The effect of NAD-299 and TCB-2 on learning and memory, hippocampal BDNF levels and amyloid plaques in Streptozotocin-induced memory deficits in male rats

Afshar, Simin; Shahidi, Siamak; Rohani, Ali Haeri; Komaki‬, Alireza; Asl, Sara Soleimani

doi:10.1007/s00213-018-4973-x

Cited by 44 publications

(30 citation statements)

References 81 publications

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“…Here, we showed that acute nicotine enhanced 5-HT 2A R-IR neurons of the DG, this might contribute to nicotine-enhanced hippocampal-dependent learning [56] considering 5-HT 2A R participates significantly to the well-documented contribution of 5-HT to memory [57,58]. TCB-2, indeed, can improve cognitive dysfunction [59] and enhance hippocampal and amygdala-dependent memory [60]. The increased expression of 5-HT 2A Rs in the neuropil of mPFC and VTA might contribute to nicotine-induced enhanced cognition [61] and positive reinforcement [18].…”

Section: Discussionmentioning

confidence: 66%

Acute and Chronic Nicotine Exposures Differentially Affect Central Serotonin 2A Receptor Function: Focus on the Lateral Habenula

Bombardi

Delicata

Tagliavia

et al. 2020

IJMS

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Nicotine addiction is a serious public health problem causing millions of deaths worldwide. Serotonin (5-hydroxytryptamine; 5-HT) is involved in central nervous system (CNS) nicotine effects, and it has been suggested as a promising pharmacological target for smoking cessation. In this regard, what is particularly interesting are the 5-HT2A receptors (5-HT2ARs) and the lateral habenula (LHb), a central area in nicotine addiction that we showed to be under a strong 5-HT2AR-modulation. Single-cell extracellular recording of LHb neurons was used to study the 5-HT2AR function by intravenously administrating the potent agonist TCB-2. Acute nicotine (2 mg/kg, intraperitoneal, i.p.) and chronic nicotine (6 mg/kg/day for 14 days) differently affected both the 5-HT2AR-immuno reactive (IR) neuron number and the 5-HT2AR immunostaining area in the different brain areas studied. After acute nicotine, TCB-2 cumulative doses (5–640 µg/kg, intravenous, i.v.) bidirectionally affected the activity of 74% of LHb recorded neurons. After chronic nicotine treatment, TCB-2 was only capable of decreasing the LHb firing rate. The expression of 5-HT2AR under acute and chronic nicotine exposure was studied in the LHb and in other brain areas involved in nicotine effects in rats by using immunohistochemistry. These data reveal that acute and chronic nicotine differentially affect the 5-HT2AR function in different brain areas and this might be relevant in nicotine addiction and its treatment.

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Section: Discussionmentioning

confidence: 66%

Acute and Chronic Nicotine Exposures Differentially Affect Central Serotonin 2A Receptor Function: Focus on the Lateral Habenula

Bombardi

Delicata

Tagliavia

et al. 2020

IJMS

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“…For example, activating 5-hydroxytryptophan 1A (5-HT1A) or 5-HT2A receptors that induce hippocampal BDNF expression has been examined. Afshar et al investigated the effects of NAD-299 (an antagonist for 5-HT1A receptor) and TCB-2 (an agonist for 5-HT2A receptor) on learning and memory function in streptozotocin (STZ)-induced memory deficit animal models [ 17 ]. In their study, rats received intracerebroventricular (icv) injection of STZ exhibited decreased discrimination index in the novel object recognition test, reduced BDNF, and increased Aβ plaques in the brain, which were reversed by treatment with NAD-299 or TCB-2 [ 17 ].…”

Section: Activation Of Bdnf/trkb System By Compoundsmentioning

confidence: 99%

“…Afshar et al investigated the effects of NAD-299 (an antagonist for 5-HT1A receptor) and TCB-2 (an agonist for 5-HT2A receptor) on learning and memory function in streptozotocin (STZ)-induced memory deficit animal models [ 17 ]. In their study, rats received intracerebroventricular (icv) injection of STZ exhibited decreased discrimination index in the novel object recognition test, reduced BDNF, and increased Aβ plaques in the brain, which were reversed by treatment with NAD-299 or TCB-2 [ 17 ]. Influence of neuropeptide Y (NPY), which is implicated as potential therapeutic target of HD, in expression of BDNF has been reported [ 18 ].…”

Section: Activation Of Bdnf/trkb System By Compoundsmentioning

confidence: 99%

Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases

Numakawa

Odaka

Adachi

2018

IJMS

227

138

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It is well known that brain-derived neurotrophic factor, BDNF, has an important role in a variety of neuronal aspects, such as differentiation, maturation, and synaptic function in the central nervous system (CNS). BDNF stimulates mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), phosphoinositide-3kinase (PI3K), and phospholipase C (PLC)-gamma pathways via activation of tropomyosin receptor kinase B (TrkB), a high affinity receptor for BDNF. Evidence has shown significant contributions of these signaling pathways in neurogenesis and synaptic plasticity in in vivo and in vitro experiments. Importantly, it has been demonstrated that dysfunction of the BDNF/TrkB system is involved in the onset of brain diseases, including neurodegenerative and psychiatric disorders. In this review, we discuss actions of BDNF and related signaling molecules on CNS neurons, and their contributions to the pathophysiology of brain diseases.

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“…For histological study, the brains of anesthetized rats from the electrophysiology test were fixed through perfusion with a paraformaldehyde solution. The brains were dehydrated, embedded in paraffin, and sliced into a series of coronal sections of 5 μm thickness according to previous studies [47,53].Then, sections were used for TdT-mediated dUTP end labeling (TUNEL) staining, in which DNA fragmentation and apoptosis were detected by a TUNEL Detection Kit (Abcam) following the manufacturer's instructions. After staining, the sections were analyzed under a light microscope (× 400, Olympus).…”

Section: Apoptosis (Tunel Assay)mentioning

confidence: 99%

Different doses of methamphetamine alter long-term potentiation, level of BDNF and neuronal apoptosis in the hippocampus of reinstated rats

et al. 2019

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Methamphetamine (METH) is a psychostimulant. The precise mechanisms of its effects remain unknown and current relapse treatments have low efficacy. However, brain-derived neurotrophic factor (BDNF) and neuronal plasticity are essential contributors, despite paradoxical reports and a lack of comprehensive studies. Therefore, we investigated the effects of different doses of METH on long-term potentiation (LTP), BDNF expression and neuronal apoptosis in the hippocampus of reinstated rats. Rats were injected intraperitoneally with METH (1, 5, or 10 mg/kg) or saline, and trained in a conditioned place preference paradigm. Following implementation of the reinstatement model, electrophysiology, western blotting and TUNEL assay were performed to assess behavior, LTP components, BDNF expression, and neuronal apoptosis, respectively. The results demonstrated that the preference scores, population spike amplitude and BDNF expression markedly decreased in the METH (10 mg/kg) group compared with the other groups. In contrast, METH (5 mg/kg) significantly increased these factors more than the control group. There was no change in variables between METH (1 mg/kg) and the control group. Also, apoptosis of the hippocampus was increased in the METH (10 mg/kg) group compared with the METH (5 mg/kg) group. These results suggest that alterations in synaptic plasticity, expression of BDNF and neuronal apoptosis in the hippocampus has a vital role in the context-induced reinstatement of METH seeking.

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The effect of NAD-299 and TCB-2 on learning and memory, hippocampal BDNF levels and amyloid plaques in Streptozotocin-induced memory deficits in male rats

Abstract: These findings suggest that 5-HT1AR blockade by NAD-299 and 5-HT2AR activation by TCB-2 improve cognitive dysfunction in icv-STZ-treated rats, and these drugs may potentially prevent the progression of AD.

Cited by 44 publications

References 81 publications

Acute and Chronic Nicotine Exposures Differentially Affect Central Serotonin 2A Receptor Function: Focus on the Lateral Habenula

Acute and Chronic Nicotine Exposures Differentially Affect Central Serotonin 2A Receptor Function: Focus on the Lateral Habenula

Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases

Different doses of methamphetamine alter long-term potentiation, level of BDNF and neuronal apoptosis in the hippocampus of reinstated rats

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