Couple study's on cannabinoids and memory and the mechanisms behind it.
The acute effects of cannabinoids on memory in humans: a review
by
Ranganathan M, D'Souza DC.
Schizophrenia Biological Research Center,
VA Connecticut Healthcare System,
West-Haven, CT, USA.
Psychopharmacology (Berl). 2006 Nov;188(4):425-44.
ABSTRACT
RATIONALE: Cannabis is one of the most frequently used substances. Cannabis and its constituent cannabinoids are known to impair several aspects of cognitive function, with the most robust effects on short-term episodic and working memory in humans. A large body of the work in this area occurred in the 1970s before the discovery of cannabinoid receptors. Recent advances in the knowledge of cannabinoid receptors' function have rekindled interest in examining effects of exogenous cannabinoids on memory and in understanding the mechanism of these effects. OBJECTIVE: The literature about the acute effects of cannabinoids on memory tasks in humans is reviewed. The limitations of the human literature including issues of dose, route of administration, small sample sizes, sample selection, effects of other drug use, tolerance and dependence to cannabinoids, and the timing and sensitivity of psychological tests are discussed. Finally, the human literature is discussed against the backdrop of preclinical findings. RESULTS: Acute administration of Delta-9-THC transiently impairs immediate and delayed free recall of information presented after, but not before, drug administration in a dose- and delay-dependent manner. In particular, cannabinoids increase intrusion errors. These effects are more robust with the inhaled and intravenous route and correspond to peak drug levels. CONCLUSIONS: This profile of effects suggests that cannabinoids impair all stages of memory including encoding, consolidation, and retrieval. Several mechanisms, including effects on long-term potentiation and long-term depression and the inhibition of neurotransmitter (GABA, glutamate, acetyl choline, dopamine) release, have been implicated in the amnestic effects of cannabinoids. Future research in humans is necessary to characterize the neuroanatomical and neurochemical basis of the memory impairing effects of cannabinoids, to dissect out their effects on the various stages of memory and to bridge the expanding gap between the humans and preclinical literature.
Cannabinoid-induced working memory impairment is reversed by a second generation cholinesterase inhibitor in rats
by
Braida D, Sala M
Department of Pharmacology,
Chemotherapy and Medical Toxicology,
University of Milan, Italy.
Neuroreport 2000 Jun 26; 11(9):2025-9
ABSTRACT
Cannabinoids which impair rat working memory appear to inhibit hippocampal extracellular acetylcholine (Ach) release and reduce choline uptake through an interaction with CB1 cannabinoid receptors. Here we report that CP 55,940, a potent bicyclic synthetic cannabinoid analog, dose-dependently impaired rat performance, when given i.p. 20 min before an eight-arm radial maze test. The selective CB1 cannabinoid receptor antagonist SR 141716A, given i.p. 20 min earlier, significantly reduced the memory deficit Pretreatment with eptastigmine, a second generation cholinesterase inhibitor, given orally 100 min before the cannabinoid agonist, relieved the memory impairment without affecting CP 55,940-induced behavioural alterations such as reduced spontaneous motor activity, analgesia and hind limb splaying. These data suggest that cannabinoid-induced working memory impairment is mediated through a central cholinergic blockade.
Cellular and molecular mechanisms underlying learning
and memory impairments produced by cannabinoids
by
Sullivan JM Molecular Neurobiology Laboratory,
The Salk Institute,
La Jolla,
California 92037, USA.
janes@AXP2.Salk.edu
Learn Mem 2000 May-Jun;7(3):132-9
ABSTRACT
Why does smoking marijuana impair learning and memory? Behavioral studies suggest that a disruption of normal hippocampal function contributes to these deficits. In vitro experiments find that cannabinoid receptor activation reduces neurotransmitter release below the levels required to trigger long-term changes in synaptic strength in the hippocampus. Cannabinoids reduce glutamate release through a G-protein-mediated inhibition of the calcium channels responsible for neurotransmitter release from hippocampal neurons. These mechanisms likely play a role in the learning and memory impairments produced by cannabinoids and by endogenous cannabinoid receptor ligands.
It can enhance creativity (and have some utility in some ADHD patients) but shouldnt be called a nootropic at all.
First study says it all.
CONCLUSIONS: This profile of effects suggests that cannabinoids impair all stages of memory including encoding, consolidation, and retrieval
Edited by medievil, 01 September 2010 - 06:42 PM.