Effects of treadmill exercise and chronic stress on anxiety-like behavior, neuronal activity, and oxidative stress in basolateral amygdala in morphine-treated rats.

The basolateral amygdala (BLA), which is sensitive to stress, is necessary for reward-seeking behavior and addiction. Regular exercise can produce various positive effects by affecting the BLA. Therefore, we aimed to investigate the effects of chronic stress and treadmill running (TR) on anxiety-like behavior, neuronal activity, lipid peroxidation (measured by malondialdehyde (MDA) levels, a marker for oxidative stress), and total thiol in BLA, in morphine-treated rats. Male Wistar rats were restricted in restraint stress and/or ran on the treadmill and treated with morphine (5 mg/kg) for 21 days. Anxiety-like behavior was evaluated using an elevated plus maze (EPM) and open field tests (OFTs), on day 22. On day 23, neuronal activity in BLA was assessed via single-unit recording. Finally, MDA and total thiol were assessed in BLA. Our results showed that chronic administration of morphine (5 mg/kg) did not affect anxiety-like behavior. However, the morphine-treated rats, subjected to chronic stress and exercise, showed fewer anxiety-like behaviors. Morphine increased BLA's MDA levels but it was prevented by TR. Glutamatergic and GABAergic basal neuronal activities were low in morphine-treated rats but after acute morphine application, there was a significant decrease in GABAergic neuronal activities in the morphine-exercise-stress (Mor-Exe-St) group. The results of this study showed that in morphine-treated rats, stress and exercise or their combination could have either co-directional or opposite effects to the chronic effects of morphine. These results indicate the existence of common pathways similar to endogenous opioids.

Pretreatment with crocin along with treadmill exercise ameliorates motor and memory deficits in hemiparkinsonian rats by anti-inflammatory and antioxidant mechanisms.

The motor symptoms of Parkinson's disease (PD) are preceded by non-motorized symptoms including memory deficits. Treatment with dopamine replacement medications, such as L-DOPA only control motor symptoms and does not meet the clinical challenges of the disease, such as dyskinesia, non-motor symptoms, and neuroprotection. The purpose of the current study was to examine the neuroprotective potential of crocin and physical exercise in an animal model of PD. Male Wistar rats ran on a horizontal treadmill and/or pretreated with crocin at a dose of 100 mg/kg. Then, 16 µg of the neurotoxin 6-hydroxydopamine (6-OHDA) was microinjected into left medial forebrain bundle. Crocin treatment and/or exercise continued for 6 more weeks. Spatial and aversive memories, rotational behaviour, inflammatory and oxidative stress parameters were assessed at the end of week 6 post surgery. The results showed that pretreatment with crocin alone and in combination with exercise decreased the total number of rotaions as compared with 6-OHDA-lesioned group. Furthermore, treatment of parkinsonian rats with crocin along with exercise training improved aversive and spatial memories. Biochemical analysis showed that crocin and exercise (alone and in combination) reduced tumor necrosis factor- (TNF) α levels in the striatum. Moreover, treatment with crocin at a dose of 100 mg/kg decreased the lipid peroxidation levels in the hippocampus, while exercise training increased the total thiol concentration. In conclusion, our findings indicated that pretreatment with crocin along with treadmill exercise ameliorated motor and memory deficits induced by 6-OHDA, which is considered to be due to their antioxidant and anti-inflammatory activities. The results suggest that combined therapy with crocin and exercise may be protective for motor and memory deficits in PD patients.

Chronic treatment with carvacrol improves passive avoidance memory in a rat model of Parkinson's disease.

The present study investigated the effects of carvacrol on motor and memory deficits as well as hyperalgesia in the 6-OHDA-lesioned rat model of Parkinson's disease. The animals were subjected to unilateral microinjection of 6-OHDA into the medial forebrain bundle and treated with carvacrol (25, 50 and 100 mg/kg, ip) for six weeks after surgery. The 6-OHDA-lesioned rats showed contralateral rotations towards the lesion side, which was accompanied by learning and memory deficits in a passive avoidance test and a decrease in tail withdrawal latency in a tail flick test at the end of week 6. The results also showed that treatment with carvacrol at a dose of 25 mg/kg ameliorated memory deficits, with no effect on rotations and hyperalgesia in lesioned rats. In conclusion, carvacrol improves memory impairments in rats with Parkinson's disease; therefore, it may serve as an adjunct therapy for the alleviation of memory deficits in Parkinson's disease patients.

Nephrogenic acute respiratory distress syndrome: A narrative review on pathophysiology and treatment.

The kidneys have a close functional relationship with other organs especially the lungs. This connection makes the kidney and the lungs as the most organs involved in the multi-organ failure syndrome. The combination of acute lung injury (ALI) and renal failure results a great clinical significance of 80% mortality rate. Acute kidney injury (AKI) leads to an increase in circulating cytokines, chemokines, activated innate immune cells and diffuse of these agents to other organs such as the lungs. These factors initiate pathological cascade that ultimately leads to ALI and acute respiratory distress syndrome (ARDS). We comprehensively searched the English medical literature focusing on AKI, ALI, organs cross talk, renal failure, multi organ failure and ARDS using the databases of PubMed, Embase, Scopus and directory of open access journals. In this narrative review, we summarized the pathophysiology and treatment of respiratory distress syndrome following AKI. This review promotes knowledge of the link between kidney and lung with mechanisms, diagnostic biomarkers, and treatment involved ARDS induced by AKI.

Chronic treatment with carvacrol improves passive avoidance memory in a rat model of Parkinson's disease / O tratamento com carvacrol melhora a memória de esquiva passiva em um modelo da doença de Parkinson em ratos

ABSTRACT The present study investigated the effects of carvacrol on motor and memory deficits as well as hyperalgesia in the 6-OHDA-lesioned rat model of Parkinson's disease. The animals were subjected to unilateral microinjection of 6-OHDA into the medial forebrain bundle and treated with carvacrol (25, 50 and 100 mg/kg, ip) for six weeks after surgery. The 6-OHDA-lesioned rats showed contralateral rotations towards the lesion side, which was accompanied by learning and memory deficits in a passive avoidance test and a decrease in tail withdrawal latency in a tail flick test at the end of week 6. The results also showed that treatment with carvacrol at a dose of 25 mg/kg ameliorated memory deficits, with no effect on rotations and hyperalgesia in lesioned rats. In conclusion, carvacrol improves memory impairments in rats with Parkinson's disease; therefore, it may serve as an adjunct therapy for the alleviation of memory deficits in Parkinson's disease patients.

RESUMO O presente estudo investigou os efeitos do carvacrol nos déficits motores e de memória, bem como na hiperalgesia, em um modelo da doença de Parkinson (DP) em ratos com lesões 6-OHDA. Os animais foram submetidos a microinjeção unilateral de 6-OHDA no feixe mediano do prosencéfalo e tratados com carvacrol (25, 50 e 100 mg / kg, ip) durante 6 semanas após a cirurgia. Os ratos com lesões 6-OHDA mostraram rotações contralaterais para o lado da lesão, que foram acompanhadas de déficits de aprendizagem e de memória em um teste de evitação passiva, e de uma diminuição da latência de retirada da cauda em um teste de cauda no final da semana 6. Os resultados também mostraram que o tratamento crônico com carvacrol a uma dose de 25 mg / kg aliviou os déficits de memória, sem efeito sobre rotações e hiperalgesia em ratos lesados. Em conclusão, o carvacrol melhora a deficiência de memória em ratos com DP e, portanto, pode servir como uma terapia complementar para aliviar os déficits de memória em pacientes com DP.

Lesion of medial prefrontal cortex reduces morphine-induced extracellular dopamine level in the ventral tegmental area: a microdialysis study in rats.

Drug addiction is a chronic disorder characterized by compulsive drug-seeking behavior despite severe negative consequences. Most abused drugs increase dopamine release in the ventral tegmental area (VTA) and in the nucleus accumbens (NA). The medial prefrontal cortex (mPFC), a part of the mesocorticolimbic dopaminergic system, receives dopaminergic projections from VTA; and in turn, sends glutamatergic projections to both VTA and NA. The present study was designed to further investigate the involvement of the mPFC in the release of dopamine in the VTA by using in vivo microdialysis and high performance liquid chromatography with electrochemical detection (HPLC­ECD). Electrical lesion of the mPFC decreased the level of dopamine in the VTA to approximately 26.8% of basal level. Acute morphine (40 mg/kg i.p.) treatment increased the level of dopamine in the VTA, while the lesion of mPFC immediately before morphine administration attenuated the effects of acute morphine on the level of dopamine. These results suggest that the mPFC modulates dopamine release into the VTA.