Chapter 6 The Endocannabinoid System During Development: Emphasis on Perinatal Events and Delayed Effects

Fride, Ester; Gobshtis, Nikolai; Dahan, Hodaya; Weller, Aron; Giuffrida, Andrea; Ben‐Shabat, Shimon

doi:10.1016/s0083-6729(09)81006-6

Cited by 80 publications

(65 citation statements)

References 88 publications

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“…Some components of the eCB system have been detected during 1) peri-implantation, where the eCB system is required for proper implantation of the trophoblast (Paria and Dey, 2000; Paria et al, 2001; Sun and Dey, 2008; Taylor et al, 2010), and 2) neurogenesis, where the eCB system is required for neurogenesis, proliferation, differentiation, migration and fasciculation of nascent neurons (Berrendero et al, 1999; Berghuis et al, 2005, 2007; Aguado et al, 2005; Bromberg et al, 2008; Harkany et al, 2008; Mulder et al, 2008; Vitalis et al 2008), reviewed in Fernández-Ruiz et al (1999), Harkany et al (2007), Anavi-Goffer et al (2009), Galve-Roperh et al (2009) and Psychoyos et al (2009). So far, very little is known regarding whether the eCB system is present in the developmental time window between peri-implantation and the start of neurogenesis, and if so, what role it plays during this time window (Anavi-Goffer et al, 2009; Fride, 2009; Psychoyos et al, 2009). This specific period corresponds to the initial stages of organogenesis, and in particular, the formation of the forebrain, midbrain and hindbrain components of the nascent brain.…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor 1 Signaling in Embryo Neurodevelopment

Psychoyos

Vinod

Cao

et al. 2012

Birth Defects Research Pt B

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In utero exposure to THC, the psychoactive component of marijuana, is associated with an increased risk for neurodevelopmental defects in the offspring by interfering with the functioning of the endocannabinoid (eCB) system. At the present time it is not clearly known whether the eCB system is present prior to neurogenesis. Using an array of biochemical techniques we analyzed the levels of CB1 receptors, eCBs (AEA and 2-AG), and the enzymes (NAPE-PLD, DAGLα, DAGLβ MAGL and FAAH) involved in the metabolism of the eCBs in chick and mouse models during development. The findings demonstrate the presence of eCB system in early embryo, prior to neurogenesis. The eCB system might play a critical role in early embryogenesis and there might be adverse developmental consequences of in utero exposure to marijuana and other drugs of abuse during this period.

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Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor 1 Signaling in Embryo Neurodevelopment

Psychoyos

Vinod

Cao

et al. 2012

Birth Defects Research Pt B

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“…Interestingly, the consequences of prenatal stress are similar to many effects of prenatal cannabinoid exposure (Fride et al, 2009), which may suggest that prenatal stress impacts on the EC system and that, vice versa, prenatal cannabinoid exposure may interfere with the ability of the foetus to cope with the stress. Early life stress in rats, due to social isolation, alters the expression of a number of genes associated with EC signalling in different brain areas, but whether this extends to cardiovascular tissues or the HPA axis is not known.…”

Section: Corticosteroids and Cardiovascular Diseasementioning

confidence: 98%

Endocannabinoids and the cardiovascular response to stress

O’Sullivan

Kendall

2011

J Psychopharmacol

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Stress activates the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS), resulting in cardiovascular responses. The endocannabinoid system (ECS), a ubiquitously expressed lipid signalling system, modulates both HPA and SNS activity. The purpose of this review is to explore the possible involvement/role of the ECS in the cardiovascular response to stress. The ECS has numerous cardiovascular effects including modulation of blood pressure, heart rate, the baroreflex, and direct vascular actions. It is also involved in a protective manner in response to stressors in cardiac preconditioning, and various stressors (for example, pain, orthostasis and social stress) increase plasma levels of endocannabinoids. Given the multitude of vascular effects of endocannabinoids, this is bound to have consequences. Beneficial effects of ECS upregulation could include cardioprotection, vasodilatation, CB(2)-mediated anti-inflammatory effects and activation of peroxisome proliferator-activated receptors. Negative effects of endocannabinoids could include mediation of the effects of glucocorticoids, CB(1)-mediated metabolic changes, and metabolism to vasoconstrictor products. It is also likely that there is a central role for the ECS in modulating cardiovascular activity via the HPA and SNS. However, much more work is required to fully integrate the role of the ECS in mediating many of the physiological responses to stress, including cardiovascular responses.

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“…During fetal life, endocannabinoids and the cannabinoid CB1 receptor are important for brain development, regulating neural progenitor differentiation and guiding axonal migration and synaptogenesis. " And further, postnatally, CB1 receptor activation by 2-arachidonoylglycerol appears to play a critical role in development and nutrition [38].…”

Section: In Utero Exposurementioning

confidence: 99%

“…The sequelae associated with prenatal cannabis exposure have been compared to the many effects of prenatal stress, "which may suggest that prenatal stress impacts on the ECS and that vice versa prenatal cannabinoid exposure may interfere with the ability of the fetus to cope with the stress" [38].…”

Section: In Utero Exposurementioning

confidence: 99%

Cannabis Induced Psychopathology

Farah¹

2017

J Addict Res Ther

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The recent trend towards legalization and commercialization of marijuana in the US has resulted in a significant drop in the perceived risks of cannabis use among all age groups. Thus, legalization has further advances the common misperception that cannabis abuse and dependence are generally safe and devoid of neuropsychiatric sequelae. Yet there are numerous acute, as well as numerous long-term neuropsychiatric consequences of cannabis use. In addition to acute psychosis and agitation, this review will discuss the long-term issues of cognitive decline, permanent psychotic disorders, syndromes of prolonged depersonalization, as well as psychological and physical dependence, and related withdrawal symptoms.Cannabis use, particularly repeated exposure, is an established contributory cause of schizophrenia by way of a classic gene-environment interaction, with the vulnerabilities associated with cannabis-induced schizophrenia involving multiple genes. There is also evidence that in utero cannabinoid exposure will impair brain maturation in developing infants and predispose them to neurodevelopmental disorders during childhood. This summary will inform clinicians of the most prevalent consequences associated with cannabis abuse and dependence, and better equip them to educate patients as to these risks. Further, there are treatments that may help patients achieve abstinence, and even neuroprotective strategies to employ in cases of new-onset cannabisinduced psychosis, as well as for cases of in utero exposure.Keywords: Schizophrenia; Cannabis abuse; Paranoia; Anxiety; Psychosis Acute Cannabis Induced PsychopathologyFor some individuals, cannabis use does not produce a calming sensation; rather, it will induce anxiety and, in some, panic attacks [1]. Numerous case reports indicate that typical panic attack symptoms often present with intense depersonalization [2]. Though possibly related to an underlying genetic vulnerability, the specifics of this interaction have yet to be discerned, however, individuals who do experience panic and anxiety symptoms during abuse are more likely to abstain from cannabis in the future [3].The mechanism of cannabis-induced paranoia and hallucinations while abusing is believed to involve the relationship between dopamine activity and endocannabinoid transmitters. Stimulation of D2 receptors in the striatum will result in the synthesis and release of endocannabinoids, which act in a retrograde fashion to inhibit GABA and glutamate activity. Researchers have speculated that due to the number of key physiological processes within the striatum dependent on D2 to endocannabinoid signaling, this process is vital for normal functions of the striatum in health [4].They further theorized that the reason antipsychotics are less effective for acute cannabis-induced psychosis is because they exert their effects through D2 blockade, while THC enters the pathway "downstream" from D2 receptors [4]. Further, acute psychosis is often a harbinger of future psychopathology, as those who experience...

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Chapter 6 The Endocannabinoid System During Development: Emphasis on Perinatal Events and Delayed Effects

Cited by 80 publications

References 88 publications

Cannabinoid Receptor 1 Signaling in Embryo Neurodevelopment

Cannabinoid Receptor 1 Signaling in Embryo Neurodevelopment

Endocannabinoids and the cardiovascular response to stress

Cannabis Induced Psychopathology

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