The effect of ghrelin on MK-801 induced memory impairment in rats

Goshadrou, Fatemeh; Kermani, Mojtaba; Ronaghi, Abdolaziz; Sajjadi, Samad

doi:10.1016/j.peptides.2013.03.022

Cited by 29 publications

(19 citation statements)

References 40 publications

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“…11,12,44,45 The experiments were conducted in accordance with the previously published protocols. 11,12,33,[45][46][47][48][49][50][51] The test was conducted over 3 days (two consecutive training days, with the test performed on the third day). The animal was placed in the white compartment in front of the door for a 30-second habituation period at the beginning of the first training day, and then the door was routinely raised up.…”

Section: In Vivo Behavioral Tests Iap Testmentioning

confidence: 99%

<p>Histamine H3 receptor antagonist E177 attenuates amnesia induced by dizocilpine without modulation of anxiety-like behaviors in rats</p>

Alachkar¹,

Khan²,

Łażewska³

et al. 2019

NDT

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Background: Alzheimer disease (AD) is the main cause of dementia in elderly people. The potential of histamine H3 receptor (H3R) antagonists as a pharmacological treatment of several neuropsychiatric diseases is well established. Methods: The novel non-imidazole-based H3R antagonist E177 was screened for its procognitive effects on the inhibitory avoidance paradigm (IAP) and novel object recognition (NOR) task in a dizocilpine (DIZ)-induced model of amnesia in male Wistar rats. Donepezil, an acetylcholine esterase inhibitor, was used as the reference drug. Results: Acute systemic treatment with E177 (1.25, 2.5, 5, and 10 mg/kg intraperitoneally [i.p.]) significantly attenuated the cognitive impairments induced by DIZ in the IAP (all P-values ,0.05, n=7), and the protective effect of the most promising dose of E177 (5 mg/kg) was abrogated when H3R agonist R-(α)-methylhistamine (RAMH; 10 mg/kg i.p.) was co-administered (P=0.281 for DIZ-amnesia group vs DIZ + E177 + RAMH group, n=7). The discrimination index calculated for E177 (5 mg/kg, i.p.) showed a significant memory-enhancing effect on DIZ-induced shortterm memory impairment in the NOR task (P,0.05, n=6), with the enhancement nullified when animals were co-administered RAMH (10 mg/kg). Moreover, the results revealed that E177 (5 and 10 mg/kg, i.p.) did not alter the anxiety levels and locomotor activity of animals naïve to the open-field test (all P-values .0.05, n=8) or the elevated plus maze test (all P-values .0.05, n=6-8), which indicated that the E177-induced enhancement of memory performance in the IAP or NOR task was unrelated to changes in emotional response or in spontaneous locomotor activity. Conclusion: The observed results suggested a possible contribution of H3Rs in the alteration of brain neurotransmitters that accompany neurodegenerative diseases, such as AD.

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Section: In Vivo Behavioral Tests Iap Testmentioning

confidence: 99%

<p>Histamine H3 receptor antagonist E177 attenuates amnesia induced by dizocilpine without modulation of anxiety-like behaviors in rats</p>

Alachkar¹,

Khan²,

Łażewska³

et al. 2019

NDT

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“…[14][15][16][17] In humans, the effects of NMDA antagonists closely resemble the clinical picture observed in schizophrenic patients in positive, negative, and cognitive symptoms. 18 An important component of learning and memory functions is long-term potentiation (LTP), which is a result of NMDA receptor activation.…”

Section: Introductionmentioning

confidence: 74%

N-methyl-D-aspartate Receptors Are Involved in Caffeine-Induced Facilitation on Memory Retention of Passive Avoidance Learning in Rats

Sarper

Ziya

ÜzümGülay

2013

Journal of Caffeine Research

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Background: Caffeine is an antagonist of adenosine receptors. It preserves cognition and reduces neurodegeneration. The MK-801, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, has also shown amnesic properties in animal models. The effect of caffeine on MK-801-induced amnesia has not been the subject of any recent study. Methods: In this study, the effects of different doses (10 and 30 mg/kg) of caffeine on Wistar male rats (eight in each group), passive-avoidance (PA) response, and the impairment of this response by the NMDA receptor antagonist MK-801 (dizocilpine) were evaluated. The PA response was examined by measuring the step-through latency, 1 and 3 days after the animals received foot-shock training. Results: When given intraperitoneally before the training session, 10 mg/kg caffeine elongated the PA response, but 30 mg/kg did not, and it even reduced the step-through latency significantly. Before and after training, administration of 0.2 mg/kg MK-801 significantly elongated the PA response. This finding showed that MK-801 had a detrimental effect on learning, consolidation, and memory. We found the first evidence that pre-training and pre-testing administration of 10 mg/kg caffeine significantly reversed the learning and memory consolidation process disrupted by MK-801. Conclusion: These results show an interaction between caffeine and the glutamatergic system, suggesting that low-dose caffeine can prevent learning deficit and amnesia produced by a NMDA antagonist in rats (model of schizophrenia in human) when injected in pre-and post-training phase and may be clinically useful for treating cognitive impairments in schizophrenia.

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“…Moreover, ghrelin exhibits numerous beneficial actions against neurotoxic challenges such as 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine exposure (Jiang et al ., ) or amyloid‐β‐1‐42 oligomer‐induced neurodegeneration (Moon et al ., ). It also prevents amnesia produced by exposure to the N ‐methyl‐ d ‐aspartate (NMDA) receptor antagonist dizolcipine (MK801) (Goshadrou et al ., ).…”

Section: Introductionmentioning

confidence: 97%

Involvement of PKA and ERK pathways in ghrelin‐induced long‐lasting potentiation of excitatory synaptic transmission in the CA1 area of rat hippocampus

Cavalier

Crouzin

Sedrine

et al. 2015

Eur J of Neuroscience

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Acute effects of ghrelin on excitatory synaptic transmission were evaluated on hippocampal CA1 synapses. Ghrelin triggered an enduring enhancement of synaptic transmission independently of NMDA receptor activation and probably via postsynaptic modifications. This ghrelin-mediated potentiation resulted from the activation of GHS-R1a receptors as it was mimicked by the selective agonist JMV1843 and blocked by the selective antagonist JMV2959. This potentiation also required the activation of PKA and ERK pathways to occur as it was inhibited by KT5720 and U0126, respectively. Moreover it most probably involved Ca(2+) influxes as both ghrelin and JMV1843 elicited intracellular Ca(2+) increases, which were dependent on the presence of extracellular Ca(2+) and mediated by L-type Ca(2+) channels opening. In addition, ghrelin potentiated AMPA receptor-mediated [Ca(2+) ]i increases while decreasing NMDA receptor-mediated ones. Thus the potentiation of synaptic transmission by GHS-R1a at hippocampal CA1 excitatory synapses probably results from postsynaptic mechanisms involving PKA and ERK activation, which are producing long-lasting enhancement of AMPA receptor-mediated responses.

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The effect of ghrelin on MK-801 induced memory impairment in rats

Cited by 29 publications

References 40 publications

<p>Histamine H3 receptor antagonist E177 attenuates amnesia induced by dizocilpine without modulation of anxiety-like behaviors in rats</p>

<p>Histamine H3 receptor antagonist E177 attenuates amnesia induced by dizocilpine without modulation of anxiety-like behaviors in rats</p>

N-methyl-D-aspartate Receptors Are Involved in Caffeine-Induced Facilitation on Memory Retention of Passive Avoidance Learning in Rats

Involvement of PKA and ERK pathways in ghrelin‐induced long‐lasting potentiation of excitatory synaptic transmission in the CA1 area of rat hippocampus

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