Suppression of outward K+ currents by WIN55212-2 in rat retinal ganglion cells is independent of CB1/CB2 receptors

Zhang, C.-Q.; Wu, Hang-Jing; Wang, S.-Y.; Yin, Shuo; Lu, Xiaoxiao; Miao, Yanying; Wang, X.-H.; Yang, Xiong‐Li; Wang, Z.

doi:10.1016/j.neuroscience.2013.08.056

Cited by 17 publications

(8 citation statements)

References 52 publications

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“…Bar=20 μm maintain normal morphology, and inhibit apoptosis of HT22 cells exposed to Aβ, and the presence of CB1 antagonist reversed these protections and CB1 receptor upregulation induced by nicotine, indicating that CB1 may be involved in the nicotine-induced protections. In fact, there are two main cannabinoid receptors expressed in the CNS, including CB1 and CB2 (Zhang et al 2013). In the hippocampus, CB1 receptors are strongly expressed (Cannarsa et al 2012), and the activation of CB1 causes neuroprotective effects (Panikashvili et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Jia

Lei

et al. 2014

J Mol Neurosci

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Emerging evidences suggest that nicotine exerts a neuroprotective effect on Alzheimer's disease (AD), yet the precise mechanism is not fully elucidated. Here, HT22 cells were exposed to amyloid beta protein fragment (Aβ)1-42 to mimic the pathological process of neuron in AD. We hypothesized that cannabinoid receptor CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 injury in HT22 cells. CB1 expression in HT22 cells was investigated by immunocytochemistry and Western blot. The injury of HT22 cells was evaluated by cellular morphology, cell viability, and lactate dehydrogenase (LDH) release. The apoptosis of HT22 cells was assessed by flow cytometry and expressions of Bcl-2 and Bax. The results demonstrated that nicotine markedly upregulated CB1 expression, increased cell viability, ameliorated cellular morphology, decreased LDH release, and reduced the apoptotic rate of HT22 cells exposed to Aβ1-42 for 24 h, while the blockade of CB1 or the inhibition of protein kinase C (PKC) partially reversed the neuroprotection. Furthermore, the blockade of CB1 reversed nicotine-induced PKC activation in HT22 cells exposed to Aβ1-42. These results suggest that CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 neurotoxicity, and the neuroprotection may be dependent on the activation of PKC.

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Section: Discussionmentioning

confidence: 99%

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Jia

Lei

et al. 2014

J Mol Neurosci

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“…Whole-cell patch-clamp recordings were performed on iPSC-derived CHAT + neurons on Day 31 after iPSC differentiation as our previous report [41]. Coverslips were placed in a bath solution made of the following (in mM): NaCl 135, KCl 3, CaCl 2 2, MgCl 2 1, glucose1 1, sucrose 10 and HEPES10, pH 7.4 adjusted with NaOH at 310mOsm.…”

Section: Methodsmentioning

confidence: 99%

Modeling the differential phenotypes of spinal muscular atrophy with high-yield generation of motor neurons from human induced pluripotent stem cells

Lin

Qian

et al. 2017

Oncotarget

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Spinal muscular atrophy (SMA) is a devastating motor neuron disease caused by mutations of the survival motor neuron 1 (SMN1) gene. SMN2, a paralogous gene to SMN1, can partially compensate for the loss of SMN1. On the basis of age at onset, highest motor function and SMN2 copy numbers, childhood-onset SMA can be divided into three types (SMA I-III). An inverse correlation was observed between SMN2 copies and the differential phenotypes of SMA. Interestingly, this correlation is not always absolute. Using SMA induced pluripotent stem cells (iPSCs), we found that the SMN was significantly decreased in both SMA III and SMA I iPSCs derived postmitotic motor neurons (pMNs) and γ-aminobutyric acid (GABA) neurons. Moreover, the significant differences of SMN expression level between SMA III (3 copies of SMN2) and SMA I (2 copies of SMN2) were observed only in pMNs culture, but not in GABA neurons or iPSCs. From these findings, we further discovered that the neurite outgrowth was suppressed in both SMA III and SMA I derived MNs. Meanwhile, the significant difference of neurite outgrowth between SMA III and SMA I group was also found in long-term cultures. However, significant hyperexcitability was showed only in SMA I derived mature MNs, but not in SMA III group. Above all, we propose that SMN protein is a major factor of phenotypic modifier. Our data may provide a new insight into recognition for differential phenotypes of SMA disease.

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“…For example, sodium, calcium, chloride, and potassium channels are involved in the phototransduction process and especially in the depolarization and the hyperpolarization of photoreceptor and bipolar cells [ 20 ]. Different studies have shown that cannabinoid agonists induced a dose-dependent reversible modulation of calcium, potassium, and chloride currents in bipolar, rod, cone, and ganglion cells [ 53 , 56 , 57 , 68 – 74 ]. These findings suggest a regulatory role of the cannabinoid system in the retinal neurotransmission at the level of photoreceptor, bipolar, and ganglion cells, which constitute three critical stages of the neural retina.…”

Section: Neurobiology Of Cannabinoids In the Retina: Neurotransmismentioning

confidence: 99%

The Endocannabinoid System in the Retina: From Physiology to Practical and Therapeutic Applications

et al. 2016

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Cannabis is one of the most prevalent drugs used in industrialized countries. The main effects of Cannabis are mediated by two major exogenous cannabinoids: ∆9-tetrahydroxycannabinol and cannabidiol. They act on specific endocannabinoid receptors, especially types 1 and 2. Mammals are endowed with a functional cannabinoid system including cannabinoid receptors, ligands, and enzymes. This endocannabinoid signaling pathway is involved in both physiological and pathophysiological conditions with a main role in the biology of the central nervous system. As the retina is a part of the central nervous system due to its embryonic origin, we aim at providing the relevance of studying the endocannabinoid system in the retina. Here, we review the distribution of the cannabinoid receptors, ligands, and enzymes in the retina and focus on the role of the cannabinoid system in retinal neurobiology. This review describes the presence of the cannabinoid system in critical stages of retinal processing and its broad involvement in retinal neurotransmission, neuroplasticity, and neuroprotection. Accordingly, we support the use of synthetic cannabinoids as new neuroprotective drugs to prevent and treat retinal diseases. Finally, we argue for the relevance of functional retinal measures in cannabis users to evaluate the impact of cannabis use on human retinal processing.

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Suppression of outward K+ currents by WIN55212-2 in rat retinal ganglion cells is independent of CB1/CB2 receptors

Cited by 17 publications

References 52 publications

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Modeling the differential phenotypes of spinal muscular atrophy with high-yield generation of motor neurons from human induced pluripotent stem cells

The Endocannabinoid System in the Retina: From Physiology to Practical and Therapeutic Applications

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