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Originally Posted by Cannabinoid mechanisms in the hippocampus and effects on memory

One of the well established effects of acute intoxication with cannabis in man is an impairment of short-term memory (the extensive literature on human studies is reviewed by Jones, 1978Go; Miller and Branconnier, 1983Go; Solowij, 1998Go; Earleywine, 2002Go). Many studies have shown significant effects on short-term memory, particularly when tests were used that depend heavily on attention (Abel, 1971Go; Mendelson et al., 1976Go). Animal studies have also found that THC, synthetic cannabinoids and anandamide cause deficits in short-term memory in spatial learning tasks (for a review see Hampson and Deadwyler, 1999Go). These include delayed matching or non-matching tests in rodents (Mallet and Beninger, 1998Go; Hampson and Deadwyler, 1999Go), performance in a radial arm maze (Stiglick and Kalant, 1985Go; Lichtman and Martin, 1996Go), and a fixed ratio food acquisition task in squirrel monkeys (Nakamura-Palacios et al., 2000Go). The effects of both cannabinoids (Lichtman and Martin, 1996Go) and anandamide (Mallet and Beninger, 1998Go) were reversed by rimonabant, indicating that they are mediated by the CB1 receptor.

A probable site for these effects is the hippocampus. Hampson and Deadwyler (1999)Go claimed that the effects of the treatment of rats with cannabinoids on short-term memory in a delayed non-matching to sample test were equivalent to the effects seen after surgical removal of the hippocampus. In each case the animals were unable to segregate information between trials in the task because of disruptions to the processing of sensory information in hippocampal circuits. CB1 receptors are expressed at high densities in the hippocampus. They are particularly abundant on the terminals of a sub-set of GABAergic basket cell interneurons, which also contain the neuropeptide cholecystokinin (Katona et al., 1999Go), and this is also the case in human hippocampus (Katona et al., 2000Go). These are presumably the GABAergic neurons involved in the endocannabinoid-mediated DSI phenomenon described above. The terminals of these cells surround large pyramidal neuron somata in the CA1–CA4 fields. GABAergic neurons in the dentate gyrus also express CB1 receptors, with terminals concentrated at the boundary of the molecular and granule cell layers (Egertová and Elphick, 2000Go). In addition CB1 receptors are expressed, at a lower level, in the glutamatergic pyramidal cells and their terminals. Cannabinoids can thus inhibit both the release of GABA and glutamate in hippocampal circuits.

The mechanisms underlying synaptic plasticity have been studied more intensely in the hippocampus than in any other brain region. In particular, the electrophysiological phenomena of long-term potentiation (LTP) and long-term depression (LTD) are thought to be involved in memory formation at glutamatergic synapses in the hippocampus. A number of studies have shown clearly that cannabinoids inhibit the induction of both LTP and LTD (for review see Elphick and Egertová, 2001Go). Cannabinoids appear to work by reducing glutamate release below the level needed to activate NMDA receptors, a requirement for LTP and LTD (Shen et al., 1996Go; Misner and Sullivan, 1999Go). Although the actions of cannabinoids in reducing GABA release from hippocampal interneurons might have been expected to increase the level of excitability of hippocampal pyramidal cells, it seems that the cannabinoid-induced reduction in glutamate release predominates. The administration of exogenous cannabinoids is, of course, wholly unphysiological and cannot mimic the effects of endocabinnoids that are released in discrete local regions in response to particular patterns of afferent inputs. CB1 receptors are capable of regulating both inhibitory and excitatory neurotransmitter release in the hippocampus and are thus capable of subtle control of synaptic plasticity. The CB1-containing GABergic interneurons are thought to control oscillatory electrical activity in the hippocampus in the theta and gamma frequencies, which plays a role in synchronizing pyramidal cell activity (Hoffman and Lupica, 2000Go). CB1 agonists decrease the power of such oscillations in hippocampal slices (Hájos et al., 2000Go) and may thus influence the synchronous activity of pyramidal cells. The physiological importance of cannabinoid-mediated DSI may be to decrease GABAergic inhibition of these cells and thus facilitate learning when hippocampal inputs are active (Wilson and Nicoll, 2001Go).

One approach to answering the question of what role the tonic release of endocannabinoids may play in hippocampal function has been to examine the effects of CB1 receptor knockout or of selective CB1 receptor antagonists. Un fortunately, these studies have so far yielded conflicting results. Bohme et al. (2000)Go reported a significant enhancement of LTP in CB1 knockout mice, and Reibaud et al. (1999)Go found a significant enhancement of memory in such animals. However, tests with the CB1 antagonist rimonabant showed no effects on LTP (Terranova et al., 1995Go) or on learning and memory in a spatial learning task (Mallet and Beninger, 1998Go), although Terranova et al. (1996Go) reported that rimonabant enhanced memory in a short-term olfactory memory test in rats (social recognition test).

Originally Posted by imported_squeek

Is a short period of time considered the next day? Or even sooner? Could you just perhaps sleep it off?