Guided by the older work from humans, research into the behavioural effects of cannabinoids concentrated on the disruption of working and short-term memory formation. This is in agreement with data suggesting marijuana-induced increases in CBF in paralimbic regions of the frontal lobes and the cerebellum, but reduced blood flow in the temporal lobe (O'Leary et al. 2002). Hypoactivity in the temporal lobe may constitute the neural basis of cognitive alterations seen in cannabis users and has prompted the search for the underlying mechanisms using behavioural paradigms that specifically activate the medial temporal lobe, or using electro-physiological recording protocols in medial temporal lobe structures. It is also in line with reductions of the cortical P300 amplitude in marijuana addicts. The P300 is an ERP reflecting attentional resource allocation and active working memory (Johnson et al. 1997). Similarly, monkeys treated with A9THC chronically have predominantly slow-wave EEGs (1-2 Hz) in hippocampus, amygdala and septum (Stadnicki et al. 1974) and present with similar deficits as human subjects (Aiger 1988; Branch et al. 1980; Evans and Wenger 1992; Gluck et al. 1973; Nakamura-Palacios et al. 2000; Schulze et al. 1988; Winsauer et al. 1999). Increased sophistication in pharmacological and physiological techniques applicable to rodents has now considerably increased our understanding of cannabinoid mechanisms in different types of memory, suggesting a modulatory role of cannabinoids and cannabinoid receptors in encoding, memory consolidation and even forgetting.
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