 in HS-WVR (P < 0.05) compared to HS. These data suggest that VWR may protect against collagen accumulation through a TGF-β-mediated pathway by improving nitric oxide bioavailability and redox balance in rats.

Механизмы поддержания экспрессии медленного миозина в волокнах постуральной мышцы при стимуляции опорных афферентов на фоне гравитационной разгрузки

The study was aimed to investigate the role of support afferentation in support of functioning the signaling mechanisms responsible for slow-type oxidative genes expression during postural soleus muscle unloading. For the investigation of the support afferentation the plantar mechanical stimulation was used. Male Wistar rats were divided into six groups (8 animals in each): two cage control groups (C), two groups hindlimb unloaded for 1 day or 3 days (1 HS, 3HS) and two hindlimb-unloaded groups with plantar mechanical stimulation 1HS+МСО; 3HS+МСО. Animals from stimulated groups received plantar stimulation during 4 hours a day, mimicking the pattern of normal animal walking. Plantar mechanical stimulation led to prevention of slow myosin I(β) and myh7b mRNAs expression decreases after 1 day of unloading. After three days of hindlimb unloading the expression of slow myosin I(β) mRNA and myh7b mRNA significantly increased in plantar stimulated group, and the expression of SOX6 mRNA in this group did not differ from control, although it was significantly increased in pure unloaded group. So, plantar mechanical stimulation prevents unloading-induced MyHC I/myh7b/SOX6 inactivation, inhibiting slow-to-fast fiber-type shift.

Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress.

BackgroundRapid Eye Movement sleep deprivation (REMSD) of rats causes inflammation of the liver and apoptotic cell death of neurons and hepatocytes. Studies also suggest that REM sleep deprivation can cause muscle as well as cardiac injury and neurodegenerative diseases.Objective and methodsThe aim of this research was to determine whether REM sleep deprivation of rats would increase the levels of reactive oxygen species (ROS) in the hepatocytes and create oxidative stress in them. We selectively deprived the rats for REM sleep using the standard flower pot method.ResultsWe observed that when rats were subjected to REM sleep deprivation, the levels of ROS in their hepatocytes increased ~184.33% compared to large platform control (LPC) group by day 9 of deprivation, but it returned towards normal level (~49.27%) after recovery sleep for 5 days. Nitric oxide synthase (iNOS) gene expression and protein levels as determined by real-time PCR and western blot analysis respectively were found to be elevated in hepatocytes of REM sleep deprived rats as compared to the LPC group. The level of nitric oxide (NO) in the hepatocytes of REMSD rats also increased by ~404.40% as compared to the LPC group but sleep recovery for 5 days normalized the effect (~135.35% compared to LPC group). We used a large platform control group as a reference group to compare with the REM sleep deprived group as the effect on the hepatocytes of both LPC group and cage control groups were not significantly different.DiscussionWe have analyzed the oxidative stress generated in the hepatocytes of rats due to REM sleep deprivation and further consequences of it. REMS deprivation not only increased the levels of ROS in the hepatocytes but also induced iNOS and NO in them. REM sleep deprived hepatocytes became more susceptible to oxidative stresses on further exposures. Furthermore, our study has great pathological and physiological.

Sleep deprivation accelerates the progression of alzheimer’s disease by influencing Aβ-related metabolism

Sleep disorders have previously been connected with the neurodegenerative pathology of Alzheimer’s disease (AD) due to the aggregation of β-amyloid(Aβ)peptides and tau proteinsinduced by sleep deprivation (SD). However, the underlying mechanisms remain unclear. Therefore, this study was performed to clarify how Aβ-related metabolism is regulated after SD. Three-month-old Sprague-Dawley rats (250–300g) were randomly divided into 5 groups: two SD groups(i.e.,SD-2d and SD-4d), two platform control groups(i.e.,PC-2d and PC-4d) and a home cage control group (CC). For the two SD groups, themodified multiple platform method (MMPM) was used to induce SD.Our experiments confirmed that SD impaired cognitive function and increased the levels of Aβ peptides, a hallmark of AD. Additionally, we found that SD significantly increasedthe levels of the β-site amyloid precursor protein (APP)-cleaving enzyme 1(BACE1, β-secretase), but had little impacton the levels of Aβ-degradationenzymes.This resultmay be the main cause of the over-expression of Aβ1-42 and Aβ1-40. Our results suggested that SD accelerates the progression of AD bymodulating Aβ-related metabolism. This findinghasimportant implications for the diagnosis and prevention of AD.

Response of Rat Tibia to Prolonged Unloading Under the Influence of Electrical Stimulation at the Dorsal Root Ganglion

Immobilization of weight bearing skeletons or microgravity results in disuse osteoporosis in both human and animals. Our previous study demonstrated that electrical stimulation at the dorsal root ganglion (DRG) with an implantable micro-electrical stimulation system (IMESS) could trigger secretion of bone anabolic calcitonin gene-related peptide (CGRP) and prevent bone loss in a short-term hindlimb unloading rat model. This study was designed to further investigate whether electrical stimulation to the DRG could prevent bone loss due to prolonged unloading. Eighteen adult rats were randomly assigned into three groups: cage control (CC), hindlimb unloading (HU), and hindlimb unloading with electrical stimulation (HUES). Electrical stimulation was applied via IMESS to the right DRGs at vertebral levels L4-L6 in HUES group for 6 weeks. Following unloading for 6 weeks, proximal tibia metaphysis was shown 64.0% decrease in bone mineral content (BMC) and 47.0% decrease in bone mineral density (BMD) in HU group while significant reduced bone lose with 2.7% increase in total BMC and only 9.2% decrease in total BMD in HUES group. Diaphyseal BMD decreased significantly in both HU and HUES group as compared with CC group. There was enhancement of CGRP expression in the DRGs in HUES group. This experimental study proved the proposed concept using electrical stimulation at the DRG for prevention of disuse-induced bone loss in a rat hindlimb suspension model.

The effects of electromagnetic radiation (2450 MHz wireless devices) on the heart and blood tissue: role of melatonin.

This study was designed to investigate the effects of 2450 MHz EMR on the heart and blood in rat and possible ameliorating effects of melatonin. Thirty-two female Wistar Albino rats were randomly grouped (by eight in each group) as follows: Group I: cage-control group (dimethysulfoxide (DMSO), 10mg/kg/day i.p. without stress and EMR. Group II: sham-control rats stayed in restrainer without EMR and DMSO (10mg/kg/day i.p.). Group III: rats exposed to 2450 MHz EMR. Group IV: treated group rats exposed to 2450 MHz EMR+melatonin (MLT) (10mg/kg/day i.p.). In the blood tissue, there was no significant difference between the groups in respect of erythrocytes GSH, GSH-Px activity, plasma LP level and vitamin A concentration (p > 0.05). However, in the Group IV, erythrocytes' LP levels (p < 0.05) were observed to be significantly decreased while plasma vitamin C, and vitamin E concentrations (p < 0.05) were found to be increased when compared to Group III. In the heart tissues, MDA and NO levels significantly increased in group III compared with groups I and II (p < 0.05). Contrary to these oxidant levels, CAT and SOD enzyme activities decreased significantly in group III compared with groups I and II (p 0.05). Besides, MLT treatment lowered the MDA and NO levels compared with group III. In conclusion, these results demonstrated that contrary to its effect on the heart, the wireless (2450 MHz) devices cause slight oxidative-antioxidative changes in the blood of rats, and a moderate melatonin supplementation may play an important role in the antioxidant system (plasma vitamin C and vitamin E). However, further investigations are required to clarify the mechanism of action of the applied 2450 MHz EMR exposure (Tab. 3, Fig. 1, Ref. 49).

Effects of chronic sleep deprivation on the myosin heavy chain isoforms of masseter muscle in rats

Objective To investigate the changes of myosin heavy chain (MyHC) isoforms in rat masseter muscle fibers caused by chronic sleep deprivation (CSD) and a possible link with the pathogenesis of temporomandibular joint disorders(TMD). Methods Total 180 male rats were randomly divided into three groups(n=60 per group): chronic sleep deprivation group (CSD), cage control group (CC), and large-platform control group (TC). Each group was further divided into three subgroups(n=20 in each group)according to the observation time point(7, 14, and 21 days). The expression of MyHC isoforms in masseter muscle fibers was investigated by real-time quantitative PCR, Western blotting and immunohistochemical staining. Results The expression of MyHC-Ⅰ, MyHC-ⅡA and MyHC-ⅡB deep and shallow masseter muscle in CSD7d group had differention with the control group(MyHC-Ⅰ: (0.314±0.005, 0.134±0.005, P 0.05), and there were no differences between the CC and TC groups at any time point. Conclusion These findings suggest that CSD alters the expression of MyHC isoforms, which may contribute to TMD pathogenesis. Key words: Chronic sleep deprivation; Temporomandibular joint disorders; Masseter muscle; Myosin heavy chain(MyHC)

The Efficiency of Zero-profile Implant in Anterior Cervical Discectomy Fusion

A prospective controlled study. The aim of this study was to compare the safety and efficacy of the zero-profile device with that of an anterior cervical plate and cage in patients undergoing anterior cervical discectomy and fusion (ACDF). A series of studies have indicated that anterior instruments produce good clinical results during ACDF. However, common implants are associated with a high rate of postoperative complications. A cervical stand-alone cage with integrated fixation for zero-profile segmental stabilization has been developed to solve this problem. A total of 46 patients with cervical radiculopathy or myelopathy were randomly treated with an anterior plate and a cage or a new zero-profile implant between September 2009 and April 2010. Patients were followed for 2 years. The operation time, blood loss, exposure to radiation, the Japan Department of Orthopedics Association (JOA) score, pain Visual Analogue Score (VAS), and dysphagia score were recorded. The operation was completed successfully in 46 patients. Twenty-three patients received an anterior plate and cage (control group) and 23 patients received the new zero-profile implant (test group). Analysis of postoperative data at all protocol-defined intervals demonstrated improvement in all clinical outcomes for both the groups when compared with the corresponding preoperative data. No significant difference in VAS and JOA score was found in the 2 treatment groups. The test group had a greater reduction in dysphagia at all follow-up intervals, compared with the control group. No adjacent segment degeneration was found in the test group, whereas 4 patients in the control group developed degeneration in adjacent segments (P=0.045). Both the groups had no adverse events associated with the implant or implant surgery. The Zero-P implant is a viable alternative to ACDF in patients with persistently symptomatic, single-level cervical disk disease. The procedure requires more technical requirements than traditional plates.

Effect of whole-body exposure to the 848.5 MHz code division multiple access (CDMA) electromagnetic field on adult neurogenesis in the young, healthy rat brain

Introduction: Whether exposure to the 848.5 MHz code division multiple access (CDMA) signal affects adult neurogenesis is unclear.Materials and methods: An animal experiment was performed with a reverberation chamber designed as a whole-body CDMA exposure system. Male Sprague-Dawley rats were assigned to three groups (n = 6 per group): Cage-control, sham-exposed, and CDMA-exposed groups. Rats in the CDMA-exposed group were exposed to the CDMA signal at a 2 W/kg whole-body specific absorption rate (SAR) for 1 or 8 h daily, 5 days per week, for 2 weeks. Rats received a single intraperitoneal injection of Bromodeoxyuridine (BrdU) to label proliferative cells daily for the last five consecutive days of CDMA signal exposure. An unbiased stereological method was used to estimate the number of BrdU+ cells in the subventricular zone (SVZ) and dentate gyrus (DG).Results: We found no significant changes in the number of BrdU+ cells in the SVZ or DG in the CDMA-exposed rats, compared with rats in the cage-control and sham-exposed groups (p > 0.05).Conclusion: Our results suggest that exposure to the CDMA signal does not affect neurogenesis in the adult rat brain, at least under our experimental conditions.

Clustered c-Fos Activation in Rat Hippocampus at the Acquisition Stage of Appetitive Instrumental Learning

To address the issue of how hippocampal neurons are involved into learning progress, we studied c-Fos expression in rat hippocampal subfields at different stages of appetitive instrumental learning. To model the first stage of learning, we pre-trained animals to approach the lever to obtain the food, and then made this behavior ineffective by not reinforcing it during the last session (“mismatch” group). Another group just acquired lever-pressing behavior at that day (“acquisition” group). Animals of the third group performed this well-trained behavior (“performance” group). The number of Fos-positive neurons in all hippocampal regions of the “mismatch” group animals was higher than in the ones of the home cage control group animals. The number of Fos-positive neurons was increased in CA1 and CA3 areas, but not in the dentate gyrus of both the “acquisition” and “performance” group animals as compared with the control group. We also found segmented c-Fos expression, which was more evident in “acquisition” group animals. Thus, our results suggest that during the first (mismatch) stage of learning hippocampal neurons are activated in an equally distributed manner. The following clustered pattern of activated CA1 neurons during the acquisition stage may reflect specialization of these neurons in respect to the specific lever-pressing behavior.

Effects of early-onset radiofrequency electromagnetic field exposure (GSM 900 MHz) on behavior and memory in rats.

Female Wistar rats, from an age of 14 days to 19 months, were exposed in the head region for 2 h per day, 5 days per week, to a GSM-modulated 900 MHz radiofrequency electromagnetic field (RF-EMF). The average specific absorption rates (SAR) in the brain were 0 (sham), 0.7, 2.5 and 10 W/kg. To ensure a primary exposure of the head region, rats were fixed in restraining tubes of different sizes according to their increasing body weight. During the experiment, a set of 4 behavioral and learning tests (rotarod, Morris water maze, 8-arm radial maze, open field) were performed 3 times in juvenile, adult and presenile rats. In these tests, no profound differences could be identified between the groups. Only presenile rats of the cage control group showed a lower activity in two of these tests compared to the other groups presumably due to the lack of daily handling. The rotarod data revealed on some testing days significantly longer holding times for the sham-exposed rat vs. the exposed rat, but these findings were not consistent. During the first year, body weights of sham-exposed and exposed rats were not different from those of the cage controls, and thereafter only marginally lower, so that the effect of stress as confounder was probably negligible. The results of this study do not indicate harmful effects of long-term RF-EMF exposure even when begun at an early age on subsequent development, learning skills and behavior in rats, even at relatively high SAR values.

Increased resistance during jump exercise does not enhance cortical bone formation.

This study sought to elucidate the effects of a low- and high-load jump resistance exercise (RE) training protocol on cortical bone of the tibia and femur mid-diaphyses. Sprague-Dawley rats (male, 6 months old) were randomly assigned to high-load RE (HRE; n = 16), low-load RE (LRE; n = 15), or cage control (CC; n = 11) groups. Animals in the HRE and LRE groups performed 15 sessions of jump RE for 5 wk. Load in the HRE group was progressively increased from 80 g added to a weighted vest (50 repetitions) to 410 g (16 repetitions). The LRE rats completed the same protocol as the HRE group (same number of repetitions), with only a 30-g vest applied. Low- and high-load jump RE resulted in 6%-11% higher cortical bone mineral content and cortical bone area compared with controls, as determined by in vivo peripheral quantitative computed tomography measurements. In the femur, however, only LRE demonstrated improvements in cortical volumetric bone mineral density (+11%) and cross-sectional moment of inertia (+20%) versus the CC group. The three-point bending to failure revealed a marked increase in tibial maximum force (25%-29%), stiffness (19%-22%), and energy to maximum force (35%-55%) and a reduction in elastic modulus (-11% to 14%) in both LRE and HRE compared with controls. Dynamic histomorphometry assessed at the tibia mid-diaphysis determined that both LRE and HRE resulted in 20%-30% higher periosteal mineralizing surface versus the CC group. Mineral apposition rate and bone formation rate were significantly greater in animals in the LRE group (27%, 39%) than those in the HRE group. These data demonstrate that jump training with minimal loading is equally, and sometimes more, effective at augmenting cortical bone integrity compared with overload training in skeletally mature rats.