The Effect of Citalopram and Thymoquinone on Reserpine-Induced Depression-Like Behaviors in Rats

WOS: 000453220100009

Increased inhibitory synaptic activity in the hippocampus (CA1) of genetic absence epilepsy rats: Relevance of kindling resistance

Purpose: Genetic absence epilepsy rats from Strasbourg (GAERS), a well-validated genetic rat model for typical absence epilepsy, are known to manifest a resistance to secondary generalization of abnormal focal electrical activity evoked by kindling. The mechanism of this resistance is still unclear. In order to understand the possible mechanism of kindling resistance, we investigated for the first time, the differences of short-term synaptic plasticity by using a paired-pulse paradigm as an indicator of GABAergic activity in CM region of hippocampus in GAERS and non-epileptic Wistar rats in-vivo

Endothelial and Autonomic Functions in Patients with Migraine

WOS: 000515122500025PubMed: 31603510Objective It has been shown that patients with migraine have endothelial dysfunction. Migraine patients with aura, especially, have more clinical manifestations of autonomic nervous system dysfunction. We aimed to evaluate the endothelial and autonomic functions in migraine patients during both migraine headache attack and headache-free periods. Design This was a cross-sectional, randomized study. Subjects and Methods A total of 130 participants (67 male and 63 female patients, minimum age = 19 years, maximum age = 71 years, mean age = 38.812.2years) were enrolled into the study. For the statistical evaluation of data, we classified the participants of the study as follows: group 1: headache (+) aura (+); group 2: headache (+) aura (-); group 3: headache (-) aura (+); group 4: headache (-) aura (-). Noninvasive evaluation of endothelial function was performed by flow-mediated dilation (FMD) and pulse wave analysis methods. Heart rate variability measurements were used for noninvasive evaluation of autonomic functions. Results Group 1 had a higher FMD ratio than the control group, group 3, or group 4 (P<0.001, P<0.001, and P=0.003, respectively). Group 4 had lower FMD ratio levels than the other migraine groups and or the control group (P<0.001). Group 3 had the highest high-frequency (HF) power levels among all migraine groups (P<0.001). Group 2 had higher low-frequency/HF ratio values than other migraineurs (P<0.001). Conclusions We concluded that endothelial dysfunction and headache are closely related. Additionally, higher parasympathetic tonus might be associated with the presence of aura

A Cannabinoid Ligand, Anandamide, Exacerbates Endotoxin-Induced Uveitis in Rabbits

SARIOGLU, YUSUF/0000-0002-9227-365XWOS: 000298292300002PubMed: 21848425Purpose: This study aimed to investigate the effects of anandamide or arachidonylethanolamide (AEA), an endogenous cannabinoid receptor agonist, on intraocular inflammation in an endotoxin-induced uveitis (EIU) model in rabbits. Methods: Forty New Zealand albino male rabbits were used (5 groups, 8 animals in each). After establishment of sufficient anesthesia, animals were taken under surgery for intravitreal injections. A maximum amount of 50 mu L of solution was injected into the central vitreous with a 30-gauge needle. In the control group, sterile saline was injected into the right eyes of the animals. Likewise, AEA (10(-5) M) in the second group, lipopolysaccharide (LPS; 100 ng) in the third group, and AEA (10(-5) M) and LPS (100 ng) in the fourth group were administered. Fifth group received 0.1 mL subtenon injection of AM251 (10(-5) M), a CB(1)-receptor antagonist, 30 min prior to intravitreal LPS (100 ng) and AEA (10(-5) M) injection. At 24 h after the surgical intervention, clinical evaluation was performed and animals were then euthanized with 100 mg/kg intravenous pentobarbital injections. Immediately after the induction of pentobarbital anesthesia, the anterior chamber of the eyes was quickly punctured using a 30-gauge needle to drain aqueous humor (AH) and obtained specimens were used for cell count, protein measurement, and microbiological contamination tests. After AH collection, enucleation was performed and enucleated material was kept for the pathological evaluation. Results: AEA caused an overall worsening of EIU in studied eyes. It significantly increased the detrimental effects of endotoxin, as assessed by clinical investigation of ocular inflammation, AH leukocyte content, and AH protein concentrations. CB(1)-receptor antagonist AM251 administration reversed some components of this AEA-induced exacerbation to significant extents. Conclusion: AEA exacerbated EIU in rabbit eyes. AM251 has been found beneficial to prevent AEA's aggravating impact on EIU. As AEA is a treatment choice for lowering intraocular pressure in ophthalmology practice, concurrent use of CB(1)-receptor antagonists may be a questionable strategy in cases of secondary glaucoma, to avoid aggravation of the present inflammation

The effect of endothelin receptor antagonists in the endotoxin-induced uveitis rabbit model

Uzun, Feyzahan/0000-0002-3050-0714WOS: 000429276400005PubMed: 28707522Purpose: To investigate the effect of Bosentan (non-selective endothelin receptor antagonist) and BQ123 (ETA receptor antagonist) on intraocular inflammation in an endotoxin-induced uveitis (EIU) rabbit model.Methods: Uveitis was induced by intravitreal injection of lipopolysaccharide (LPS). The animals were divided into 7 groups and there were six rabbits in each group (saline, saline and ethanol, bosentan, BQ123, lipopolysaccharide (LPS), bosentan and LPS, BQ123 and LPS-injected groups). Bosentan and BQ123 were applied before LPS injection. Aqueous humour was collected at 24th hour post-injections and enucleation was performed for the evaluation of histopathological changes.Results: BQ123 decreased clinical score, cell counts and protein amount more than bosentan and it was significant for cell counts (p=0.018). Bosentan significantly diminished inflammatory reactions more than BQ123 as shown in histopathological specimens (p=0.002).Conclusions: ETA receptor blockage is effective on uveitis treatment by its protective effect on blood aqueous barrier

Supply-Demand Mismatch Transients in Susceptible Peri-infarct Hot Zones Explain the Origins of Spreading Injury Depolarizations

Peri-infarct depolarizations (PIDs) are seemingly spontaneous spreading depression-like waves that negatively impact tissue outcome in both experimental and human stroke. Factors triggering PIDs are unknown. Here, we show that somatosensory activation of peri-infarct cortex triggers PIDs when the activated cortex is within a critical range of ischemia. We show that the mechanism involves increased oxygen utilization within the activated cortex, worsening the supply-demand mismatch. We support the concept by clinical data showing that mismatch predisposes stroke patients to PIDs as well. Conversely, transient worsening of mismatch by episodic hypoxemia or hypotension also reproducibly triggers PIDs. Therefore, PIDs are triggered upon supply-demand mismatch transients in metastable peri-infarct hot zones due to increased demand or reduced supply. Based on the data, we propose that minimizing sensory stimulation and hypoxic or hypotensive transients in stroke and brain injury would reduce PID incidence and their adverse impact on outcome