Nd binding research [62, 64, 6669]. Incidentally, CB1 was also found in brain places like

Nd binding research [62, 64, 6669]. Incidentally, CB1 was also found in brain places like thalamus and cortex, known to influence visual output [7072], at the same time as in trabecular meshwork, Schlemm’s canal and ciliary body, where also CB2 is expressed [66, 7375]. Several studies demonstrated the presence of TRPV1 along with other TRP subunits at mRNA and protein level in mammalian and ��-Bisabolene In stock nonmammalian retina, and in a selection of neuronal and glial cells of this region; however, results remained controversial, possibly due to the use of distinct antibodies and staining protocols [35, 63, 7681]. Interestingly, TRPV1 might play a major functional part within the inner retina, given that it was not detected in photoreceptors and bipolar cells [63]. As for GPR55, its presence has been documented only in the inner segments of rod photoreceptors of monkey retina, suggesting a function part in scotopic vision [65, 69]. Indeed, retinal function has been assessed by various flash electroretinogram (ERG) measurements in the presence of selective antagonists of CB1 and CB2, suggesting the involvement of eCB signaling in the modulation of retinal response. ECS can also be involved in neurotransmission within the retina. Indeed, by acting on ionic currents and electrical potentials, it may modulate the release of many neurotransmitters including dopamine, noradrenaline, GABA and glutamate, that control synaptic activity in retinal ganglion cells and consequently modulate visual response [8287]. Additionally, AEA, 2AG and their congener Npalmitoylethanolamine (PEA) happen to be measured by gas chromatographymass spectrometry in human ocular tissues, Lufenuron manufacturer demonstrating an general larger content of 2AG when compared with AEA in human retina, in addition to a content material change upon retinal degenerative diseases [75, 88, 89]. 2AG and AEA levels are high in retina with DR and agerelated macular degeneration [89], whereas glaucoma sufferers have lowered levels of 2Neuroprotection by (endo)Cannabinoids in Glaucoma and Retinal Neurodegenerative DiseasesCurrent Neuropharmacology, 2018, Vol. 16, No.AG and PEA without modifications in AEA in the very same patients [88]. Moreover, FAAH expression is exceptional in different layers of retina, from OPL to GCL (ganglion cell layer) in rats, zebrafishes, gold fishes, monkeys and humans [64, 90, 91], and FAAH activity can be measured inside the identical species and especially in mice and rats, exactly where it truly is larger in rods, bipolar cells, horizontal cells, amacrine cells, Muller cells and ganglion cells. Furthermore, NAPEPLD was identified in the retina of rodents as well as other mammals [90], and not too long ago the presence of DAGL and MAGL mRNAs was documented in rat retina [41], extending previous data on their localization in the course of postnatal improvement [62]. Far more particularly, DAGL was located to be expressed in the postsynaptic terminals of cone bipolar cells, whereas MAGL inside the IPL and OPL [92]. Localization of ECS components in retina is schematically depicted in Fig. (1). four. PHYTOCANNABINOIDS, IOP REDUCTION AND RETINAL PROTECTION The initial evidence to get a constructive role of pCBs in retina protection dates back towards the `70s, when smoking marijuana was identified to reduce IOP in a smaller number of subjects [93]. Then, several experimental findings demonstrated that oral or intravenous administration of THC to human subjects with glaucoma reduces IOP, although with development of tolerance and considerable education of systemic blood pressure and tachycardia [9497]. Rather, single sublingual administration of THC tempo.