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the Endocannabinoid & System Autism

regament
11.09.2018

Content:

  • the Endocannabinoid & System Autism
  • Endocannabinoid System as Novel Therapeutic Target for Autism Treatment
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  • Autism spectrum disorder (ASD) defines a group of neurodevelopmental disorders whose symptoms include impaired communication and. Autism Spectrum Disorder (ASD) disease has become a mounting The Endocannabinoids System (ES) consists of a family of locally. Int J Mol Sci. Sep 7;18(9). pii: E doi: /ijms The Endocannabinoid System and Autism Spectrum Disorders: Insights from Animal.

    the Endocannabinoid & System Autism

    Advice Feb 5, 0. Home News Latest News. Post a Job Job Dashboard. No comments so far. Be first to leave comment below. Cancel reply Your email address will not be published. Recent Posts View all. February Advice Feb 5, 0. Subscribe to our Newsletter. I agree to my submitted data being stored and used to receive newsletters. Recently, several studies highlight a key involvement of endocannabinoid EC system in autism pathophysiology [ 2 ]. Endocannabinoids are arachidonic acid derived compounds and together with their receptors and the associated enzymes, they the EC system, an intricate network of lipid signalling pathways [ 3 ].

    Beyond autism, EC system is also involved in several other psychiatric disorders i. This system is also a key regulator of other metabolic and cellular pathways involved in ASDs, such as food intake, energy metabolism, immune system controlling. Early studies in animal models demonstrated that BTBR mice show an abnormal regulation of dopamine levels functioning with an up-regulated CB2A gene expression [ 5 ].

    In addition, in the valproic acid induced model of autism, alterations in the brain's endocannabinoid system have been reported in a newest research [ 6 ]. Autism is a human pathology: However, specific pharmacological approaches aimed at modifying EC signaling in the brain of NLGN3 mutant mice are required to establish whether the observed alterations of the EC system directly contribute to the ASD-like phenotype in these mouse models.

    In addition to the genetically modified rodent models of ASD, several inbred mouse strains incorporate face validity as ASD models, because they display robust and well-replicated social deficits and repetitive behaviors.

    These inbred strains are considered to be models of idiopathic autism, as their ASD-like phenotype is not caused by known genetic mutations.

    Among these, of particular interest is the BTBR mouse, which has been the most extensively characterized. BTBR mice display deficits in behavioral tasks modeling the core domains of ASD, including reduced play and social approach behavior [ 54 , 55 ] and restricted-repetitive behaviors [ 55 , 56 ]. These mice also show pronounced cognitive impairments [ 57 ] as well as an exaggerated response to stress that is associated with high blood levels of corticosterone [ 58 ].

    Overall, a number of BTBR behaviors are consistent with autism, and many of the anatomical features in this strain are consistent with those present in autistic patients [ 59 ].

    Thus far, only one study has investigated the effects of a manipulation of the EC system in the BTBR mouse model [ 45 ]. The authors showed that increasing AEA levels via acute administration of URB completely reversed the social impairment in the three chamber apparatus, an effect that was not attributable to reduced anxiety. Although the most commonly suggested etiology of ASD is through the hereditary genetic characteristics identified as high risk genes for ASD, exposure to environmental factors in the prenatal and early postnatal periods imposes a significant contribution to ASD development [ 60 , 61 ].

    Relevant environmental manipulations in rodents must be conducted using the same agents that have been correlated with human ASD. Well-known environmental risk factors for ASD in humans are maternal infections and valproic acid VPA exposure at the time of neural tube closure. The EC system has been studied in two environmental-based models: Among environmental animal models that show both construct and face validity to ASD, the VPA rat model represents an excellent system to test and develop novel behavioral and drug therapies.

    This model demonstrates many of the structural and behavioral features that can be observed in individuals with autism, thus enabling definition of relevant pathways of developmental dysregulation resulting from environmental manipulation [ 62 ]. VPA is an anti-epileptic drug with an identified histone deacetylase inhibitor property [ 63 , 64 ].

    Several studies have shown that gestational VPA treatment may cause neural tube defects [ 65 ], as well as cognitive impairments [ 66 ] in children. This is consistent with animal studies indicating that the offspring of female rats injected with VPA on the Moreover, prenatal exposure to VPA induces sex-related differences in behavior that are greater in males than females [ 68 ], thus mimicking the imbalanced gender ratio observed in ASD patients [ 69 ].

    Of note, enhancing AEA signaling through inhibition of its degradation partially mitigated the behavioral phenotype induced by prenatal VPA exposure. Similarly, URB treatment normalized communication abnormalities of VPA-exposed pups in the homing test, and reversed their social deficits in the three-chamber and social play behavior tests [ 74 ]. Overall, available data in the VPA rat model suggest that altered AEA-mediated signaling may contribute to communication and social deficits associated with ASD, and support a role of FAAH in the regulation of social behavioral deficits.

    Both viral and bacterial infections during pregnancy have been linked to an increased risk to develop ASD in the offspring [ 76 ].

    Exposure to influenza virus or maternal immune activation MIA induced by polyinosine: C or LPS in rodents at the time of closure of the neural tube seems to be related to the onset of ASD-like behaviors in the offspring [ 77 ]. Hence, the offspring of dams injected with poly I: C between GD 9. In addition, prenatal LPS exposure increases anxiety, decreases social interactions [ 81 ] and impairs learning and memory [ 82 ] in mice.

    In rats, gestational LPS exposure also decreases prepulse inhibition in the male offspring [ 83 ]. These behavioral phenotypes in the offspring were correlated with synaptic abnormalities, including increased cell density and excitability of pyramidal neurons, enhanced postsynaptic glutamatergic responses to NMDA-induced synaptic plasticity, as well as altered glia reactivity [ 84 ].

    Although post-natal LPS administration is not recognized as a model of ASD, data collected further suggest that FAAH inhibition may represent a potential approach for the treatment of disorders involving impaired sociability. Early-life inflammation induced by a single LPS injection at postnatal day PND 14 decreased adolescent social play and non-play behavior both in male and in female rats. A similar improvement was observed after direct PF injection into the basolateral amygdala, suggesting that altered AEA signaling in this brain region plays a central role in mediating LPS-induced social impairments at least in females.

    Many morphological and neurochemical abnormalities have been reported in ASD patients as well as in animal models, reflecting the heterogeneous and complex nature of this group of disorders.

    Such diversity poses a great challenge and hampers the identification of possible common pathophysiological mechanisms in ASD. However, very little information has been thus far available regarding the possible mechanisms through which the EC system could affect ASD-like behaviors.

    For instance, the reported prosocial effects of AEA in animal models of ASD might arise from an interaction with oxytocin, a neuropeptide that promotes parental and social bonding. Indeed, recent evidence has highlighted that oxytocin stimulates AEA release in the nucleus accumbens, a key region for the reinforcing properties of both natural rewards and drugs of abuse, and, importantly, AEA-mediated signaling is required for the prosocial effects of this neuropeptide [ 91 ].

    This suggests that oxytocin-driven AEA signaling may be defective in ASD; hence, a correction of such deficits supposedly offers a novel strategy to treat the social impairments associated with ASD. Additionally, it has been shown that the amelioration of cognitive deficits after chronic rimonabant administration in Fmr1 knockout mice was associated with the normalization of the hippocampal mTOR signaling pathway [ 42 ], suggesting that the procognitive effects elicited by CB1 receptor blockade may be partly dependent upon restoration of this signaling pathway in the hippocampus.

    This is consistent with the observation that mTOR signaling is crucially involved in memory consolidation [ 92 ], and its genetic modulation prevents some of the pathological features in Fmr1 knockout mice [ 93 ]. There is also evidence that ECs might modulate ASD symptoms via interaction with immune system cells. Indeed, changes in AEA metabolism and CB2 receptors were observed in peripheral blood mononuclear cells [ 95 ] and blood monocyte-derived macrophage cells [ 96 ] from autistic patients, suggesting that the EC system could play a role in the immunological dysfunctions associated with ASD.

    As retrograde EC signaling at CB1 receptors is a key regulator of synaptic plasticity both at inhibitory and excitatory synapses in the adult brain [ 99 ], dysfunctions of the EC system could sustain ASD phenotypes as a consequence of unbalanced excitatory and inhibitory neurotransmission.

    Understanding the time course of the alterations of the EC system in animal models of ASD could help to dissect the contribution of this system in the pathogenesis of these neurodevelopmental conditions. Although the preclinical findings seem to suggest that pharmacological interventions aimed at modulating the EC system could be beneficial for relieving symptoms associated with ASD Table 2 , their preliminary nature does not allow any definite conclusion to be drawn concerning potential therapeutic exploitations.

    Effects of pharmacological manipulations of the endocannabinoid EC system in animal models of autism spectrum disorder ASD. Converging data indicate that enhancing AEA signaling through inhibition of its degradation exerts prosocial effects in different animal models of ASD.

    In addition, CB1 receptor blockade, either acute or chronic, seems to have beneficial effects towards cognitive deficits, at least in mouse models of FXS. Remarkably, in most of the studies, the drugs were administered systemically. However, the alterations of the EC system reported in animal models of ASD Table 3 appear to be different depending on the brain region considered, possibly suggesting a different contribution to ASD-like symptoms.

    If so, any potential therapeutic approach is unlikely to involve a single targeted molecule. National Center for Biotechnology Information , U. Int J Mol Sci. Published online Sep 7. Find articles by Marina Gabaglio. Author information Article notes Copyright and License information Disclaimer. Received Jul 24; Accepted Sep 4. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution CC BY license http: This article has been cited by other articles in PMC.

    Abstract Autism spectrum disorder ASD defines a group of neurodevelopmental disorders whose symptoms include impaired communication and social interaction with restricted or repetitive motor movements, frequently associated with general cognitive deficits. Introduction Endocannabinoids ECs are arachidonic acid-derived compounds that, together with their receptors and the associated metabolic enzymes, constitute the endocannabinoid EC system, a neuromodulatory network of lipid signaling pathways [ 1 ].

    Table 1 Pharmacological modulators of the endocannabinoid EC system tested in animal models of autism spectrum disorder ASD. Open in a separate window. EC-modulation of ASD-Like Behaviors According to the Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders DSM-5 , ASD comprises a heterogeneous group of neurological conditions characterized by impaired social communication functions and the presence of restricted, repetitive patterns of behavior or interests that start to emerge in the early developmental period.

    Neuroligin-3 NLGN3 Mouse Models NLGNs are postsynaptic cell adhesion molecules required for synaptic function; they orchestrate the maturation and function of both excitatory and inhibitory synapses in the mammalian brain [ 46 , 47 ]. BTBR Mouse Model In addition to the genetically modified rodent models of ASD, several inbred mouse strains incorporate face validity as ASD models, because they display robust and well-replicated social deficits and repetitive behaviors.

    The EC System in Environmental-Based Models Although the most commonly suggested etiology of ASD is through the hereditary genetic characteristics identified as high risk genes for ASD, exposure to environmental factors in the prenatal and early postnatal periods imposes a significant contribution to ASD development [ 60 , 61 ]. Prenatal VPA Exposure Among environmental animal models that show both construct and face validity to ASD, the VPA rat model represents an excellent system to test and develop novel behavioral and drug therapies.

    Postnatal LPS Injection Both viral and bacterial infections during pregnancy have been linked to an increased risk to develop ASD in the offspring [ 76 ]. Possible Mechanisms Many morphological and neurochemical abnormalities have been reported in ASD patients as well as in animal models, reflecting the heterogeneous and complex nature of this group of disorders.

    Conclusions Although the preclinical findings seem to suggest that pharmacological interventions aimed at modulating the EC system could be beneficial for relieving symptoms associated with ASD Table 2 , their preliminary nature does not allow any definite conclusion to be drawn concerning potential therapeutic exploitations.

    Table 2 Effects of pharmacological manipulations of the endocannabinoid EC system in animal models of autism spectrum disorder ASD. Conflicts of Interest The authors declare no conflict of interest. The endocannabinoid system and its modulation by phytocannabinoids.

    Endocannabinoids as regulators of transient receptor potential TRP channels: A further opportunity to develop new endocannabinoid-based therapeutic drugs.

    Endocannabinoid System as Novel Therapeutic Target for Autism Treatment

    Early studies suggest that the endocannabinoid system may mediate social problems, in patients with autism, so it may be a treatment target in. The endocannabinoid (EC) system represents a major neuromodulatory system involved in the regulation of emotional responses, behavioral reactivity to. By Joseph Rosado, MD, MBA. Autism spectrum disorder (ASD) is a developmental disability that can cause significant social, communication.

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    gromila1992

    Early studies suggest that the endocannabinoid system may mediate social problems, in patients with autism, so it may be a treatment target in.

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