The density of Golgi-impregnated dendritic spines from adult rat posterodorsal medial amygdala neurons displays no evidence of hemispheric or dorsal/ventral differences

The posterodorsal medial amygdaloid nucleus (MePD) is a sexually dimorphic area in the rat brain and dendritic spines are specialized postsynaptic sites involved with local neural plasticity. Previous electrophysiological data showed that prepubertal males have more excitatory synapses than females in the left MePD. Besides, dorsal and ventral MePD neurons have a heterogeneous expression of estrogen receptors α or β in mating-responsive neurons in females. Based on these findings, the “single-section” Golgi method was employed in adult rats (n = 6 in each group) to reveal: (1) the effect of hemispheric laterality in the density of dendritic spines in the MePD of males and diestrus females, and (2) the density of dendritic spines in the MePD dorsal and ventral subregions in proestrus females (mean values from n = 48 neurons for each experimental variable). There were no statistically significant differences for sex, laterality or the interaction of these factors in the dendritic spine density between males and diestrus females (p > 0.2), nor for the dorsal and the ventral MePD dendritic spine density in proestrus females (p > 0.1). These findings complement current knowledge about the rat MePD and suggest that the number of proximal dendritic spines is not lateralized at adulthood. Furthermore, the differential expression of estradiol receptors in the dorsal and ventral MePD did not lead to distinct spine number in these subregions when circulating ovarian steroids peak in proestrus.     

Descriptive findings on the morphology of dendritic spines in the rat medial amygdala

The rat posterodorsal medial amygdala (MePD) is a brain area in which gonadal hormones induce notable plastic effects in the density of dendritic spines. Dendritic spines are post-synaptic specializations whose shape and spacing change neuronal excitability. Our aim was to obtain new data on the dendritic spines morphology and density from MePD neurons using the carbocyanine dye DiI under confocal microscopy. In adult male rats, the dendritic spine density of the medial branches of the left MePD (mean ± SD) was 1.15 ± 0.67 spines/dendritic μm. From the total sampled, approximately 53% of the spines were classified as thin, 22.5% as “mushroom-like”, and 21.5% as stubby/wide. Other spine shapes (3%) included those ramified, with a filopodium-like or a gemule appearance, and others with a protruding spinule. Additional experiment joining DiI and synaptophysin (a pre-synaptic protein) labeling suggested synaptic sites on dendritic shafts and spines. Dendritic spines showed synaptophysin puncta close to their head and neck, although some spines had no evident labeled puncta on them or, conversely, multiple puncta appeared upon one spine. These results advance previous light microscopy results by revealing features and complexities of the dendritic spines at the same time that give new insight on the possible synaptic organization of the adult rat MePD.     

Comparative effects of risedronate,atorvastatin, estrogen and SERMs on bone mass and strength in ovariectomized rats

Objective

The aim of this study was to investigate bone protective effects of risedronate, atorvastatin, raloxifene and clomiphene citrate in ovariectomized rats.

Methods

Our study was conducted on 63 rats at Experimental Research Center of Celal Bayar University. Six-month-old rats were divided into seven groups. There were five drug administered ovariectomized groups, one ovariectomized control group without drug administration and one non-ovariectomized control group without drug administration. Eight weeks postovariectomy, rats were treated with the bisphosphonate risedronate sodium, the statin atorvastatin, the estrogen 17β-estradiol and the selective estrogen receptor modulators (SERMs) raloxifene hydrochloride and clomiphene citrate by gavage daily for 8 weeks. At the end of the study, rats were killed under anesthesia. For densitometric evaluation, left femurs and tibiae were removed. Left femurs were also used to measure bone volume. Right femurs were used for three-point bending test.

Results

Compared to ovariectomized group, femur cortex volume increased significantly in non-ovariectomized group (p = 0.016). Compared to non-ovariectomized group, distal femoral metaphyseal and femur midshaft bone mineral density values were significantly lower in ovariectomized group (p = 0.047). In ovariectomy + atorvastatin group, whole femur and femur midshaft bone mineral density and three-point bending test maximal load values were significantly higher than ovariectomized group (p = 0.049, 0.05, and 0.018). When compared to the ovariectomized group, no significant difference was found with respect to femoral maximum load values in groups treated with risedronate, estrogen, raloxifene and clomiphene (p = 0.602, 0.602, 0.75, and 0.927). In ovariectomy + risedronate group, femur midshaft bone mineral density values were significantly higher than the values in ovariectomized group (p = 0.023). When compared to ovariectomized group, no significant difference was found with respect to femur midshaft bone mineral density values in groups treated with estrogen, raloxifene and clomiphene (p = 0.306, 0.808, and 0.095).

Conclusions

While risedronate sodium prevented the decrease in bone mineral density in ovariectomized rats, atorvastatin maintained mechanical characteristics of bone and also prevented the decrease in bone mineral density as risedronate sodium.     

Bridging the transition from cancer patient to survivor: Pilot study results of the Cancer Survivor Telephone Education and Personal Support (C-STEPS) program

Objective

To develop a feasibility study of a theory-driven telephone counseling program to enhance psychosocial and physical well-being for cancer survivors after treatment.

Methods

Participants (n = 66) were recruited from two Colorado hospitals with self-administered questionnaires at baseline and two weeks post-intervention. The one group, intervention only design included up to six thematic telephone counseling sessions over three months. Topics included nutrition, physical activity, stress management, and medical follow-up. Primary outcomes were cancer-specific distress, self-reported fruit and vegetable consumption and physical activity.

Results

Of 66 subjects, 46 completed at least one counseling module and the follow-up assessment (70% retention rate). Mean satisfaction was 9 out of 10, and all participants would recommend C-STEPS to other survivors. Cancer-specific distress (Impact of Event Scale – Intrusion subscale) decreased for entire study population (p < 0.001) and stress management session participants (p < 0.001). Fruit and vegetable consumption increased for nutrition and exercise session participants (p = 0.02) and the entire sample (p = NS). Physical activity increased in the entire group (p = 0.006) and for nutrition and exercise session participants (p = 0.01).

Conclusion and practice implications

C-STEPS is a feasible telephone counseling program that transcends geographic barriers, demonstrating the potential to decrease distress and promote coping and healthy lifestyles among cancer survivors.     

Delayed peripheral administration of the N-terminal tripeptide of IGF-1 (GPE) reduces brain damage following microsphere induced embolic damage in young adult and aged rats

We have previously reported that peripheral administration of GPE prevents neuronal injury after ischemic reperfusion injury in young adult rats. This study examined the ameliorating effects of GPE-treatment after embolic injury induced by microsphere injection in young adult and aged male rats. Unilateral injury was induced by injecting microspheres into the right internal carotid artery in both young adult (3–4 months) and aged (16–17 months) male rats. Either GPE (12 mg/kg) or the vehicle was infused intravenously over 1 h starting 3 h after embolic injury and the degree of brain injury, astrocytosis and vascular remodeling were examined using histological and immunohistochemical analysis 8 days later. Changes in core temperature, blood glucose concentration, oxygen saturation and heart rate were monitored. Microsphere injection induced multiple sites of focal damage in the ipsilateral subcortical regions. Massive numbers of microglia accumulated within the core of the tissue damage whereas astrocytes were located in the penumbra. There was no difference in the degree of brain injury between the young and aged control rats. However the aged rats showed less injury-induced astrocytosis and greater vascular remodeling. Intravenous infusion of GPE 3 h after the injury reduced overall damage scores in both young (p < 0.01) and aged rats (p < 0.05). GPE-treatment reduced astrocytosis in young, but not aged animals and did not significantly alter the vascular remodeling in either age group. The data suggested that the neuroprotection of the tripeptide is independent of cerebral reperfusion and is not age selective.     

Involvement of neuronal nitric oxide synthase in cognitive impairment in isoflurane-treated rats

The underlying causes of post-operative cognitive dysfunction (POCD) in elderly patients remain to be elucidated. In order to explore possible contributory mechanisms, we tested the effects of isoflurane anesthesia on (i) expression of hippocampal neuronal nitric oxide synthase (nNOS) and (ii) the relationship of changes in nNOS expression to cognitive dysfunction in isoflurane-treated aged rats. Our results indicate that isoflurane treatment leads to significant changes in correct reactions (F = 28.35, p < 0.001), initiative avoidances (F = 29.33, p < 0.001), and total reaction time (TRT) (F = 6.99, p < 0.05) of treated rats in the Y-maze test. Isoflurane-treated rats had fewer correct reactions and initiative avoidances in the Y-maze test 24 and 48 h after 2 h of isoflurane anesthesia compared with control group rats (p < 0.05). TRTs to complete 20 trials of the Y-maze test increased significantly 48 h after 2 h anesthesia. The number of nNOS-positive hippocampal neurons decreased 24 h after anesthesia, corresponding to an increased mean immunostaining grey-scale value. These data show that isoflurane causes a transient decrease in expression of hippocampal nNOS in aged rats during early post-anesthesia stages, and that the transient decrease of nNOS is closely correlated with cognitive impairment in isoflurane-treated aged rats.     

Prenatal ozone exposure abolishes stress activation of Fos and tyrosine hydroxylase in the nucleus tractus solitarius of adult rat

Ozone (O₃) is widely distributed in the environment, with high levels of air pollution. However, very few studies have documented the effects on postnatal development of O₃ during pregnancy. The long-term effects of prenatal O₃ exposure in rats (0.5 ppm 12 h/day from embryonic day E5 to E20) were evaluated in the adult nucleus tractus solitarius (NTS) regulating respiratory control. Neuronal response was assessed by Fos protein immunolabeling (Fos-IR), and catecholaminergic neuron involvement by tyrosine hydroxylase (TH) labeling (TH-IR). Adult offspring were analyzed at baseline and following immobilization stress (one hour, plus two hours’ recovery); immunolabeling was observed by confocal microscopy. Prenatal O₃ increased the baseline TH gray level per cell (p < 0.001). In contrast, the number of Fos-IR cells, Fos-IR/TH-IR colabeled cells and proportion of TH double-labeled with Fos remained unchanged. After stress, the TH gray level (p < 0.001), number of Fos-IR cells (p < 0.001) and of colabeled Fos-IR/TH-IR cells (p < 0.05) and percentage of colabeled Fos-IR/TH-IR neurons against TH-IR cells (p < 0.05) increased in the control group. In prenatal-O₃ rats, immobilization stress abolished these increases and reduced the TH gray level (p < 0.05), indicating that prenatal O₃ led to loss of adult NTS reactivity to stress. We conclude that long-lasting sequelae were detected in the offspring beyond the prenatal O₃ exposure. Prenatal O₃ left a print on the NTS, revealed by stress. Disruption of neuronal plasticity to new challenge might be suggested.     

Stressful experience has opposite effects on dendritic spines in the hippocampus of cycling versus masculinized females

Stress increases associative learning and the density of dendritic spines in the hippocampus of male rats. In contrast, exposure to the same stressor impairs associative learning and reduces spine density in females. These effects in females are most evident when they are in the proestrus phase of the estrous cycle. An injection of testosterone at the time of birth masculinizes the female brain. In adulthood, masculinized females respond like males do to stress, i.e. they learn better. Here, we hypothesized that stress would increase spine densities on pyramidal neurons in area CA1 of the hippocampus of masculinized females, because stress enhances learning ability in both males and masculinized females. To test this, we used Golgi impregnation to stain tissue from masculinized and cycling females that were exposed to an acute stressor and sacrificed 1 day later. There was a significant interaction between stressor exposure and testosterone treatment at birth (p < 0.001). In general, cycling females that were stressed tended to possess fewer spines on apical and basal dendrites in the CA1 area of the hippocampus, whereas the masculinized females possessed significantly more spines after the stressor. These findings underscore the plastic nature of dendritic spines. They suggest that their response to stress in adulthood is organized by the presence of testosterone during very early development. Such a process may represent a mechanism for altering learning abilities after an acute traumatic experience.     

Influence of substitutive ovarian steroids in the nuclear and cell body volumes of neurons in the posterodorsal medial amygdala of adult ovariectomized female rats

The volumes of the neuronal nucleus and the cell body in the left posterodorsal medial amygdala (MePD) of adult ovariectomized (OVX) female rats submitted to different hormonal therapies were studied here, aiming to reveal possible influence of substitutive sex steroids in these morphological parameters. One week following ovariectomy and at the end of treatments, brains were cut to semi-thin sections (1 μm) and stained with 1% toluidine blue for stereological estimations, carried out using the Cavalieri method and the technique of point counting. Both the volume of the neuronal nucleus and the soma showed a statistically significant difference when comparing the data among OVX females treated with vehicle (V), estradiol (EB) alone, EB plus progesterone (EB + P) or P alone [n = 5 rats in each group; one-way ANOVA test, P < 0.01 in both cases]. The Tukey test showed that OVX and EB + P treated females had higher mean neuronal nucleus and somatic volumes when compared to V (P < 0.01) or EB alone (P < 0.01). Also, OVX females treated with P alone showed larger mean neuronal nucleus and somatic volumes when compared to V (P < 0.05). These results suggest that the neuronal nucleus and the somatic volumes can be modulated by substitutive ovarian hormones administered to OVX females, for which P can lead to higher results. These findings reveal additional epigenetic actions of the sex steroids in the MePD and new neuronal morphological features in adult female rats.     

Central ghrelin treatment stimulates ACTH cells in normal-fed,food-restricted and high-fed rats: An immunohistomorphometric and hormonal study

Changes in feeding regime represent serious stress, while ghrelin is considered a key player in energy balance. We investigated the effects of intracerebroventricular (ICV) ghrelin application on pituitary adrenocorticotropic (ACTH) cells in rats fed diets differing in energy content. Before the ICV treatment, male Wistar rats were subjected to three different feeding regimes for 4 weeks: normal-fed (NF), food-restricted (FR) or high-fed (HF) (n = 3 × 14). At the age of 8 weeks, rats from each group were divided into two subgroups and given ICV, either ghrelin (G; 1 μg ghrelin/5 μl PBS, n = 7) or solvent alone (5 μl PBS, n = 7) every 24 h for 5 days. The immunohistochemical appearance and quantitative morphology of pituitary ACTH cells were evaluated, as well as peripheral ACTH and corticosterone levels. Central ghrelin administration increased (p < 0.05) ACTH cell volumes in GNF, GFR and GHF rats by 8.1%, 11.8% and 9.1%, respectively, compared to the controls, while significant increases in ACTH cell volume density were observed in GNF and GHF rats. Circulating ACTH and corticosterone levels were elevated (p < 0.05) in GNF and GFR rats by 72.8% and 80.8%, respectively, when compared to the corresponding controls. Thus, central ghrelin administration stimulated the pituitary-adrenal axis under preserved and negative energy balance states.     

Labisia pumila extract regulates body weight and adipokines in ovariectomized rats

Objective

We investigated the effects of a standardized water extract of Labisia pumila var. alata (LPva), and compared to estrogen replacement (ERT), on body weight gain, uterus weight, adipose tissue mRNA and protein levels of adipokines in ovariectomized (OVX) rats.

Methods

Eight-week-old OVX Sprague-Dawley rats were administered orally with either 10 mg/kg/day (LPva10), 20 mg/kg/day (LPva20) or 50 mg/kg/day (LPva50) of LPva for 30 days. Sham-operated (Sham) and estrogen-treated OVX rats (ERT, 0.625 mg/kg/day) served as controls. Plasma adipokines were measured, and mRNA expressions of the adipokines were determined in the adipose tissues.

Results

ERT- and LPva50-treated OVX rats showed significantly less (p < 0.05) weight gain compared to untreated OVX rats. Ovariectomy caused plasma leptin levels to decrease significantly (p < 0.05), but when treated with LPva or ERT, plasma leptin increased significantly to levels higher or comparable to that seen in the Sham group. The mRNA expression of leptin was higher in the LPva-treated animals than in all other groups. In contrast, the elevated plasma resistin concentrations in OVX rats were significantly reduced in rats given ERT (p < 0.05) and LPva extracts (p < 0.05). There was no difference in adiponectin levels in all groups. The uterus to body weight ratio of untreated OVX rats was significantly low compared to Sham (p < 0.05), but showed dose-dependent increase upon treatment with LPva.

Conclusion

The present study provides first evidence that LPva exerts uterotrophic effect and regulates body weight gain by modulating secretion of leptin and resistin, and expression of the adipokines in adipose tissues.     

Class I antiarrhythmic drugs produced a spinal anesthetic effect in rats

Class I antiarrhythmic drugs are commonly used to treat cardiac rhythm disorders. Some of those drugs were recently reported to have both a cutaneous analgesic and a neural blocking effect. We evaluated whether these drugs have a spinal anesthetic effect. Three Class I antiarrhythmic drugs (class IA: quinidine, IB: mexiletine, and IC: flecainide) were tested. After they had been intrathecally injected in rats, the potencies and durations of these drugs on spinal anesthesia were recorded. Bupivacaine, a commonly used local anesthetic, and 5% dextrose solution were used as controls. Bupivacaine, flecainide, quinidine, and mexiletine produced a dose-related spinal blockade of motor function, proprioception, and nociception, but dextrose solution produced no spinal anesthetic effect. The descending order of potency was bupivacaine > flecainide > quinidine > mexiletine (p < 0.05 for all differences). On an equipotent basis, flecainide, quinidine, and bupivacaine produced similar durations of action, all of which were significantly longer than that of mexiletine (p < 0.05). In conclusion, intrathecal injections of Class I antiarrhythmic drugs produced a dose-related spinal anesthetic effect. These drugs may be potential candidates for developing new local anesthetics.     

Differential alterations of GABA(A) receptor (α1, β2, γ2 subunit) expression and increased seizure susceptibility in rat offspring from morphine-addicted mothers: beneficial effect of dextromethorphan

Recent study demonstrated a close relationship between cerebellum atrophy and symptom severity of pediatric maltreatment-related posttraumatic stress disorder (PTSD). It has also been known that females are more vulnerable than males in developing anxiety disorders after exposure to traumatic stress. The mechanisms are unknown. Because cannabinoid receptors (CB₁ and CB₂) are neuroprotective and highly expressed in the cerebellum, we investigated cerebellar CB expression in stressed rats. Young male and female Sprague-Dawley rats were given 40 unpredictable electric tail-shocks for 2 h daily on 3 consecutive days. CB₁ and CB₂ mRNA and protein levels in rat cerebellum and brain stem were determined using quantitative real-time PCR and Western blot, respectively. Two-way ANOVA revealed significant gender and stress effects on cerebellar CB₁ mRNA expression, with females and non-stressed rats exhibiting higher CB₁ mRNA levels than the males (3 fold, p < 0.01) and stressed rats (30%, p < 0.01), respectively. CB₁ and CB₂ mRNA levels in brain stem were also greater in female rats than males (p < 0.01, p < 0.05, respectively). Repeated stress increased the level of phosphorylated CB₁ receptors, the inactivated CB₁, in rat cerebellum (p < 0.01), particularly in female rats as revealed by the significant gender × stress interaction. Thus, repeated severe stress caused greater CB₁ mRNA suppression and CB₁ receptor phosphorylation in female cerebellum that could lead to increased susceptibility to stress-related anxiety disorders including PTSD.     

Group II metabotropic glutamate receptors in the striatum of non-human primates: dysregulation following chronic cocaine self-administration

The purpose of this study was to investigate the possible effects of a treadmill training program on regeneration in young (3-month-old) and mature (13-month-old) rats with sciatic nerve crush using functional, electrophysiological, and morphometric analyses. When compared to both the young and mature untrained injury groups, those groups that underwent a treadmill training showed improved sensorimotor function evaluated by narrow beam test (p < 0.04 and p < 0.001, respectively), while muscle action potential amplitude was only greater in the young group (p < 0.02). The treadmill training program was able to reduce myelinated fiber density in the young group (p < 0.001), which appeared to increase after nerve injury (poly-innervation), but decreased with training, which means that the innervation became more functional. The data indicate that treadmill training is able to promote functional, electrophysiological and morphological recovery in young animals. However, in mature animals, improvement was only seen in terms of functional recovery.     

Fluoxetine augments ventilatory CO2 sensitivity in Brown Norway but not Sprague Dawley rats

The Brown Norway (BN; BN/NHsdMcwi) rat exhibits a deficit in ventilatory CO₂ sensitivity and a modest serotonin (5-HT) deficiency. Here, we tested the hypothesis that the selective serotonin reuptake inhibitor fluoxetine would augment CO₂ sensitivity in BN but not Sprague Dawley (SD) rats. Ventilation during room air or 7% CO₂ exposure was measured before, during and after 3 weeks of daily injections of saline or fluoxetine (10 mg/(kg day)) in adult male BN and SD rats. Fluoxetine had minimal effects on room air breathing in BN and SD rats (p > 0.05), although tidal volume (V_T) was reduced in BN rats (p < 0.05). There were also minimal effects of fluoxetine on CO₂ sensitivity in SD rats, but fluoxetine increased minute ventilation, breathing frequency and V_T during hypercapnia in BN rats (p < 0.05). The augmented CO₂ response was reversible upon withdrawal of fluoxetine. Brain levels of biogenic amines were largely unaffected, but 5-HIAA and the ratio of 5-HIAA/5-HT were reduced (p < 0.05) consistent with selective and effective 5-HT reuptake inhibition. Thus, fluoxetine increases ventilatory CO₂ sensitivity in BN but not SD rats, further suggesting altered 5-HT system function may contribute to the inherently low CO₂ sensitivity in the BN rat.     

Sustained acceleration of colonic transit following chronic homotypic stress in oxytocin knockout mice

Acute restraint stress delays gastric emptying and accelerates colonic transit via central corticotropin releasing factor (CRF) in rats. In contrast, central oxytocin has anxiolytic effects and attenuates the hypothalamus–pituitary–adrenal (HPA) axis in response to stress. Our recent study showed that up regulated oxytocin expression attenuates hypothalamic CRF expression and restores impaired gastric motility following chronic homotypic stress in mice. We studied the effects of acute and chronic homotypic stress on colonic transit and hypothalamic CRF mRNA expression in wild type (WT) and oxytocin knockout (OXT-KO) mice. Colonic transit was measured following acute restraint stress or chronic homotypic stress (repeated restraint stress for 5 consecutive days). ⁵¹Cr was injected via a catheter into the proximal colon. Ninety minutes after restraint stress loading, the entire colon was removed. The geometric center (GC) was calculated to evaluate colonic transit. Expression of CRF mRNA in the supraoptic nucleus (SON) was measured by real time RT-PCR. Colonic transit was significantly accelerated following acute stress in WT (GC = 8.1 ± 0.8; n = 7) and OXT KO mice (GC =9.4 ± 0.3; n = 7). The accelerated colonic transit was significantly attenuated in WT mice (GC = 6.6 ± 0.5; n = 9) following chronic homotypic stress while it was still accelerated in OXT KO mice (GC = 9.3 ± 0.5; n = 8). The increase in CRF mRNA expression at the SON was much greater in OXT-KO mice, compared to WT mice following chronic homotypic stress. It is suggested that oxytocin plays a pivotal role in mediating the adaptation mechanism following chronic homotypic stress in mice.     

Base excision repair pathway genes polymorphism in prostate and bladder cancer risk in North Indian population

Purpose

Carcinogens causes DNA damage, including oxidative lesions that are removed efficiently by the base excision repair (BER) pathway. Variations in BER genes may reduce DNA repair capacity, leading to development of urological cancers.

Methods

This study included 195 prostate cancer (PCa) and 212 bladder cancer (BC) patients and 250 controls who had been frequency matched by age, sex, and ethnicity. We genotyped XRCC1 Exon 6 (C > T), 9 (G > A), 10 (G > A), OGG1 Exon 7 (C > G) and APE1 Exon 5 (T > G) genes polymorphism using PCR-RFLP and ARMS.

Results

GA of XRCC1 Exon 9 demonstrated increased risk with PCa as well as in BC (p = 0.001; p = 0.006). Similarly variant containing genotype revealed association with PCa (p = 0.031). Haplotype of XRCC1 also associated with significant risk for PCa and BC. The APE1 GG genotype showed a decreased risk of BC (OR = 0.25; p = 0.017). Variant genotype GG of OGG1 demonstrated significant risk with BC (p = 0.028).

Conclusions

Our observations suggested increased risk for PCa and BC in case of GA genotype for XRCC1, and variant GG in case of OGG1. However APE1 GG genotype conferred a protective association with BC susceptibility. Larger studies and the more SNPs in the same pathway are needed to verify these findings.     

Tuning the gain of somato-sympathetic reflexes by stimulation of the thoracic spine in humans

In animals, somatic stimulation of the limbs can evoke sympathetic reflexes of supraspinal origin. In addition, spinal reflexes can be elicited by stimulation of somatic tissues of the trunk. However, limited evidence is available concerning the specific modulation of sympathetic reflexes by afferents from the thoracic spine. This has also been largely overlooked in healthy humans. The aim of the present study was to determine whether tonic noxious heat (NH) applied to the skin over T3–T5 could segmentally increase supraspinal sympathetic reflexes (skin conductance responses – SCRs) induced by phasic electrical stimulation of the sural nerve. In addition, the effect of spinal manipulation (SM) on SCR amplitude and SCR amplification by NH was investigated. During the control session, palmar and plantar SCR amplitude was stable, showing no significant modulation. During NH and SM, however, palmar SCR amplitude was respectively increased and decreased in comparison to baseline, leading to a robust difference in SCR amplitude between the 2 conditions (p < 0.001). Moreover, these changes were also significantly and marginally different compared to the control session (p = 0.041 and p = 0.053, respectively). Interestingly, when applied immediately before NH, SM had a preventive effect on palmar SCR amplification induced by NH. In sharp contrast, changes in plantar SCRs were not significantly different between sessions (p = 0.42). Altogether, these results indicate that somatic stimulation of the thoracic spine may modulate somato-sympathetic reflexes segmentally in conscious, healthy volunteers.     

Antihyperglycemic and antihyperlipidemic effect of Rumex patientia seed preparation in streptozotocin-diabetic rats

Background and objective:Rumex patientia (RP) could exert beneficial health effects to ameliorate metabolic diseases. The effect of subchronic feeding of RP seeds was evaluated on serum glucose and lipid profile in streptozotocin (STZ)-diabetic rats. Methods: Wistar rats were divided into control, RP-treated control, diabetic, glibenclamide-treated diabetic, and RP-treated diabetic groups. For induction of diabetes, streptozotcin was administered at a dose of 60 mg/kg. Meanwhile, RP-treated groups received RP seed powder mixed with standard pelleted food at a weight ratio of 6% for 4 weeks. Serum glucose and lipid levels were determined before the study and at 2nd and 4th weeks after the study in addition to the oxidative stress markers in hepatic tissue. Results: Serum glucose was significantly lower in RP-treated diabetic rats at 2nd and 4th weeks as compared to untreated diabetics (p < 0.05 and p < 0.01, respectively). Serum total cholesterol and triglyceride levels did not show significant reductions in RP-treated diabetic rats as compared to untreated diabetics. Serum HDL-cholesterol, however, significantly increased (p < 0.05) and LDL-cholesterol showed a significant reduction (p < 0.05) in RP-treated diabetic rats as compared to untreated diabetics (p < 0.05). RP also attenuated the increased malondialdehyde (MDA) content and reduced activity of superoxide dismutase (SOD) in hepatic tissue. Conclusion: Subchronic treatment of diabetic rats with RP could lessen the abnormal changes in blood glucose level and to improve lipid profile regarding HDL- and LDL-cholesterol in part due to its attenuation of lipid peroxidation in hepatic tissue.