Effects on development.
ABSTRACT This chapter will review the effects produced on neural development by maternal consumption of cannabinoids during gestation and lactation, with emphasis in the maturation of several neurotransmitter systems (dopamine, serotonin, opioids, cannabinoids, etc.) and possible modifications in their functional expression at the behavioral or neuroendocrine levels. In addition, we have analyzed the possible existence of a sexual dimorphism in these ontogenic effects of cannabinoids, as well as the possible molecular mechanism underlying such effects. In general, the results discussed support the view that exposure to cannabinoids during critical periods of development produces marked modifications in the functional expression of diverse neuronal systems in adulthood. Furthermore, the functions of endocannabinoids in the brain are large not only in adulthood, but also in the period of prenatal and postnatal development. Thus, endocannabinoids have been reported to be present in early ages and to play a role in the process of brain development: neural proliferation and migration, axonal elongation, synaptogenesis and/or myelogenesis.
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ABSTRACT: The active component of the marijuana plant Cannabis sativa, Delta9-tetrahydrocannabinol (THC), produces numerous beneficial effects, including analgesia, appetite stimulation and nausea reduction, in addition to its psychotropic effects. THC mimics the action of endogenous fatty acid derivatives, referred to as endocannabinoids. The effects of THC and the endocannabinoids are mediated largely by metabotropic receptors that are distributed throughout the nervous and peripheral organ systems. There is great interest in endocannabinoids for their role in neuroplasticity as well as for therapeutic use in numerous conditions, including pain, stroke, cancer, obesity, osteoporosis, fertility, neurodegenerative diseases, multiple sclerosis, glaucoma and inflammatory diseases, among others. However, there has been relatively far less research on this topic in the eye and retina compared with the brain and other organ systems. The purpose of this review is to introduce the "cannabinergic" field to the retinal community. All of the fundamental works on cannabinoids have been performed in non-retinal preparations, necessitating extensive dependence on this literature for background. Happily, the retinal cannabinoid system has much in common with other regions of the central nervous system. For example, there is general agreement that cannabinoids suppress dopamine release and presynaptically reduce transmitter release from cones and bipolar cells. How these effects relate to light and dark adaptations, receptive field formation, temporal properties of ganglion cells or visual perception are unknown. The presence of multiple endocannabinoids, degradative enzymes with their bioactive metabolites, and receptors provides a broad spectrum of opportunities for basic research and to identify targets for therapeutic application to retinal diseases.Progress in Retinal and Eye Research 09/2008; 27(5):501-26. DOI:10.1016/j.preteyeres.2008.07.002 · 9.90 Impact Factor
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ABSTRACT: In the United States, marijuana is one of the drugs most abused by adolescents, with females representing a growing number of users. In previous studies, treatment of adolescent female rats with morphine significantly altered brain reward systems in future offspring. As both cannabinoid and opioid systems develop during adolescence, it was hypothesized that early exposure to cannabinoids would induce similar transgenerational effects. In the current study, female rats were treated with the cannabinoid receptor (CB1/CB2) agonist WIN 55,212-2 or its vehicle for three consecutive days during adolescent development (30 days of age), and were subsequently mated in adulthood (60 days of age). The adolescent and adult male offspring of these WIN 55,212-2 (WIN-F1)- or vehicle (VEH-F1)-treated females were tested for their response to morphine using the conditioned place preference (CPP) paradigm. Both adolescent and adult WIN-F1offspring exhibited greater sensitivity to morphine CPP than their VEH-F1 counterparts. Collectively, the findings provide additional evidence of transgenerational effects of adolescent drug use.Journal of Psychopharmacology 04/2012; 26(10):1348-54. DOI:10.1177/0269881112443745 · 2.81 Impact Factor
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ABSTRACT: Adolescence is a developmental period characterized by neuronal remodeling and the maturation of adult emotionality, reproductive behavior and social behavior. We examined whether chronic cannabinoid exposure in adolescent rats alters female sexual motivation, estrous cyclicity, sucrose preference, and CB(1)R expression in adulthood. Female rats were administered with the synthetic cannabinoid agonist, CP-55,940 (0.4 mg/kg, intraperitoneal), daily during adolescent development (PND 35-45). In a subset of subjects, socio-sexual motivation was investigated in adulthood (PND 75-86) using a runway apparatus. Estrous cyclicity was tracked in adulthood via vaginal cytology and a single-mount test. A two-bottle sucrose preference test was also conducted to determine whether predicted changes in socio-sexual motivation might be linked to alterations in hedonic processing. CB(1)R expression was examined in two separate subsets of subjects, one sacrificed following drug treatment (PND 46) and one before behavioral testing (PND 74). Drug treatment significantly decreased adult preference for a male conspecific (sexual motivation), as assessed by both Run Time and Proximity Time, but did not affect estrous cyclicity or sucrose preference. CP-55,940 treatment also induced immediate, but transient, decreases in CB(1)R expression in the ventromedial nucleus of the hypothalamus and amygdala. Drug treatment did not affect CB(1)R expression in the nucleus accumbens (core or shell) or globus pallidus at either time point. We suggest that the endocannabinoid system may play a role in the maturation of neuroendocrine axes and adult female reproductive behavior, and that chronic exposure to cannabinoids during adolescence disrupts these neurodevelopmental processes.Pharmacology Biochemistry and Behavior 07/2011; 100(1):157-64. DOI:10.1016/j.pbb.2011.07.006 · 2.82 Impact Factor