Background:The G protein-coupled receptor 55 (GPR55) is a mammalian orphan receptor that awaits a formal classification. There are an increasing number of reports directed to know the physiology and pathophysiology of this receptor. Lamentably, its functions in the central nervous system (CNS) have been scarcely elucidated.Methods:A bibliographic search in PubMed database about GPR55 actions in the CNS was made. The information was grouped for brain structures to facilitate the interpretation. Finally, we constructed a schematic representation of the current knowledge about the potential participation of GPR55 in some physiological and pathophysiological events.Results:Seventy nine papers were included in the review. Only few of them showed data about GPR55 (mRNA/protein) expression in multiple brain areas. The rest showed findings in different preparations both in vitro and in vivo conditions that allowed us to speculate a potential activity of GPR55 in the different brain areas.Conclusion:GPR55 mRNA is expressed in several brain areas as the hippocampus, hypothalamus, frontal cortex and cerebellum; but due to the lack of information, only some speculative information about its function in these regions has been suggested. Therefore, this review provide relevant information to motivate further research about GPR55 physiology/pathophysiology in the CNS.
Endocannabinoids (eCBs) are involved in the hippocampal mechanisms of spatial learning and memory in rats. Although eCBs exert many of their actions on spatial learning and memory via CB1 receptors, the putative cannabinoid receptor GPR55 (expressed in the hippocampus, cortex, forebrain, cerebellum and striatum) seems to be also involved. To investigate the potential role of GPR55 in spatial learning and memory, Wistar rats received bilateral infusions of lysophosphatidylinositol (LPI, GPR55-agonist) into the hippocampus 5-minutes before training-phase in the Barnes-maze (BM). This manipulation increased the use of serial navigation while preventing the learning of spatial navigation strategy and decreasing the use of random activity to find the escape-tunnel in the BM. In contrast, CID16020046 (GPR55-antagonist) increased the use of random activity at the expense of spatial and serial navigation strategies. Finally, CID16020046 significantly reduced the time spent in the target zone during a retention test. Our results suggest: (i) a potential role of GPR55 in developing navigation strategies; (ii) a prospective function for LPI acting in hippocampal CA1 (probably via GPR55) to perform a serial navigation strategy; and (iii) a potential role of GPR55 in the mechanisms involved in spatial memory (object placement memory).
We have previously reported that maternal separation (MS) for 3 h daily during the first two postnatal weeks increases wakefulness, whereas it reduces sleep in rats. Oleamide, an agonist of the cannabinoid receptor type 1, increases sleep in MS rats to such a level that we cannot differentiate their sleep patterns from those of their non-MS (NMS) siblings. However, 2-arachidonoylglycerol (2-AG), an endocannabinoid, infused into the lateral hypothalamus of NMS rats at the beginning of the dark phase of the cycle increases rapid eye movement sleep and the expression of c-Fos on the rapid eye movement sleep promoting melanin-concentrating hormone neurons. We recorded the sleep-wake cycle of adult rats subjected to MS for 3 h daily from postnatal days 2 to 16, as well as in their NMS siblings. Besides the electrodes for recording the sleep-wake cycle, a couple of cannulae aimed bilaterally to the lateral hypothalamus were implanted to infuse 2-AG. We found that administration of 2-AG into the lateral hypothalamus of MS rats at the beginning of the light phase of the cycle restores sleep, whereas sleep and wakefulness of NMS rats under 2-AG infusion do not show any significant change.
Temporal lobe epilepsy (TLE) is a common form of medically intractable partial epilepsy. Although seizures originate in mesial temporal structures, there are widespread abnormalities of gray and white matter beyond the temporal lobes that negatively impact on functional networks and cognition. Previous studies have focused either on the global impact on functional networks, or on the functional correlates of specific cognitive abilities. Here, we use a step-wise approach to evaluate the link between whole-brain functional connectivity (FC) anomalies to overall cognitive performance, and how such abnormal connectivity alters the fronto-parietal brain regions involved in working memory (WMem), a cognitive disability often reported by TLE patients. We evaluated 40 TLE patients and 36 healthy subjects through extensive cognitive testing, resting-state functional magnetic resonance imaging (rs-fMRI), and task-based fMRI using Sternberg's task to evaluate WMem. As a group, TLE patients displayed cognitive abnormalities across different domains, although considerable within-group variability was identified. TLE patients showed disruptions of functional networks between and within the default mode network (DMN) and task-positive networks (TPN) resulting in associations with cognitive performance. Furthermore, during the WMem task, TLE patients showed abnormal activity of fronto-parietal regions that was associated with other forms of memory, and alterations of seed-based connectivity analyses. Our results show that different degrees of abnormal functional brain activity and connectivity are related to the severity of cognitive disabilities across cognitive spheres. Differential activity between patients and healthy subjects suggest potential compensatory mechanisms to preserve adequate cognitive performance.
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