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  1. #1

    Danni da cannabis sul cervello

    Quali sono i danni da abuso di cannabis sul cervello? Come agisce a livello di neuroni?
    Mi indicate qualche testo o articolo per approfondire questo argomento?

  2. #2
    Data registrazione
    non ho un doc preciso da consigliarti ma ti suggerisco di cercare in rete fabrizio schifano, ci sono molti doc disponibili. schifano in particolare si occupa di tossicodipendenza e pat psichiatriche.

    ciao laura

  3. #3
    Postatore OGM L'avatar di willy61
    Data registrazione
    Albino (BG)
    Blog Entries
    High times for memory: cannabis disrupts temporal coordination among hippocampal neurons. By: Soltesz, Ivan; Staley, Kevin. Nature Neuroscience, Dec2006, Vol. 9 Issue 12, p1461-1463, 3p, 1 diagram; Abstract: The article reports on the findings of a study which seeks to evaluate if endogenous cannabinoids interrupt coordination among hippocampal hormones. The researchers have investigated the effects of cannabinoid administration on hippocampal ensemble activity in rats. Details of the experiment are offered. The researchers found that endogenous cannabinoid does not affect coordination among hippocampal hormones, as well as it does not regulate learning. DOI: 10.1038/nn1206-1461 (AN 23211056)

    Lack of Hippocampal Volume Change in Long-term Heavy Cannabis Users. By: Tzilos, Golfo K.; Cintron, Christina B.; Wood, Jonas B. R.; Simpson, Norah S.; Young, Ashley D.; Pope, Harrison G.; Yurgelun-Todd, Deborah A.. American Journal on Addictions, Jan/Feb2005, Vol. 14 Issue 1, p64-72, 9p Abstract: The effects of cannabis smoking on the morphology of the hippocampus are still unclear, especially because previous human studies have examined primarily younger, shorter-term users. We used magnetic resonance imaging to invest:;gate these effects in a group of 22 older, long-term cannabis users (reporting a mean (SD] of 20,100 [13,900] lifetime episodes of smoking) and 26 comparison subjects with no history of cannabis abuse or dependence. When compared to control subjects, smokers displayed no significant adjusted differences in volumes of gray matter, white matter, cerebrospinal fluid, or left and right hippocampus. Moreover, hippocampal volume in cannabis users was not associated with age of onset of use nor total lifetime episodes of use. These findings are consistent with recent literature suggesting that cannabis use is not associated with structural changes within the brain as a whole or the hippocampus in particular. [ABSTRACT FROM AUTHOR] DOI: 10.1080/10550490590899862 (AN 16257046)

    β-Endorphin elevations in the ventral tegmental area regulate the discriminative effects of Δ-9-tetrahydrocannabinol. By: Solinas, M.; Zangen, A.; Thiriet, N.; Goldberg, S.R.. European Journal of Neuroscience, Jun2004, Vol. 19 Issue 12, p3183-3192, 10p Abstract: β-Endorphin is an endogenous opioid that produces behavioral effects similar to heroin and morphine and is released in the nucleus accumbens by cocaine, amphetamine and ethanol, suggesting a general involvement in the reinforcing effects of abused drugs. Here we show that, in rats, Δ-9-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, produces large increases in extracellular levels of β-endorphin in the ventral tegmental area and lesser increases in the shell of the nucleus accumbens. We then used a two-lever choice THC-discrimination procedure to investigate whether THC-induced changes in endogenous levels of β-endorphin regulate the discriminative effects of THC. In rats that had learned to discriminate injections of THC from injections of vehicle, the opioid agonist morphine did not produce THC-like discriminative effects but markedly potentiated discrimination of THC. Conversely, the opioid antagonist naloxone reduced the discriminative effects of THC. Bilateral microinjections of β-endorphin directly into the ventral tegmental area, but not into the shell of the nucleus accumbens, markedly potentiated the discriminative effects of ineffective threshold doses of THC but had no effect when given alone. This potentiation was blocked by naloxone. Together these results indicate that certain psychotropic effects of THC related to drug abuse liability are regulated by THC-induced elevations in extracellular β-endorphin levels in brain areas involved in opiate reward and reinforcement processes. [ABSTRACT FROM AUTHOR] DOI: 10.1111/j.0953-816X.2004.03420.x (AN 13546954)

    Add AddedThe effects of adolescent cannabis use on educational attainment: a review. By: Lynskey, Michael; Hall, Wayne. Addiction, Nov2000, Vol. 95 Issue 11, p1621-1630, 10p Abstract: This paper reviews research examining the link between cannabis use and educational attainment among youth. Cross-sectional studies have revealed significant associations between cannabis use and a range of measures of educational performance including lower grade point average, less satisfaction with school, negative attitudes to school, increased rates of school absenteeism and poor school performance. However, results of cross-sectional studies cannot be used to determine whether cannabis use causes poor educational performance, poor educational performance is a cause of cannabis use or whether both outcomes are a reflection of common risk factors. Nonetheless, a number of prospective longitudinal studies have indicated that early cannabis use may significantly increase risks of subsequent poor school performance and, in particular, early school leaving. This association has remained after control for a wide range of prospectively assessed covariates. Possible mechanisms underlying an association between early cannabis use and educational attainment include the possibility that cannabis use induces an 'amotivational syndrome' or that cannabis use causes cognitive impairment. However, there appears to be relatively little empirical support for these hypotheses. It is proposed that the link between early cannabis use and educational attainment arises because of the social context within which cannabis is used. In particular, early cannabis use appears to be associated with the adoption of an anti-conventional lifestyle characterized by affiliations with delinquent and substance using peers, and the precocious adoption of adult roles including early school leaving, leaving the parental home and early parenthood. [ABSTRACT FROM AUTHOR] DOI: 10.1080/09652140020000867 (AN 3865782)

    Cannabis and cognitive dysfunction: Parallels with endophenotypes of schizophrenia? By: Solowij, Nadia; Michie, Patricia T.. Journal of Psychiatry & Neuroscience, Jan2007, Vol. 32 Issue 1, p30-52, 23p Abstract (English): Currently, there is a lot of interest in cannabis use as a risk factor for the development of schizophrenia. Cognitive dysfunction associated with long-term or heavy cannabis use is similar in many respects to the cognitive endophenotypes that have been proposed as vulnerability markers of schizophrenia. In this overview, we examine the similarities between these in the context of the neurobiology underlying cognitive dysfunction, particularly implicating the endogenous cannabinoid system, which plays a significant role in attention, learning and memory, and in general, inhibitory regulatory mechanisms in the brain. Closer examination of the cognitive deficits associated with specific parameters of cannabis use and interactions with neurodevelopmental stages and neural substrates will better inform our understanding of the nature of the association between cannabis use and psychosis. The theoretical and clinical significance of further research in this field is in enhancing our understanding of underlying pathophysiology and improving the provision of treatments for substance use and mental illness. [ABSTRACT FROM AUTHOR] (AN 23490194)

    Cannabis and motor function: fMRI changes following 28 days of discontinuation. Pillay, Srinivasan S.; Rogowska, Jadwiga; Kanayama, Gen; Experimental and Clinical Psychopharmacology, Vol 16(1), Feb 2008. pp. 22-32. [Journal Article] Abstract: The authors hypothesized that supplementary motor cortex (SMA) and anterior cingulate cortex (ACC) activation in chronic cannabis users, studied 4 to 36 hours after their last episode of use, would disappear by Day 28 of abstinence during finger-tapping tests. Eleven cannabis users and 16 comparison subjects were scanned during right (RFT) and left (LFT) finger-tapping tasks on a GE 1.5 Tesla scanner retrofitted with a whole body echo planar coil. Image analyses were conducted in SPM99 using an ROI approach to define each Brodmann area (BA). Differences in cerebral activation were examined in the left and right primary motor cortex (BA4), SMA (BA6), and ACC (BA24 and BA32 separately). The authors found diminished activation for contralateral BA6 from Day 0 to Day 28. For LFT, the authors also found: ipsilaterally diminished BA6 activation on Day 7, but not Day 0 or Day 28; ipsilaterally diminished BA32 activation on Day 0, but not Day 7 or Day 28; contralaterally diminished BA 4 activation on Day 28, but not Day 0 or Day 7; and contralaterally diminished BA32 activation on Day 0 and Day 28, but not Day 7. For RFT, the authors found ipsilaterally diminished BA32 activation on Days 0 and 7 but not on Day 28; contralaterally diminished BA32 activation on Days 0, 7, and 28; and ipsilaterally diminished BA6 activation on Days 0, 7, and 28. These results suggest that residual diminished brain activation is still observed after discontinuing cannabis use in motor cortical circuits. (PsycINFO Database Record (c) 2008 APA, all rights

    Spatial working memory performance and fMRI activation interaction in abstinent adolescent marijuana users. Padula, Claudia B.; Schweinsburg, Alecia D.; Tapert, Susan F.; Psychology of Addictive Behaviors, Vol 21(4), Dec 2007. pp. 478-487. [Journal Article] Abstract: Previous studies have suggested neural disruption and reorganization in adult marijuana users. However, it remains unclear whether these effects persist in adolescents after 28 days of abstinence and, if they do, what Performance × Brain Response interactions occur. Adolescent marijuana users (n=17) and controls (n=17) aged 16-18 years were recruited from local schools. Functional magnetic resonance imaging data were collected after 28 days' monitored abstinence as participants performed a spatial working memory task. Marijuana users show Performance × Brain Response interactions in the bilateral temporal lobes, left anterior cingulate, left parahippocampal gyrus, and right thalamus (clusters ≥1358 μl; p<.05), although groups do not differ on behavioral measures of task performance. Marijuana users show differences in brain response to a spatial working memory task despite adequate performance, suggesting a different approach to the task via altered neural pathways. (PsycINFO Database Record (c) 2007 APA, all rights reserved)

    Early adolescent cannabis exposure and positive and negative dimensions of psychosis. By: Stefanis, N. C.; Delespaul, P.; Henquet, C.; Bakoula, C.; Stefanis, C. N.; van Os, J.. Addiction, Oct2004, Vol. 99 Issue 10, p1333-1341, 9p Abstract: To investigate the effect of exposure to cannabis early in adolescence on subclinical positive and negative symptoms of psychosis.Cross-sectional survey in the context of an ongoing cohort study.Government-supported general population cohort study.A total of 3500 representative 19-year olds in Greece.Subjects filled in the 40-item Community Assessment of Psychic Experiences, measuring subclinical positive (paranoia, hallucinations, grandiosity, first-rank symptoms) and negative psychosis dimensions and depression. Drug use was also reported on.Use of cannabis was associated positively with both positive and negative dimensions of psychosis, independent of each other, and of depression. An association between cannabis and depression disappeared after adjustment for the negative psychosis dimensions. First use of cannabis below age 16 years was associated with a much stronger effect than first use after age 15 years, independent of life-time frequency of use. The association between cannabis and psychosis was not influenced by the distress associated with the experiences, indicating that self-medication may be an unlikely explanation for the entire association between cannabis and psychosis.These results add credence to the hypothesis that cannabis contributes to the population level of expression of psychosis. In particular, exposure early in adolescence may increase the risk for the subclinical positive and negative dimensions of psychosis, but not for depression. [ABSTRACT FROM AUTHOR] DOI: 10.1111/j.1360-0443.2004.00806.x (AN 14410519)

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