Intraamygdaloid microinjection of acylated-ghrelin influences passive avoidance learning

Tóth, K.; László, Kristóf; Lukács, E; Lénárd, László

doi:10.1016/j.bbr.2009.03.031

Cited by 42 publications

(22 citation statements)

References 31 publications

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“…Similarly, only a slight cognitive impairment was seen in rats that survived for 5 weeks following SAH (Takata et al, 2008). Since memory function was intact 48 h after SAH-induced cerebral injury, the previously-demonstrated stimulatory effects of centrallyadministered ghrelin on memory retention (Carlini et al, 2008;Tó th et al, 2009) were not seen. Thus, the influence of ghrelin on learning processes and memory needs to be further explored in chronic SAH.…”

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confidence: 73%

The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats

Erşahin

Toklu

Erzik

et al. 2010

Journal of Neurotrauma

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To elucidate the putative neuroprotective effects of ghrelin in subarachnoid hemorrhage (SAH)-induced brain injury, Wistar albino rats (n = 54) were divided into sham-operated control, saline-treated SAH, and ghrelin-treated (10 microg/kg/d IP) SAH groups. The rats were injected with blood (0.3 mL) into the cisterna magna to induce SAH, and were sacrificed 48 h after the neurological examination scores were recorded. In plasma samples, neuron-specific enolase (NSE), S-100beta protein, TNF-alpha, and IL-1beta levels were evaluated, while forebrain tissue samples were taken for the measurement of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species levels, myeloperoxidase (MPO), Na(+)-K(+)-ATPase activity, and DNA fragmentation ratio. Brain tissue samples containing the basilar arteries were obtained for histological examination, while cerebrum and cerebellum were removed for the measurement of blood-brain barrier (BBB) permeability and brain water content. The neurological scores were impaired at 48 h after SAH induction, and SAH caused significant decreases in brain GSH content and Na(+)-K(+)-ATPase activity, and increases in chemiluminescence, MDA levels, and MPO activity. Compared with the control group, the protein levels of NSE, S-100beta, TNF-alpha, and IL-1beta in plasma were also increased, while ghrelin treatment prevented all SAH-induced alterations observed both biochemically and histopathologically. The results demonstrate that ghrelin alleviates SAH-induced oxidative brain damage, and exerts neuroprotection by maintaining a balance in oxidant-antioxidant status, by inhibiting proinflammatory mediators, and preventing the depletion of endogenous antioxidants evoked by SAH.

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confidence: 73%

The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats

Erşahin

Toklu

Erzik

et al. 2010

Journal of Neurotrauma

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“…We focused on the amygdala, a relevant brain region involved in the regulation of emotional response (Carlini et al, 2004, Toth et al, 2009, Toth et al, 2010. In addition to the aforementioned receptor, Crhr1, the data point to a number of interesting novel potential target genes for ghrelin's central effects, although further confirmation and exploration would be required to demonstrate that these are important for ghrelin's effects on mood.…”

Section: 8mentioning

confidence: 99%

Central administration of ghrelin alters emotional responses in rats: behavioural, electrophysiological and molecular evidence

et al. 2011

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“…This suggests a unique central role of ghrelin [25], in addition to its role as a peripheral hormone secreted by gastric endocrine glands [1]. Later on, ghrelinergic neurons have been detected also in the cerebral cortex [26-28] indicating that ghrelin might be involved in higher activities in the central nervous system, like reward, mood, learning and memory [29-32]. The central role of ghrelin has been further supported by the findings that ghrelin induces neurogenesis, as first described in the rat dorsal motor nucleus of the vagus nerve [33] and the nucleus of the solitary tract [34] and, subsequently in cultured hippocampal progenitor cells [35], the hippocampus of adult mice [36], and the rat spinal cord [37,38].…”

Section: Introductionmentioning

confidence: 99%

Ghrelin accelerates synapse formation and activity development in cultured cortical networks

Stoyanova

Feber

2014

BMC Neurosci

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BackgroundWhile ghrelin was initially related to appetite stimulation and growth hormone secretion, it also has a neuroprotective effect in neurodegenerative diseases and regulates cognitive function. The cellular basis of those processes is related to synaptic efficacy and plasticity. Previous studies have shown that ghrelin not only stimulates synapse formation in cultured cortical neurons and hippocampal slices, but also alters some of the electrophysiological properties of neurons in the hypothalamus, amygdala and other subcortical areas. However, direct evidence for ghrelin’s ability to modulate the activity in cortical neurons is not available yet. In this study, we investigated the effect of acylated ghrelin on the development of the activity level and activity patterns in cortical neurons, in relation to its effect on synaptogenesis. Additionally, we quantitatively evaluated the expression of the receptor for acylated ghrelin – growth hormone secretagogue receptor-1a (GHSR-1a) during development.ResultsWe performed electrophysiology and immunohistochemistry on dissociated cortical cultures from neonates, treated chronically with acylated ghrelin. On average 76 ± 4.6% of the cortical neurons expressed GHSR-1a. Synapse density was found to be much higher in ghrelin treated cultures than in controls across all age groups (1, 2 or 3 weeks). In all cultures (control and ghrelin treated), network activity gradually increased until it reached a maximum after approximately 3 weeks, followed by a slight decrease towards a plateau. During early developmental stages (1–2 weeks), the activity was much higher in ghrelin treated cultures and consequently, they reached the plateau value almost a week earlier than controls.ConclusionsAcylated ghrelin leads to earlier network formation and activation in cultured cortical neuronal networks, the latter being a possibly consequence of accelerated synaptogenesis.

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Intraamygdaloid microinjection of acylated-ghrelin influences passive avoidance learning

Cited by 42 publications

References 31 publications

The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats

The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats

Central administration of ghrelin alters emotional responses in rats: behavioural, electrophysiological and molecular evidence

Ghrelin accelerates synapse formation and activity development in cultured cortical networks

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