Effects of pinealectomy and the treatment with melatonin on the temporal lobe epilepsy in rats

Lima, Edson Alves de; Soares, José Maria; Garrido, Yaima del Carmen Sanabria; Valente, Sandra Gomes; Priel, Margareth Rose; Baracat, Edmund Chada; Cavalheiro, Ésper A.; Naffah-Mazzacoratti, Maria da Graça; Amado, Débora

doi:10.1016/j.brainres.2005.02.027

Cited by 56 publications

(29 citation statements)

References 31 publications

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“…Pinealectomy facilitates epileptogenesis in some species and increases seizure activity (De and melatonin has been reported to either reverse (Yildrim et al, 2013) or to be ineffective (De Lima et al, 2005) in this pinealectomy-induced enhancement of seizure susceptibility.…”

Section: Melatonin and Epilepsymentioning

confidence: 99%

“…Several studies have reported that melatonin deficit due to pinealectomy exacerbates epileptogenesis and is associated with neuronal loss in particular brain structures, such as the hippocampus and amygdala (De Lima et al, 2005;Janjoppi et al, 2006;Yildrim et al, 2013); moreover, a deficit of melatonin can negatively affect the HPA axis (Weidenfeld et al, 1993). Indeed, exogenous melatonin has been shown to abolish the circadian pattern of spontaneous epileptic seizures and to exert beneficial effects on seizure 7 frequency, neuronal damage, status epilepticus (SE)-induced oxidative stress, and behavioral complications concomitant with epilepsy (Tchekalarova et al, 2013, Petkova at el., 2014Atanasova et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

Tchekalarova

Moyanova

Fusco

et al. 2015

Brain Research Bulletin

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Abstract\ud \ud There is emerging evidence of the beneficial role of the melatonin system in a wide range of psychiatric and neurologic disorders, including anxiety, depression, and epilepsy. Although melatoninergic drugs have chronobiotic and antioxidant properties that positively influence circadian rhythm desynchronization and neuroprotection in neurodegenerative disorders, studies examining the use of melatonin for epilepsy's comorbid psychiatric and neurological symptomatology are still limited. Preclinical and clinical findings on the beneficial effects of the melatonin system on anxiety, depression, and epilepsy suggest that melatoninergic compounds might be effective in treating comorbid behavioral complications in epilepsy beyond regulation of a disturbed sleep-wake cycle

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Section: Melatonin and Epilepsymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

Tchekalarova

Moyanova

Fusco

et al. 2015

Brain Research Bulletin

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“…In another study involving the central nervous system (CNS), Lima et al 38 have observed that the administration of melatonin to pinealectomized mice induced to epilepsy with pilocarpine caused a reduction in the number of TUNEL-positive cells in various limbic areas of the CNS. This indicates a neuroprotector effect of this hormone during the epileptic state, suggesting that it can be used as adjuvant in anticonvulsive therapy.…”

Section: Melatonin Action In Apoptosismentioning

confidence: 99%

Melatonina: modulador de morte celular

Ferreira

Maganhin

Simões

et al. 2010

Rev. Assoc. Med. Bras.

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Apoptosis or planned cell death is a biological phenomenon that is essential for the development and maintenance of a cell population. In this process, senescent or damaged cells are eliminated after activation of a cell death program involving participation of pro-apoptotic molecules (Fas, Bax, caspases 2,3,6,7, 8 and 9). Molecule activation causes typical morphological changes, such as cell shrinkage, loss of adhesion to the extracellular matrix and neighboring cells, chromatin condensation, DNA fragmentation and formation of apoptotic bodies. Anti-apoptotic molecules (Bcl-2, FLIP) block the emergence and evolution of these cell changes and prevent cell death. The balance between pro-and anti-apoptotic molecules ensures tissue homeostasis. When apoptosis is out of control, it contributes to the emergence of several neoplastic, autoimmune and neurodegenerative diseases. Several inducing and inhibiting agents of apoptosis are recognized as potential weapons in the fight against disorders related to cell proliferation and death among, among which stand hormones out. Melatonin has been reported as an important anti-apoptotic agent in various tissues by reducing cell calcium uptake, mitigating the production of oxygen reactive species and decreasing pro-apoptotic proteins, such as Bax. The knowledge of new agents capable of acting on the course of apoptosis is important and valuable for developing further therapies against various diseases. Thus, the objective of this review was to clarify the main aspects of cell death by apoptosis and the role of melatonin in this process

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“…In rats subjected to pinealectomy, a significant increase in lipid peroxidation products and a marked reduction of the antioxidative enzymes have been shown [1,2,12,14,15,24,32]. These changes are invariably reversed by melatonin substitution [13,14,24,28].…”

mentioning

confidence: 99%

“…Pharmacological Reports, 2010, 62, 864 873 aggravate ischemic damage in the brain and spinal cord and facilitate epileptogenic processes [1,14]. In rats subjected to pinealectomy, a significant increase in lipid peroxidation products and a marked reduction of the antioxidative enzymes have been shown [1,2,12,14,15,24,32].…”

mentioning

confidence: 99%

Pinealectomy aggravates acute pancreatitis in the rat

Jaworek

Żwirska-Korczala

Szklarczyk

et al. 2010

Pharmacological Reports

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Abstract:Melatonin, a pineal indoleamine, protects the pancreas against acute damage; however, the involvement of the pineal gland in the pancreatoprotective action of melatonin is unknown. The primary aim of this study was to determine the effects of pinealectomy on the course of acute caerulein-induced pancreatitis (AP) in rats. AP was induced by a subcutaneous infusion of caerulein (25 µg/kg) into pinealectomized or sham-operated animals. Melatonin (5 or 25 mg/kg) was given via intraperitoneal (ip) injection 30 min prior to the induction of AP. The pancreatic content of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal (MDA + 4HNE) and the activity of an antioxidative enzyme, glutathione peroxidase (GSH-Px), were measured in each group of rats. Melatonin blood levels were measured by radioimmunoassay (RIA). In the sham-operated rats, AP was confirmed with histological examination and manifested as pancreatic edema and an increase in the blood lipase level (by 1,500%). In addition, the pancreatic content of MDA + 4HNE was increased by 200%, and pancreatic glutathione peroxydase (GSH-Px) activity was reduced by 40%. Pinealectomy significantly aggravated the histological manifestations of AP, reduced the GSH-Px activity and markedly augmented the levels of MDA + 4HNE in the pancreas of rats with or without AP as compared to sham-operated animals. Melatonin was undetectable in the blood of the pinealectomized rats with or without AP. Treatment with melatonin (25 mg/kg, ip) prevented the development of AP in the sham-operated rats and significantly reduced pancreatic inflammation in the animals previously subjected to pinealectomy. In conclusion, pineal melatonin contributes to the pancreatic protection through the activation of the antioxidative defense mechanism in pancreatic tissue as well as its direct antioxidant effects.

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Effects of pinealectomy and the treatment with melatonin on the temporal lobe epilepsy in rats

Cited by 56 publications

References 31 publications

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

Melatonina: modulador de morte celular

Pinealectomy aggravates acute pancreatitis in the rat

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