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Held in Kings College, University of London, May 1-2 2007 Conference abstracts The
central nervous system and endocannabinoids The major endocannabionoid 2-arachidonoyl glycerol (2-AG) has been identified both in the central nervous system and in the periphery. Stressful stimuli-traumatic brain injury (TBI) for example - enhance brain 2-AG levels in mice. 2-AG, both of endogenous and exogenous origin, has been shown to be neuroprotective in in-vivo models of closed head injury, ischemia and excitotoxicity. These effects may derive from the ability of cannabinoids to act through various biochemical mechanisms including inhibition of glutamate release or direct blockade of NMDA receptors, inhibition of intracellular calcium mobilization, action as reactive oxygen species (ROS) scavengers, inhibition of pro- flammatory cytokines and inhibition of NF-kB activation. 2-AG also helps repair the blood brain barrier after TBI. The
endocannabinoids act via multiple receptors, of which the CB1 receptors
are most abundant in the CNS. We Arachidonoyl-L-serine
(ARA-S) is an endogenous constituent of the endocannabionoid family,
which we recently Indeed,
a preliminary study revealed that mice, injected with ARA-S after
injury, displayed a significantly greater ----------------------------- Endocannabinoids
and development The active components of cannabis function by stimulating the CB1 cannabinoid receptor in the brain. These receptors have normal functions, and the brain makes its own molecules (called endocannabinoids) to activate them. Diacylglycerol lipase (DAGL) activity generates 2-arachidonyl glycerol (2-AG), the most abundant endocannabinoid in the nervous system. Insights into novel roles for endocannabinoids during development, and in the adult, are emerging based on a full understanding of where and when the DAGLs are expressed. The enzymes are first expressed by newly differentiated neurons, supporting an important role for the enzymes in axonal growth and guidance. The enzymes become restricted to post-synaptic sites at all CB1 positive synapses in the adult nervous system where they are well placed to synthesize, on demand, an endocannabinoid for the retrograde control of synaptic strength and neuroprotection. The enzymes are also expressed by neural stem cells in the adult brain where they play a role in the generation of new neurons throughout life. The cloning and characterisation of these enzymes paves the way for a better understanding of the factors that regulate endocannabinoid signalling, a pathway that can now be viewed as having multiple functions throughout the developing and adult brain. ----------------------------- Cannabis,
cognition and schizophrenia ----------------------------- A
functional MRI study of the effects of cannabis on the brain Cannabis use can induce psychotic symptoms and anxiety and can alter cognitive and emotional processing. We used functional neuroimaging to investigate the neurocognitive basis of these effects, using experimental tasks that engage processes known to be modulated by cannabis use. Methods Subjects
were 15 healthy males who were not regular cannabis users. Each
subject was studied on 3 occasions, Results During
the encoding phase of the memory task THC attenuated activation
in the left temporal cortex compared to Conclusions The
different symptomatic and cognitive effects of cannabis can be related
to the influence of THC and CBD on ----------------------------- Cannabis
exposure and the developing brain: long-term gateway effects? Epidemiological studies suggest that early regular use of cannabis increases the risk of initiating the use of other illicit drugs. Whether there is a causal relationship between early cannabis exposure and the progression to the use of other illicit drugs is still highly debated. One strategy to directly evaluate the neurobiological relationship of prior cannabis experience with other illicit drugs independent of cultural and social factors is the use of experimental animal models. The presentation will provide results from animal models showing long-term cannabis-induced disturbances of reward neural systems. ----------------------------- Cannabis
use: an important risk factor for psychosis? This presentation is based on findings from an epidemiological study among 2,076 children and adolescents from the general population who were followed up into adulthood. In young adulthood, information on lifetime cannabis (and other illicit drug) use and lifetime psychotic features was obtained. At previous assessments behavioural and emotional problems were assessed. Cannabis use predicted future psychotic symptoms. However, the reverse, psychotic symptoms predicting cannabis use, was also found. The prediction of psychotic symptoms by cannabis use could not be explained by high levels of behavioural or emotional problems in general. Remarkably, MDMA use predicted psychotic symptoms as well. Implications for mental health policies will be discussed. ----------------------------- Cannabis
an dpsychotic symptoms, is htere a causal link? This presentation will use data from the Christchurch Health & Development Study (CHDS) to examine the linkages between exposure to cannabis use and rates of psychosis/psychotic symptoms. The CHDS is a longitudinal study of a birth cohort of 1,265 children born in 1977 that has been studied to the age of 30. Key issues to be examined include: confounding; reverse causality; and the pathways linking cannabis use to the development of psychotic symptoms. The implications of these findings for the regulation of cannabis use and supply will be considerable. ----------------------------- Genetic
moderation of cannabis-induced psychosis Observational studies have shown that gene X environment interactions may underlie the association between cannabis use and psychosis. A double-blind placebo controlled study in which patients with a psychotic illness, relatives of patients and healthy controls were exposed to delta-9-THC, showed that a functional polymorphism in the cathechol-0-methyltransferase gene moderates the acute effects of cannabis on cognition and psychosis outcome. A momentary assessment technique was furthermore used to assess differences between patients and controls in the effects of cannabis in daily life. These data show that psychosis liability is associated with differential sensitivity to both the psychosis-inducing and mood-enhancing effects of cannabis. The temporal dissociation between acute rewarding effects and sub-acute psychotogenic effects may be instrumental in explaining the circle of deleterious use in patients with psychotic illness. ----------------------------- Use
of cannabis in a East-London first episode psychosis sample: data
from the GAP, genetics and psychosis study Background: Exposure to cannabis is associated with a risk of developing psychosis. Individual sceptibility depends on age of onset of cannabis abuse and on genotype (Arseneault et al., 2004; Caspi et al., 2005). In the general population cannabis use is associated with lower educational achievement (Macleod et al, 2004). There are not study addressing this association in individuals with psychosis. In this study we investigate whether early age at first cannabis use is associated with longer and regular use and whether cannabis use predicts level of educational achievement in a first-episode psychotic population. Method: We
collected demographic, clinical and cannabis use (age at first use,
frequency, length of use) information Results: 110
(55%) smoked cannabis, eighty-nine were male and 21 female. We collected
data on age at first use on Among
those who commenced cannabis use before age 16, the mean length
of cannabis use was 9,5 years Condusion: Early age at first use of cannabis is associated with longer and regular use in patients with their first episode of psychosis. Counterintuitively, our data also show that frequent cannabis use is associated with higher academic achievement in a first episode psychotic population. This is not due to the non-users being of lower age. Further analyses will be conducted to explore this interesting finding. ----------------------------- Day 2 Interventions
for cannabis use disorder: an overview Cannabis is the most widely used illicit substance in the Western world with more than one in four young people in the UK having ever used it. Worldwide, its use is increasingly recognised as a source of morbidity, with recent concerns focusing on its contribution to psychosis in young people. In 1996 it was estimated in Australia, that more disability-adjusted healthy years of life were lost due to cannabis use and dependence than to HIV, Hepatitis B and Hepatitis C combined. In addition, there is a growing demand for cannabis dependence treatment locally and internationally. This paper will provide an overview of the evidence to support psycho-social interventions for cannabis use disorder and discuss the promising pharmacotherapies, and specific interventions for co-occurring cannabis dependence and other psychological disorders, currently under investigation internationally. ----------------------------- Stoned,
cold sober: psychological interventions for cannabis and alcohol
use among people with psychosis ----------------------------- Psychotherapeutic
interventions for cannabis abuse and/or dependence in outpatient
settings Cannabis
use disorder is the most commonly occurring illicit substance use
disorder in the general population. ----------------------------- Personality
and Cannabis use ----------------------------- CBD
vs. THC: imaging differences ----------------------------- he
effects of delta-9-THC in healthy individuals and individuals with
schizophrenia In
light of the growing preclinical evidence of cannabinoid-dopamine
interactions, we then sought to determine These
data provide the first evidence in humans that we are aware of that
cannabinoid and dopamine systems have ----------------------------- Cannabidiol
as an antipsychotic - new perspectives Background: The human endocannabinoid system interacts with various neurotransmitter systems and the endocannabinoid anandamide was found significantly elevated in CSF and inversely correlated to psychopathology (Giuffrida et al. 2004) providing a link to the neurobiology of schizophrenia. While delta-9-tetrahydrocannabinol, the psychoactive compound of Cannabis sativa shows psychedelic properties, the major herbal cannabinoid compound cannabidiol was suggested recently a re- uptake inhibitor of anandamide. In addition potential antipsychotic properties have been hypothezised. Methods. We performed an explorative, 4-week, double-blind, controlled clinical trial on the effects of purified cannabidiol in acute schizophrenia compared to the antipsychotic amisulpride. The antipsychotic properties of bothwere the primary target of the study. Furthermore side effects and anxiolytic capabilities of both treatments were investigated. Results: 42
patients fulfilling DSM-IV criteria of acute paranoid schizophrenia
or schizophreniform psychosis participated in the study. Both treatments
were associated with a significant decrease of psychotic symptoms
after Conclusions: Cannabidiol
proved substantial antipsychotic properties in acute schizophrenia.
This is in line with our suggestion of an adaptive role of the endocannabinoid
system in paranoid schizophrenia, and raises further evidence that
this adaptive mechanism may represent a valuable target for antipsychotic
treatment strategies.
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