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OBJECTIVE: This study aimed to test the association between anthropometric measures and risk of developing hypertension. METHODS: We did a systematic search using PubMed and Scopus, from inception up to January 2017. Prospective cohort studies reporting the risk estimates of hypertension for three or more quantitative categories of indices of general and abdominal adiposity were included. Summary relative risks were calculated using random-effects models. RESULTS: Fifty-seven prospective cohort studies were included. Summary relative risks were 1.49 (95% confidence interval [CI]: 1.41, 1.58; I2  = 97.4%, n = 50) for a five-unit increment in body mass index, 1.27 (95%CI: 1.15, 1.39; I2  = 95.0%, n = 14) for a 10-cm increment in waist circumference, 1.16 (95%CI: 1.09, 1.23; I2  = 77.8%, n = 5) for weight gain equal to a one-unit increment in BMI, and 1.37 (95%CI: 1.24, 1.51; I2  = 76.4%, n = 8) and 1.74 (95%CI: 1.35, 2.13; I2  = 58.9%, n = 4) for a 0.1-unit increment in waist-to-hip ratio and waist-to-height ratio, respectively. The risk of hypertension increased continuously with increasing all anthropometric measures, and also along with weight gain. CONCLUSION: Being as lean as possible within the normal body mass index range may be the best suggestion in relation to primary prevention of hypertension.

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Prenatal morphine exposure throughout pregnancy can induce a series of neurobehavioral and neurochemical disturbances by affecting central nervous system development. This study was designed to investigate the effects of an enriched environment on behavioral deficits and changes in hippocampal brain-derived neurotrophic factor (BDNF) levels induced by prenatal morphine in rats. On pregnancy days 11-18, female Wistar rats were randomly injected twice daily with saline or morphine. Offspring were weaned on postnatal day (PND) 21. They were subjected to a standard rearing environment or an enriched environment on PNDs 22-50. On PNDs 51-57, the behavioral responses including anxiety and depression-like behaviors, and passive avoidance memory as well as hippocampal BDNF levels were investigated. The light/dark (L/D) box and elevated plus maze (EPM) were used for the study of anxiety, forced swimming test (FST) was used to assess depression-like behavior and passive avoidance task was used to evaluate learning and memory. Prenatal morphine exposure caused a reduction in time spent in the EPM open arms and a reduction in time spent in the lit side of the L/D box. It also decreased step-through latency and increased time spent in the dark side of passive avoidance task. Prenatal morphine exposure also reduced immobility time and increased swimming time in FST. Postnatal rearing in an enriched environment counteracted with behavioral deficits in the EPM and passive avoidance task, but not in the L/D box. This suggests that exposure to an enriched environment during adolescence period alters anxiety profile in a task-specific manner. Prenatal morphine exposure reduced hippocampal BDNF levels, but enriched environment significantly increased BDNF levels in both saline- and morphine-exposed groups. Our results demonstrate that exposure to an enriched environment alleviates behavioral deficits induced by prenatal morphine exposure and up-regulates the decreased levels of BDNF. BDNF may contribute to the beneficial effects of an enriched environment on prenatal morphine-exposed to rats.

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Progesterone (PROG) is promising as an important protective agent against various injuries to the nervous system. The present study was designed to investigate whether starting PROG administration, when symptomatology is already established, would alleviate the expression of nociceptive behaviors (mechanical allodynia and thermal hyperalgesia) and electrophysiological changes in a chronic constriction injury (CCI) model of neuropathic pain in rats. Male rats were given PROG (1.5, 3, 6 and 12 mg/kg, i.p.) 12 days after CCI induction, and dosing continued daily until day 26. Behavioral tests were done immediately before surgery (day 0) and on days 12, 26, 28, and 35 post-CCI, and were followed by electrophysiological measurements in the last day. PROG at doses of 6 or 12 mg/kg reduced both the thermal hyperalgesia and mechanical allodynia induced by CCI. Electrophysiological data indicated that CCI-induced animals had a remarkable decrement of both compound muscle and nerve action potential amplitudes recorded in the gastrocnemius muscle and sural nerve, respectively. CCI also caused a significant reduction in motor and sensory conduction velocities measured in the sural and tibial nerves, respectively. PROG at doses of 6 or 12 mg/kg induced a significant recovery of all electrophysiological changes. Our data indicated that starting PROG therapy when symptomatology is already established, and continuing it for a sufficient period of time, may have a therapeutic effect. This suggests that PROG may offer new strategies for the treatment of neuropathic pain.

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This study was designed to examine the effect of voluntary exercise on hippocampal long-term potentiation (LTP) in morphine-dependent rats. The rats were randomly distributed into the saline-sedentary (Sal/Sed), the dependent-sedentary, the saline-exercise (Sal/Exc), and the dependent-exercise (D/Exc) groups. The Sal/Exc and the D/Exc groups were allowed to freely exercise in a running wheel for 10 days. The Sal/Sed and the morphine-sedentary groups were kept sedentary for the same extent of time. Morphine (10 mg/kg) was injected bi-daily (12 h interval) during 10 days of voluntary exercise. On day 11, 2h after the morphine injection, the in vivo LTP in the dentate gyrus of the hippocampus was examined. The theta frequency primed bursts were delivered to the perforant path for induction of LTP. Population spike (PS) amplitude and the field excitatory post-synaptic potentials (fEPSP) slope were measured as indices of increase in synaptic efficacy. Chronic morphine increased the mean basal EPSP, and augmented PS-LTP. Exercise significantly increased the mean baseline EPSP and PS responses, and augmented PS-LTP in both saline and morphine-treated groups. Moreover, the increase of PS-LTP in the morphine-exercise group was greater (22.5%), but not statistically significant, than that of the Sal/Exc group. These results may imply an additive effect between exercise and morphine on mechanisms of synaptic plasticity. Such an interaction between exercise and chronic morphine may influence cognitive functions in opiate addicts.

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BACKGROUND AND THE PURPOSE OF THE STUDY: Pentoxifylline (PTX) is a non-specific cytokite pain in several animal models and humans. However, long-term therapeutic effects of PTX on neuropathic pain in a rat model of chronic constriction injury (CCI) are not completely clear. This study was conducted to examine the effect of long-term administration of PTX on neuropathic pain in rats. METHODS: Neuropathic pain was induced by sciatic nerve ligation using of CCI model in rats. Rats were randomly assigned into sham, CCI-saline treated, and CCI-PTX treated (30 or 60 mg/kg ip) groups. PTX or saline administered at 30 min before CCI and daily for 14 days post-CCI. At the days of 3, 7, 11 and 14 following CCI, by using standard methods effects of thermal hyperalgesia, thermal and mechanical allodynia in all groups were examined using the standard methods. RESULTS: The CCI-saline treated group showed a significant increase in mechanical and thermal allodynia, and thermal hyperalgesia as compared with the sham group in the tested days. Administration of the higher dose of PTX (60 mg/kg/day), but not the lower dose (30 mg/kg/day) significantly reduced mechanical and thermal allodynia, as compared with the CCI-saline treated group on days of 3, 7, 11 and 14 (all P values<0.001). Also, both doses of PTX significantly reduced thermal hyperalgesia as compared with the CCI-saline treated group on these days (all P values<0.001). CONCLUSION: Results of this study show that chronic administration of PTX reduces the neuropathic pain in a rat model of CCI. Thus, this drug may have a therapeutic application in the treatment and management of neuropathic pain in humans.

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There is an obesity epidemic worldwide, which has been increasing in recent years. An epidemiologic cross-sectional study was conducted among 3799 persons who were 30-70 years old in Semnan Province, Iran. Multistage cluster sampling was performed, and subjects were selected from urban and rural populations. Body weight, height and waist circumference (WC) were measured, and body mass index (BMI) and waist to hip ratio (WHR) were calculated. Overweight and obesity were defined as 25 < or = BMI < 30 and > or =30 respectively in men with WHR > or = 0.9 or WC > or = 102 cm, and women with WHR > or = 0.8 or WC > or = 88 cm were considered centrally obesite. Prevalence of obesity and overweight was 26.3% and 40.6% respectively. Prevalence of obesity was more among women (39.5%) than men (14.5%) with central obesity prevalence using WHR and WC cut-points of 72.2% and 26.6% respectively. There was a significant association between obesity and age, gender, residential area and educational level (P < 0.01). In conclusion, prevalence of obesity and overweight among 30-70 years old, especially among women, was higher than expected. A comprehensive educational programme on obesity risk factors and obesity-related diseases is necessary.

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The beneficial effects of exercise on learning and memory are well documented but the effects of prenatal exposure to maternal exercise on offspring are not clear yet. Using a two-trial-per-day Morris water maze for five consecutive days, succeeded by a probe trial 2 days later we showed that maternal voluntary exercise (wheel running) by pregnant rats increased the acquisition phase of the pups' learning. Maternal forced swimming by pregnant rats increased both acquisition and retention phases of the pups' learning. Also we found that the rat pups whose mother was submitted to forced-swimming during pregnancy had significantly higher brain, liver, heart and kidney weights compared with their sedentary counterparts. On the other hand we estimated the cell number of different regions of the hippocampus in the rat pups. We found that both exercise models during pregnancy increased the cell number in cornus ammonis subregion 1 (CA1) and dentate gyrus of the hippocampus in rat pups. To determine the role that noradrenergic and serotonergic neurotransmission and N-methyl-D-aspartate (NMDA) receptors hold in mediation of the maternal exercise in offspring, we used N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), p-chloroamphetamine (PCA) and MK-801 to eliminate or block the above systems, respectively. Blocking the NMDA receptors, significantly abolished learning and memory in rat pups from all three experimental groups. Elimination of noradrenergic or serotonergic input did not significantly attenuate the learning and memory in rat pups whose mothers were sedentary, while it significantly reversed the positive effects of maternal exercise during pregnancy on rat pups' learning and memory. The presented results suggest that noradrenergic and serotonergic systems in offspring brain seem to have a crucial specific role in mediating the effects of maternal physical activity during pregnancy on rat pups' cognitive function in both models of voluntary and forced exercise.

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Reactivation of stabilized memories returns them to a labile state and causes them to undergo extinction or reconsolidation processes. Although it is well established that administration of glucocorticoids after training enhance consolidation of contextual fear memories, but their effects on post-retrieval processes are not known. In this study, we first asked whether administration of corticosterone after memory reactivation would modulate subsequent expression of memory in rats. Additionally, we examined whether this modulatory action would depend upon the strength of the memory. We also tested the effect of propranolol after memory reactivation. Adult male Wistar rats were trained in a fear conditioning system using moderate (0.4 mA) or high shock (1.5 mA) intensities. For reactivation, rats were returned to the chamber for 90 s 24h later. Immediately after reactivation, rats were injected with corticosterone (1, 3 or 10mg/kg) or vehicle. One, 7 and 14 days after memory reactivation, rats were returned to the context for 5 min, and freezing behavior was scored. The findings indicated that corticosterone when injected after memory reactivation had no significant effect on recall of a moderate memory, but it impaired recall of a strong memory at a dose of 3mg/kg. Propranolol (5mg/kg) given after the reactivation treatment produced a modest impairment that persisted over three test sessions. Further, the results showed that corticosterone, but not propranolol deficit was reversed by a reminder shock. These findings provide evidence that administration of glucocorticoids following memory reactivation reduces subsequent retrieval of strong, but not moderate, contextual conditioned fear memory likely via acceleration of memory extinction. On the other hand, propranolol-induced amnesia may result from blockade of reconsolidation process. Further studies are needed to determine the underlying mechanisms.

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Previous studies indicated that stress levels of glucocorticoid hormones (cortisol in humans, and corticosterone in rodents) induce impairment of long-term memory retrieval, but the underlying mechanisms (genomic or nongenomic) are not clear. To clarify this issue, we investigated the involvement of brain corticosteroid receptors and protein synthesis in the corticosterone-induced impairment of memory retrieval. Young rats were trained in the water maze task with six trials per day for 6 consecutive days. Retention of the spatial training was assessed 24 h after the last training session with a 60-s probe trial. Experiments included intraventricular injections of anisomycin, a specific protein synthesis inhibitor or specific antagonists for both types of corticocosteroid receptors (mineralocorticoid receptor, MR, and glucocorticoids receptor, GR) before corticosterone administration shortly before retention testing. The results showed that administration of anisomycin did not change the corticosterone response. Administration of the MR, but not GR, antagonist blocked the corticosterone-induced response dose dependently. These findings provide evidence for the view that glucocorticoids impair memory retrieval through nongenomic mechanisms involving an interaction with central MRs.

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A peripheral injection of glucose has been found to improve memory in rats, but the underlying mechanisms are unknown. One possible mechanism by which peripheral glucose might act on memory storage is by regulating ATP-sensitive potassium (K-ATP) channels. The present study investigated the effects of K-ATP channel modulators (minoxidil, a K-ATP channel opener and glibenclamide, a K-ATP channel closer) on memory enhancement induced by peripheral injection of glucose in an inhibitory avoidance task. Rats were trained in a one trial inhibitory avoidance task (50 Hz, 1 mA, 3 s footshock), and minoxidil (12.5,25 or 50 mg/kg) or glibenclamide (2.5,5,10 or 20 mg/kg) was injected interaperitoneally (I.P) 30 min before training. Immediately after training the rats were injected with glucose (100 mg/kg, I.P). Retention was tested 2 days later. The results indicate that systemic post-training injection of glucose improved memory storage and this effect was attenuated and enhanced by pretreatment of minoxidil and glibenclamide, respectively. The drug minoxidil or glibenclamide alone did not significantly affect memory storage. This shows that K-ATP channels mediate the memory improving effects of systemic glucose.

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Numerous studies in the past have dealt with the role of serotonergic system lesions in tasks aimed at measurement of cognitive behavior, but the literature concerning the role of serotonin in cognition remains controversial. Rats with electrolytic lesions of the median raphe nucleus (MRN) were found to display a profound impairment in both the acquisition and retention of spatial memory task. In this study, the lidocaine inactivation was employed to evaluate the involvement of the rat's median raphe nucleus in reference and working memory versions of the Morris water maze (MWM) task. Lidocaine (0.5 microl, 2%) was injected through a single cannula aimed at the MRN; control groups were treated in the same way with a 0.5 microl injection of saline. In Experiment 1, rats were trained in a reference memory version of the MWM with two blocks of four trials per day for three consecutive days, with intra-cerebral injection made 5 min before training. No significant difference was found. In Experiment 2, intra-cerebral injection was applied immediately after two blocks of four trials, and in Experiment 3, the drug was injected 5 min before retention test in rats that had received eight trials per day on three consecutive days. Again, no significant difference between control and treatment groups was found. These results indicate that MRN has no role in acquisition, consolidation and retrieval of spatial reference memory. In subsequent experiments, rats were trained in a working memory version of the MWM task to find a new target position in trial 1, and retrieval was tested 75 min later. MRN inactivation 5 min before (Experiment 4) and immediately after the acquisition trial (Experiment 5) enhanced spatial working memory. It is concluded that normal activity of the MRN has no role in formation and retrieval of reference memory, but it has an inhibitory role in working memory. Our results are confirmed with other studies suggesting that the serotonergic system has a different role in long-term and short-term memory. Interaction with other neurotransmitter systems like acetylcholine may be involved in this case.

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Involvement of median raphe nucleus (MRN) in acquisition, consolidation and retrieval of passive avoidance (PA) was investigated with functional suppression of this area by lidocaine. Rats carrying a chronically implanted cannula aimed at the MRN were trained on a step-through passive avoidance task and received intra-MRN injection of lidocaine or saline 5 min before training or 5, 90 and 360 min after acquisition trial or 5 min before the retrieval test. Lidocaine MRN inactivation had no effect on PA learning. Lidocaine injected 5 and 90 min after the acquisition trial significantly enhanced avoidance of the dark compartment in comparison with the control group injected with saline. But PA retention was not affected by lidocaine injected 360 min after acquisition or 5 min before training. Retention latency significantly increased, when lidocaine injected 5 min before retrieval test. Step-through latency of naive rats was not affected by MRN blockade. Furthermore, reversible inactivation of MRN did not have a significant effect on locomotor activity. Our results indicate that the MRN contributes to PA consolidation at least until 90 min after acquisition and involves in PA retrieval. It is concluded that functional ablation of the MRN may disrupt the inhibitory actions of MRN projections to sub-cortical circuits participating in PA memorization and retrieval.

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This study examined the role of the nucleus tractus solitarius (NTS) and amygdala in mediating the effects of bombesin (BBS) on retention of inhibitory avoidance training by reversibly inactivating these regions with lidocaine immediately following training. In Expt. 1, peripheral injection of different doses of BBS (1, 2.5, 5, 10 or 20 microg/kg) to unoperated rats immediately after training in one trial inhibitory avoidance task (1 mA, 1.5 s footshock) produced a dose-dependent response on retention test scores which was given two days after training. In Expts. 2 and 3, rats were surgically implanted unilaterally with cannula tip placed above the NTS or amygdala, were trained in task and then received unilateral injections of saline or lidocaine (2%, 0.5 microl) into the NTS or amygdala and peripheral injections of saline or BBS (5 microg/kg). The results showed that the memory enhancing effect of BBS was attenuated by unilateral inactivation of the NTS or amygdala. These findings indicate that the NTS and amygdala are involved in mediating the memory modulating effects of peripheral BBS on memory storage.

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We assessed the effects of reversible inactivation of the medial septal area (MSA) on long-term potentiation (LTP) and recurrent inhibition in the dentate gyrus of urethane-anesthetized rats, in vivo. The septal input to the hippocampus was temporarily eliminated by injection of tetrodotoxin (TTX, 10 ng/l microliter) into the MSA. In Experiment 1, LTP inducibility was examined in the perforant-dentate gyrus synapses in the MSA inactivated and control rats by 2 high-frequency stimulation (HFS), 5 min apart, applied to the perforant pathway (PP). The magnitude of potentiation was evaluated as the percentage change in the population spike (PS) amplitude at 5, 30, 60 or 120 min after the second HFS. The PS amplitude in the MSA inactivated rats was significantly lower than those of control group at 120 but not 5, 30 or 60 min after the second HFS. The MSA inactivation itself had no effect on the basal responses evoked by test stimuli. In Experiment 2, the MSA inactivation did not affect the efficacy of recurrent inhibition in the perforant-dentate gyrus synapses produced by paired pulses applied to the PP at 10- and 20-ms interpulse intervals. These results indicate that: (1) although hippocampal synapses can be still potentiated after the HFS in the MSA inactivated animals, a faster decay of LTP may be due to elimination of the MSA output amplification on synaptic responses mediated by excitatory amino acids; and (2) the recurrent inhibition mechanism in the dentate gyrus of the hippocampus is not probably affected by the MSA inactivation.

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Involvement of the medial septal area (MSA) in reference memory and working memory versions of the Morris water maze (MWM) task was investigated in rats with reversible inactivation of this area by drugs injected through a single cannula aimed at the MSA. In Experiment 1, rats were trained in a reference memory version of the MWM with two blocks of four trials per day for 3 consecutive days. Acquisition was impaired by pretrial MSA injection of 10 ng tetrodotoxin (TTX) in 1 microliter saline but not of saline alone into MSA. In Experiment 2, intraseptal injection of TTX (10 ng, 1 microliter) immediately after two blocks of four trials had no effect on the consolidation of spatial reference memory. In Experiment 3, intraseptal injection of TTX (10 ng, 1 microliter) impaired retrieval of well established spatial reference memory in rats which had received 8 trials per day for 3 consecutive days. In Experiments 4 and 5, rats were trained in a working memory version of MWM task to find a new target position in trial 1 and retrieval of this information was tested 75 min later in trial 2. Intraseptal injection of lidocaine (4%, 1 microliter) prior to training impaired working memory performance while immediately posttraining injection of lidocaine had no effect. It is concluded that normal activity of the MSA is necessary for the memory formation at the time of training but its involvement in posttraining consolidation is unlikely. The MSA function is required for retrieval of well established spatial reference memory.

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Involvement of the medial septal area (MSA) in consolidation and retrieval of passive avoidance response (PAR) was investigated with functional suppression of this area by tetrodotoxin (TTX). Rats carrying a chronically implanted cannula aimed at the MSA were trained on a step-through passive avoidance task and received intraseptal injection of 5 ng TTX dissolved in 1 microliter saline 5, 90 and 360 min after the acquisition trial or 60 min before the retrieval test. TTX injected 5 and 90 min after the acquisition trial significantly reduced avoidance of the dark compartment in comparison with the control group injected with saline. PAR was not impaired by septal TTX injected 360 min after acquisition or 60 min before the retrieval test. Step-through latency of naive rats was not affected by septal blockade. The results indicate that the MSA contributes to PAR consolidation at least 90 min after acquisition but its involvement in PAR retrieval is unlikely. It is concluded that functional ablation of the MSA may disrupt integrity of subcortical circuits participating in PAR learning.

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Tolerance to ketamine (KET) induced blockade of cortical spreading depression (CSD) was investigated in 31 rats anesthetized with pentobarbital. CSD was elicited by injection of 1 microl of 5% KCl into cortex at 15 min intervals and monitored by recording the accompanying slow potential waves. After control recording, five injections of KET (50 mg/kg) were applied at 75 min intervals. The first KET injection elicited CSD blockade lasting for 30-45 min at the near and for 60-75 min at the far electrode. The CSD blocking effect of subsequent injections gradually declined and was not recognizable after the fifth KET injection. MK-801 (2.5 mg/kg) injected to rats with fully developed KET tolerance 30 min after the last KET dose, failed to block CSD. Without KET pretreatment the same dosage of MK-801 induced CSD blockade lasting more than 1 h. KET tolerance did not prevent local CSD blockade in a cortical area superfused with 10(-3) mol/l AP5. It is concluded that repeated applications of KET may induce some conformational changes at binding site(s) in the N-methyl-D-aspartate (NMDA) controlled channels shared by both KET and MK-801.

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1. Subcutaneous injection (s.c.) of apomorphine (0.1-0.5 mg/kg) and intraperitoneal administration (i.p.) of quinpirole (0.01-0.25 mg/kg), physostigmine (0.05-0.2 mg/kg) and pilocarpine (0.75-3 mg/kg, i.p.) but not neostigmine (0.1-1 mg/kg) induced ejaculation in rats. 2. The responses of drugs were reduced by morphine (1-6 mg/kg, s.c.) pretreatment. 3. The inhibitory effect of morphine was reversed by naloxone (1.5 mg/kg, s.c.). 4. Naloxone (0.75-3 mg/kg, s.c.) alone induced slight but significant ejaculation. 5. Ejaculatory responses induced by apomorphine and quinpirole but not those by physostigmine and pilocarpine were reduced by sulpiride (100 mg/kg, i.p.) pretreatment. 6. Domperidone (1-30 mg/kg, i.p.) did not change the response induced by apomorphine. 7. Pretreatment of animals with the cholinergic antagonist atropine (10 mg/kg, i.p.) decreased the frequency of ejaculation induced by apomorphine, quinpirole, physostigmine or pilocarpine. 8. It may be concluded that D-2 activation induces ejaculation through influence on cholinergic mechanisms and morphine inhibits the ejaculation induced by activation of both cholinergic and dopaminergic systems via opiate receptor sites.

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Intraperitoneal (IP) administration of bombesin (BBS; 2.5-20 micrograms/kg) induced a dose-dependent inhibition of food intake. The effect was decreased by intraventricular (ICV) administration of bombesin receptor antagonist [Leu14-psi (CH2NH)-Leu13] (3 micrograms/rat) but not by the D1 antagonist SCH 23390, the D2 antagonists sulpiride and pimozide, the dopamine antagonist cis-flupentixol, adrenoceptor blockers phenoxybenzamine or propranolol and serotonergic antagonist methergoline. It is concluded that BBS-induced suppression of feeding may be mediated through central BBS receptors, and is independent of interaction with brain catecholaminergic system.

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