Effects of carnosine on amygdaloid-kindled seizures in Sprague–Dawley rats

Jin, Chunlei; Yang, Lixia; Wu, Xi; Li, Q.; Ding, Meiping; Fan, Yanying; Zhang, W. P.; Luo, Jianhong; Chen, Z.

doi:10.1016/j.neuroscience.2005.06.066

Cited by 71 publications

(53 citation statements)

References 39 publications

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“…This may be due to the insufficient strength of disinhibition effect of carnosine; however, it may also have an alternative explanation. According to the decrease rather than increase of the first spike in the evoked response following prolonged application of carnosine, it is presumable that carnosine might have inhibitory effects on both principal pyramidal neurons and interneurons in the hippocampal CA1 region, such as a decrease of glutamate release (Jin et al, 2005;Shen et al, 2007). The inhibitory action on the pyramidal neurons could decrease the first spike in the evoked response and thereby prevent the occurrence of spontaneous bursts.…”

Section: Discussionmentioning

confidence: 99%

“…Ratio of paired-pulse evoked PS (%) using i.p. doses of 200~1500 mg/kg (Jin et al, 2005;Wu et al, 2006;Zhu et al, 2007). Since carnosine can penetrate blood-brain barrier easily (Crush, 1970), the corresponding concentrations in the brain of these i.p.…”

Section: Fig4 Effects Of Carnosine and Ptx On The Paired-pulse Deprementioning

confidence: 99%

“…Because it can penetrate the blood-brain barrier (BBB) easily and has few side effects, the therapeutic potentials of carnosine to some brain disorders have attracted great attention. Recent investigations have shown that carnosine has inhibitory effects on both electric stimulation-kindled seizures and chemically-induced seizures (Jin et al, 2005;Wu et al, 2006;Zhu et al, 2007). It suggests that carnosine may be used as a new anticonvulsant to treat epilepsy.…”

Section: Introductionmentioning

confidence: 99%

“…For example, carnosine can significantly decrease the glutamate release in some brain regions, such as the amygdala and hippocampus (Jin et al, 2005;Shen et al, 2007). It can also decrease the seizure duration and prolong the seizure latency (Jin et al, 2005;Wu et al, 2006;Zhu et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Effects of carnosine on the evoked potentials in hippocampal CA1 region

Feng

Zheng

Wang

2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To directly examine the effects of carnosine on neuronal excitation and inhibition in rat hippocampus in vivo. Methods: Artificial cerebrospinal fluid with carnosine was directly administrated over the exposed rat hippocampus. The changes of neuron activity in the CA1 region of hippocampus were evaluated by orthodromically-and antidromically-evoked potentials, as well as paired-pulse stimulation paradigm. Results: In both orthodromic and antidromic response potentials, carnosine transformed population spikes (PSs) with single spike into epileptiform multiple spikes. In addition, similar to the effect of γ-aminobutyric acid A (GABA A ) antagonist picrotoxin, carnosine decreased paired-pulse stimulating depression significantly.However, no significant change was observed in the spontaneous field potentials during the application of carnosine. Conclusion:The results indicate a disinhibition-induced excitation effect of carnosine on the CA1 pyramidal neurons. It provides important information against the application of carnosine as a potential anticonvulsant in clinical treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Fig4 Effects Of Carnosine and Ptx On The Paired-pulse Deprementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of carnosine on the evoked potentials in hippocampal CA1 region

Feng

Zheng

Wang

2009

J. Zhejiang Univ. Sci. B

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“…102,103 We recently reported that the metabolic carnosine-histidine-histamine pathway also exists in the CNS. 30,104 Carnosine prevents amygdaloid kindling seizures in rats by partial transformation to histamine. Given the relationship between carnosine and histamine, carnosine is proposed as a new histaminergic drug that can replace histamine and avoid inflammation.…”

Section: ■ Prospects For Histamine-related Agents In Cerebral Ischemiamentioning

confidence: 99%

Role of Histamine and Its Receptors in Cerebral Ischemia

Chen

2012

ACS Chem. Neurosci.

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Histamine is recognized as a neurotransmitter or neuromodulator in the brain, and it plays a major role in the pathogenic progression after cerebral ischemia. Extracellular histamine increases gradually after ischemia, and this may come from histaminergic neurons or mast cells. Histamine alleviates neuronal damage and infarct volume, and it promotes recovery of neurological function after ischemia; the H1, H2, and H3 receptors are all involved. Further studies suggest that histamine alleviates excitotoxicity, suppresses the release of glutamate and dopamine, and inhibits inflammation and glial scar formation. Histamine may also affect cerebral blood flow by targeting to vascular smooth muscle cells, and promote neurogenesis. Moreover, endogenous histamine is an essential mediator in the cerebral ischemic tolerance. Due to its multiple actions, affecting neurons, glia, vascular cells, and inflammatory cells, histamine is likely to be an important target in cerebral ischemia. But due to its low penetration of the blood-brain barrier and its wide actions in the periphery, histamine-related agents, like H3 antagonists and carnosine, show potential for cerebral ischemia therapy. However, important questions about the molecular aspects and pathophysiology of histamine and related agents in cerebral ischemia remain to be answered to form a solid scientific basis for therapeutic application.

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Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Shen

Zhang

et al. 2007

Cell Biochemistry & Function

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Carnosine (beta-alanyl-histidine) is a naturally occurring dipeptide that has been characterized as a putative hydrophilic antioxidant. The protective function of carnosine has been demonstrated in neuronal cells under ischemic injury. The purpose of this study was to investigate the effects of carnosine on oxygen-glucose deprivation (OGD)-induced degranulation and histamine release from mast cells. Cultured mast cells were exposed to OGD for 4 h, and then the degranulation was observed immediately by microscopy. Histamine release was analyzed by high-performance liquid chromatography (HPLC). OGD caused degranulation of mast cells, and increased histamine and lactate dehydrogenase (LDH) release. Carnosine (at a concentration of 5 mM) alone did not produce any appreciable effect on degranulation, histamine, and LDH release from mast cells under normal condition, but significantly inhibited the degranulation, histamine, and LDH release of mast cells induced by OGD. These results indicate that carnosine can protect mast cells from degranulation and histamine release and it may be an endogenous mast cell stabilizer in the pathological processes induced by ischemia.

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Effects of carnosine on amygdaloid-kindled seizures in Sprague–Dawley rats

Cited by 71 publications

References 39 publications

Effects of carnosine on the evoked potentials in hippocampal CA1 region

Effects of carnosine on the evoked potentials in hippocampal CA1 region

Role of Histamine and Its Receptors in Cerebral Ischemia

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

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