scholarly journals Anxiolytic Effects of Acanthopanax senticosus HARMS Occur via Regulation of Autonomic Function and Activate Hippocampal BDNF–TrkB Signaling

Molecules ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. 132 ◽  
Author(s):  
Shouhei Miyazaki ◽  
Hirotaka Oikawa ◽  
Hideo Takekoshi ◽  
Masako Hoshizaki ◽  
Masato Ogata ◽  
...  
Keyword(s):  
Autonomic Function ◽  
Nervous Activity ◽  
Anxiolytic Effect ◽  
Gastric Ulcers ◽  
Sympathetic Nervous Activity ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Acanthopanax Senticosus ◽  
Sprague Dawley Rats ◽  
Bdnf Signaling

Mental stress, such as anxiety and conflict, causes physiological changes, such as changes in autonomic nervous activity and gastric ulcers. In addition, stress induces glucocorticoids and changes the hippocampal brain-derived neurotrophic factor (BDNF) expression levels. We previously reported that Acanthopanax senticosus HARM (ASH) prevents stress-induced gastric ulcers. Thus, we investigated the potential anxiolytic effect and influence of ASH on the hippocampus BDNF-related protein in male Sprague-Dawley rats fed 1% and 5% ASH extract-containing food for one week using novelty suppressed feeding (NSF) and improved elevated beam walking (IEBW) tests. ASH treatment significantly decreased latency to eat in the NSF test and increased the time spent on the open arm in the IEBW test. ASH5% treatment showed a significant decrease in LFnu, indicative of sympathetic nervous activity, and a significant increase in HFnu, indicative of parasympathetic nervous activity, in the NSF test. In addition, ASH1% and ASH5% treatments significantly decreased LFnu and significantly increased HFnu in the IEBW test. ASH5% treatment significantly increased hippocampal BDNF protein expression in both Western blotting and immunohistochemistry experiments. Our findings suggest that anxiolytic effects of ASH occur via the regulation of autonomic function and increased hippocampal BDNF signaling.

scholarly journals Combination of syringaresinol–di–O–β-d-glucoside and chlorogenic acid shows behavioral pharmacological anxiolytic activity and activation of hippocampal BDNF–TrkB signaling

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Shouhei Miyazaki ◽  
Yoshio Fujita ◽  
Hirotaka Oikawa ◽  
Hideo Takekoshi ◽  
Hideaki Soya ◽  
...  
Keyword(s):  
Protein Expression ◽  
Chlorogenic Acid ◽  
Nervous Activity ◽  
Low Frequency ◽  
Anxiolytic Activity ◽  
Gastric Ulcers ◽  
Sympathetic Nervous Activity ◽  
Sprague Dawley ◽  
Acanthopanax Senticosus ◽  
Frequency Power

Abstract Mental stress, such as anxiety and conflict, causes physiological changes such as dysregulation of autonomic nervous activity, depression, and gastric ulcers. It also induces glucocorticoid production and changes in hippocampal brain-derived neurotrophic factor (BDNF) levels. We previously reported that Acanthopanax senticosus HARMS (ASH) exhibited anxiolytic activity. Thus, we attempted to identify the anxiolytic constituents of ASH and investigated its influence on hippocampal BDNF protein expression in male Sprague Dawley rats administered chlorogenic acid (CHA), ( +)-syringaresinol–di–O–β-d-glucoside (SYG), or a mixture of both (Mix) for 1 week using the open field test (OFT) and improved elevated beam walking (IEBW) test. As with ASH and the benzodiazepine anxiolytic cloxazolam (CLO), Mix treatment significantly increased locomotor activity in the OFT. CHA and Mix increased the time spent in the open arm in the IEBW test. SYG and Mix treatment inhibited the significant increase in normalized low-frequency power, indicative of sympathetic nervous activity, and significant decrease in normalized high-frequency power, indicative of parasympathetic nervous activity, as observed in the IEBW test. SYG and Mix treatment significantly increased hippocampal BDNF protein expression. The combination of CHA and SYG possibly induces anxiolytic behavior and modulates autonomic regulation, activates hippocampal BDNF signaling as with ASH.

scholarly journals RNAi silencing of brain klotho potentiates cold-induced elevation of blood pressure via the endothelin pathway

2010 ◽  
Vol 41 (2) ◽  
pp. 120-126 ◽  
Author(s):  
Xiuqing Wang ◽  
Zhongjie Sun
Keyword(s):  
Blood Pressure ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Control Shrna ◽  
Sympathetic Nervous ◽  
Subsequent Activation ◽  
And Control

Klotho is a recently identified antiaging gene. Brain endothelin-1 (ET1) is important in the regulation of blood pressure (BP). We hypothesized that silence of brain klotho potentiates cold-induced elevation of BP via the endothelin pathway. To silence brain klotho, we constructed adeno-associated virus (AAV) carrying rat klotho small interference hairpin RNA (KL-shRNA). AAV carrying ET1-shRNA was used to silence brain ET1. Scrambled shRNA was used as Control-shRNA. Three groups of male Sprague-Dawley rats (6 rats/group) received KL-shRNA, KL-shRNA plus ET1-shRNA, and Control-shRNA, respectively, via intracerebroventricular injection. BP was monitored daily using a telemetry system. All animals were exposed to a moderate cold environment (5°C) at 12 days after gene delivery. KL-shRNA significantly increased BP by 9 days of exposure to cold, while BP in the Control-shRNA group remained unchanged. ET1-shRNA abolished KL-shRNA-induced elevation of BP during cold exposure. Interestingly, KL-shRNA increased brain ET1 expression and plasma norepinephrine level, suggesting that silencing of brain klotho increased ET1 production and the sympathetic nervous activity. The KL-shRNA-induced increase in sympathetic nervous activity was mediated by ET1 because it could be abolished by silencing of ET1. These results demonstrated that silencing of brain klotho potentiated and expedited cold-induced elevation of BP by upregulation of ET1 and the subsequent activation of the sympathetic nervous system.

scholarly journals Aerobic Exercise Prevents Depression via Alleviating Hippocampus Injury in Chronic Stressed Depression Rats

2020 ◽  
Vol 11 (1) ◽  
pp. 9
Author(s):  
Jie Kang ◽  
Di Wang ◽  
Yongchang Duan ◽  
Lin Zhai ◽  
Lin Shi ◽  
...  
Keyword(s):  
Aerobic Exercise ◽  
Mild Stress ◽  
Glutamatergic System ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Sprague Dawley Rats ◽  
Immobility Time ◽  
Neurotoxic Effects ◽  
Swimming Test ◽  
Underlying Mechanisms

(1) Background: Depression is one of the overwhelming public health problems. Alleviating hippocampus injury may prevent depression development. Herein, we established the chronic unpredictable mild stress (CUMS) model and aimed to investigate whether aerobic exercise (AE) could alleviate CUMS induced depression-like behaviors and hippocampus injury. (2) Methods: Forty-eight healthy male Sprague-Dawley rats (200 ± 20 g) were randomly divided into 4 groups (control, CUMS, CUMS + 7 days AE, CUMS + 14 days AE). Rats with AE treatments were subjected to 45 min treadmill per day. (3) Results: AE intervention significantly improved CUMS-induced depressive behaviors, e.g., running square numbers and immobility time assessed by the open field and forced swimming test, suppressed hippocampal neuron apoptosis, reduced levels of phosphorylation of NMDA receptor and homocysteine in hippocampus, as well as serum glucocorticoids, compared to the CUMS rats. In contrast, AE upregulated phosphorylation of AMPAR receptor and brain-derived neurotrophic factor (BDNF) hippocampus in CUMS depression rats. The 14 day-AE treatment exhibited better performance than 7 day-AE on the improvement of the hippocampal function. (4) Conclusion: AE might be an efficient strategy for prevention of CUMS-induced depression via ameliorating hippocampus functions. Underlying mechanisms may be related with glutamatergic system, the neurotoxic effects of homocysteine, and/or influences in glucocorticoids-BDNF expression interaction.

scholarly journals The Protective Effect of Testosterone on Indomethacin Induced Gastric Ulcer in Female Sprague Dawley Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-5
Author(s):  
U. Akpamu ◽  
H. O. Otamere ◽  
I. O. Ernest-Nwoke ◽  
C. N. Ekhator ◽  
U. C. Osifo
Keyword(s):  
Gastric Ulcer ◽  
Female Rats ◽  
Gastric Ulcers ◽  
Standard Laboratory ◽  
Sprague Dawley ◽  
Gastric Mucus ◽  
Ulcer Index ◽  
Sprague Dawley Rats ◽  
Group A ◽  
Group B

Gastric ulcer has shown association with changes in sex hormones, with impact exacerbated in males. Also, males are known to be more exposed to ulcer risk factors. This study investigates the effect of testosterone on indomethacin induced gastric ulcers in adult female rats. Eighteen female rats (225 ± 25 g body weight) were randomly assigned to 3 groups under standard laboratory condition. After acclimatization, animals fasted for 40 hrs but were given water ad libitum. Group A served as control while group B served as the ulcer control, in which ulcer was induced without treatment using indomethacin (40 mg/kg single orally dose). Group C was pretreated with testosterone (1 mg/kg IM) eight hours before ulcer induction. Eight hours after ulcer induction, animals were sacrificed and the stomach was harvested for analysis. Results showed a significant reduction in mucus content in groups C (0.79±0.11 g) and B (0.87±0.02 g) compared to A (1.11±0.03 g). Gastric mucus pH was significantly acidic in group B (4.40±0.55) compared to C (5.20±0.45) and A (5.80±0.45). There was a significantly higher ulcer index in group B (4.60±0.55 mm) compared to C (3.60±0.89 mm) and testosterone pretreatment resulted in a 21.74% ulcer inhibition. Although weak, the findings suggest that testosterone might protect the gastric mucosa against NSAIDs in females.

scholarly journals Chronic Inflammatory Pain Management by BDNF Modulation: A Comparative Study of Gabapentin, Indomethacin and Their Combination on Arthritis Rat Model

2021 ◽  
Author(s):  
Sameera Khurshid ◽  
Zaid Abdul Razzak ◽  
Shabana Usman Simjee
Keyword(s):  
Nitric Oxide ◽  
Total Protein ◽  
Protein Concentration ◽  
Low Dose ◽  
Sprague Dawley ◽  
Total Protein Concentration ◽  
Bdnf Expression ◽  
Treatment Groups ◽  
Sprague Dawley Rats ◽  
Dose Combination

Abstract Brain derived neurotropic factors (BDNF) can be secreted either as a pro-BDNF or a mature form (mBDNF) through γ-amino-butyric acid (GABAA) receptors activation. Depolarization of GABA neurons in spinal cord can be mediated through N-methyl-D-aspartate (NMDA) receptor due to the exogenous secretion of over expressed BDNF. This over expressed BDNF further modulate the excitation and sensitization of nociceptors. We investigated the modulation of BDNF by GABAA agonist i.e., gabapentin, indomethacin (non-steroidal anti-inflammatory) and their low-dose combination on adjuvant-induced inflammatory arthritis. Mycobacterium tuberculosis H37Ra strain, as adjuvant, was injected in the tail base of female Sprague-Dawley rats. Gabapentin (5 mg/kg), indomethacin (5 mg/kg) and low dose combination of gabapentin (1.5 mg/kg) + indomethacin (2.5 mg/kg) were used. Paw edema was measure by plethysmometer and chronic pain was measured by plantar apparatus. Nitric oxide, peroxide and superoxide dismutase levels were also measured to analyze the free radical and antioxidant balance in different treatment groups along with the total protein concentration. Significant reduction of nitric oxide, peroxide as well as total protein concentration was found in low dose combination. Immunohistochemistry data also showed that the low dose combination has more potential in lowering the BDNF expression in cortex as well as in hippocampus region of brain as compared to their mono therapies. Our study suggested that low-dose combination of gabapentin and indomethacin has a significant impact on lowering the chronic and its associated markers as compare to their monotherapy. Thus indicated the additive effects of the combination therapy on neuropathic pain.

scholarly journals 7,8-Dihydroxyflavone Enhances Cue-Conditioned Alcohol Reinstatement in Rats

2020 ◽  
Vol 10 (5) ◽  
pp. 270 ◽  
Author(s):  
Samuel J. Hogarth ◽  
Elvan Djouma ◽  
Maarten van den Buuse
Keyword(s):  
Body Weight ◽  
Progressive Ratio ◽  
Ethanol Exposure ◽  
Ethanol Solution ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Self Administration ◽  
Bdnf Expression ◽  
Sprague Dawley Rats

Alcohol use disorder (AUD) is a detrimental disease that develops through chronic ethanol exposure. Reduced brain-derived neurotrophic factor (BDNF) expression has been associated with AUD and alcohol addiction, however the effects of activation of BDNF signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown. We therefore trained male and female Sprague Dawley rats in operant chambers to self-administer a 10% ethanol solution. Following baseline acquisition and progressive ratio (PR) analysis, rats were split into drug and vehicle groups during alcohol lever extinction. The animals received two weeks of daily IP injection of either the BDNF receptor, TrkB, agonist, 7,8-dihydroxyflavone (7,8-DHF), or vehicle. During acquisition of alcohol self-administration, males had significantly higher absolute numbers of alcohol-paired lever presses and a higher PR breakpoint. However, after adjusting for body weight, the amount of ethanol was not different between the sexes and the PR breakpoint was higher in females than males. Following extinction, alcohol-primed reinstatement in male rats was not altered by pretreatment with 7,8-DHF when adjusted for body weight. In contrast, in female rats, the weight-adjusted potential amount of ethanol, but not absolute numbers of active lever presses, was significantly enhanced by 7,8-DHF treatment during reinstatement. Analysis of spontaneous locomotor activity in automated photocell cages suggested that the effect of 7,8-DHF was not associated with hyperactivity. These results suggest that stimulation of the TrkB receptor may contribute to reward craving and relapse in AUD, particularly in females.

BDNF shifts excitatory-inhibitory balance in the paraventricular nucleus of the hypothalamus to elevate blood pressure

2021 ◽  
Author(s):  
Daniella Thorsdottir ◽  
Zachary Einwag ◽  
Benedek Erdos
Keyword(s):  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Viral Vectors ◽  
Cardiovascular Responses ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Sprague Dawley Rats ◽  
The Central Nervous System ◽  
Inhibitory Signaling ◽  
Signaling Components

Presympathetic neurons in the paraventricular nucleus of the hypothalamus (PVN) play a key role in cardiovascular regulation. We have previously shown that brain-derived neurotrophic factor (BDNF), acting in the PVN, increases sympathetic activity and blood pressure and serves as a key regulator of stress-induced hypertensive responses. BDNF is known to alter glutamatergic and GABA-ergic signaling broadly in the central nervous system, but whether BDNF has similar actions in the PVN remains to be investigated. Here, we tested the hypothesis that increased BDNF expression in the PVN elevates blood pressure by enhancing NMDA receptor (NMDAR)- and inhibiting GABAA receptor (GABAAR)-mediated signaling. Sprague Dawley rats received bilateral PVN injections of AAV2 viral vectors expressing GFP or BDNF. Three weeks later, cardiovascular responses to PVN injections of NMDAR and GABAAR agonists and antagonists were recorded under α-chloralose-urethane anesthesia. Additionally, expressions of excitatory and inhibitory signaling components in the PVN were assessed using immunofluorescence. Our results showed that NMDAR inhibition led to a greater decrease in blood pressure in the BDNF vs GFP group, while GABAAR inhibition led to greater increases in blood pressure in the GFP group compared to BDNF. Conversely, GABAAR activation decreased blood pressure significantly more in GFP vs BDNF rats. In addition, immunoreactivity of NMDAR1 was upregulated, while GABAAR-a1 and K+/Cl- cotransporter 2 were downregulated by BDNF overexpression in the PVN. In summary, our findings indicate that hypertensive actions of BDNF within the PVN are mediated, at least in part, by augmented NMDAR and reduced GABAAR signaling.

The Effect of Age and Strain Differences on the Incidence of Restraint-Induced Oral and Gastric Ulcers in Three Strains of Rats

1972 ◽  
Vol 51 (2) ◽  
pp. 619-625 ◽  
Author(s):  
D.K. Whittaker ◽  
T.R. Wilson
Keyword(s):  
Wistar Rats ◽  
Strain Differences ◽  
Gastric Ulcers ◽  
Sprague Dawley ◽  
Oral Ulcers ◽  
Sprague Dawley Rats ◽  
Different Strains ◽  
Strain Dependent ◽  
Effect Of Age

Restraint of different strains of rat has been shown to be capable of inducing both oral and gastric ulcers. Hooded Wistar rats were most susceptible to gastric ulcers, whereas Sprague-Dawley rats had the highest incidence of oral ulcers. The causative mechanisms probably differ and are strain dependent.

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