Referências para a pesquisa com Juliana

Potential role of the cannabinoid receptor CB1 in rapid eye movement sleep rebound.
Navarro L, Martínez-vargas M, Murillo-rodríguez E, Landa A, Méndez-díaz M, Prospéro-garcía O. Neuroscience. 2003;120(3):855-9.

[Cannabinoid receptor 1 expression and pathological changes in rat hippocampus after deprivation of rapid eye movement sleep]
[Article in Chinese]
Jiang PF, Zhu T, Xia ZZ. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2006 Sep;35(5):535-40.

Sleep modulates cannabinoid receptor 1 expression in the pons of rats.
Martínez-Vargas M, Murillo-Rodríguez E, González-Rivera R, Landa A, Méndez-Díaz M, Prospro-García O, Navarro L. Neuroscience. 2003;117(1):197-201.

Oleamide modulates memory in rats.
Murillo-Rodríguez E, Giordano M, Cabeza R, Henriksen SJ, Méndez Díaz M, Navarro L, Prospéro-García O. Neurosci Lett. 2001 Nov 2;313(1-2):61-4.
Grupo de Neurociencias, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, A Postal 70-250 Mexico, D. F. 04510, Mexico.

Oleamide is a recently described lipid, obtained from the cerebrospinal fluid of sleep-deprived cats. It has been observed that oleamide possesses several biological effects, such as sleep induction, and immunological suppression as well as serotonin and gamma-aminobutyric acid receptors activation. In addition, oleamide also binds to the cannabinoid receptors. In this study, we have observed that oleamide facilitates memory extinction in a passive avoidance paradigm, reduces core temperature and pain perception, but does not affect significantly locomotion. These results suggest that oleamide modulates memory processes. However, we do not know if oleamide impairs the retrieval of the memory associated to the "not go" behavior, or facilitates the fast re-learning of the "go" behavior. In addition, since these effects are also induced by marijuana and anandamide, it is very likely that oleamide may be affecting the cerebral cannabinoid system to induce its effects.

Short-term memory is modulated by the spontaneous release of endocannabinoids: evidence from hippocampal population codes.
Deadwyler SA, Goonawardena AV, Hampson RE. Behav Pharmacol. 2007 Sep;18(5-6):571-80.

Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157-1083, USA. sdeadwy@wfubmc.edu
Population codes derived from ensembles of hippocampal neurons were assessed to determine whether endocannabinoids were active when rats performed a delayed-nonmatch-to-sample (DNMS) short-term memory task. Multivariate discriminant analyses of the firing patterns of ensembles of CA1 and CA3 hippocampal neurons extracted representations of information encoded at the time of the sample response (SmR codes) during individual DNMS trials. The 'strength' or distinctiveness of trial-specific SmR codes in normal sessions was compared with sessions in which either rimonabant, the well-characterized cannabinoid CB1 receptor antagonist, or WIN 55212-2 (WIN-2), a cannabinoid CB1 receptor agonist, were administered. Results show that performance on trials with delay intervals longer than 10 s was facilitated by rimonabant (2.0 mg/kg) owing to a significantly increased frequency of trials with stronger SmR codes. In contrast, WIN-2 (0.35 mg/kg) suppressed the strength of SmR codes necessary to perform trials with delays greater than 10 s. The positive influence of rimonabant on performance indicated that the action of endocannabinoids was to reduce SmR code strength, resulting in trials that were at risk for errors if the delay exceeded 10 s. Thus endocannabinoids, like exogenously administered cannabinoids, reduced hippocampal encoding necessary to perform long-delay trials. The findings therefore indicate a direct relationship between the actions of endocannabinoids on hippocampal processes and the ability to encode information into short-term memory.

Endocannabinoid signaling and synaptic plasticity in the brain.
Zhu PJ. Crit Rev Neurobiol. 2006;18(1-2):113-24.

Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health and National Chemical Genomics Center, National Human Genome Research Institute, Bethesda, MD, USA. pzhu@mail.nih.gov
Repetitive firing neuron or activation of synaptic transmission plays an important role in the modulation of synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). These activity-dependent changes in synaptic efficacy are thought to be critical to learning and memory; however, the underlying mechanisms remain to be defined. Endogenous cannabinoids (eCBs) are diffusible modulators that are released from depolarized postsynaptic neurons and act on presynaptic terminals. Persistent release of eCBs can lead to long-term modulation of synaptic plasticity in the brain. Given a broad distribution of eCB receptors in the brain, the eCB signaling system could contribute to use-dependent modification of brain functions.

Effects of intra-amygdala infusion of CB1 receptor agonists on the reconsolidation of fear-potentiated startle.
Lin HC, Mao SC, Gean PW. Learn Mem. 2006 May-Jun;13(3):316-21. Epub 2006 May 16.
Institute of Basic Medical Sciences and Department of Pharmacology, National Cheng-Kung University, Tainan, Taiwan. bailu@mail.nih.gov

The cannabinoid CB1 receptor has been shown to be critically involved in the extinction of fear memory. Systemic injection of a CB1 receptor antagonist prior to extinction training blocked extinction. Conversely, administration of the cannabinoid uptake inhibitor AM404 facilitated extinction in a dose-dependent manner. Here we show that bilateral infusion of CB1 receptor agonists into the amygdala after memory reactivation blocked reconsolidation of fear memory measured with fear-potentiated startle. The effect was dose-dependent and could be blocked by AM251, a specific CB1 receptor antagonist. In contrast, the effect of CB1 agonists on reconsolidation was no longer seen if memory reactivation was omitted. Concomitant with block of reconsolidation, CB1 agonist-treated animals did not exhibit shock-induced reinstatement or spontaneous recovery of fear. The absence of recovery was not attributable to permanent damage to the amygdala in WIN-treated rats, nor did the effect result from alteration of baseline startle or shock reactivity. These results suggest that CB1 agonists could impair fear memory via blocking reconsolidation.

Se eu tivesse conhecimento dessas referências (especialmente a última) o paper com meu irmão ficaria bem mais fortalecido... Vamos ver a nova versão com a Juliana...