نقل عصبي
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↑  "Endocannabinoid signaling in midbrain dopamine neurons: more than physiology?". Current Neuropharmacology. ج. 5 ع. 4: 268–77. ديسمبر 2007. DOI:10.2174/157015907782793612. PMC:2644494. PMID:19305743. Thus, it is conceivable that low levels of CB1 receptors are located on glutamatergic and GABAergic terminals impinging on DA neurons [127, 214], where they can fine-tune the release of inhibitory and excitatory neurotransmitter and regulate DA neuron firing.
Consistently, in vitro electrophysiological experiments from independent laboratories have provided evidence of CB1 receptor localization on glutamatergic and GABAergic axon terminals in the VTA and SNc.
↑  "Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far". Frontiers in Neuroscience. ج. 7: 256. ديسمبر 2013. DOI:10.3389/fnins.2013.00256. PMC:3868890. PMID:24391536. Direct CB1-HcrtR1 interaction was first proposed in 2003 (Hilairet et al., 2003). Indeed, a 100-fold increase in the potency of hypocretin-1 to activate the ERK signaling was observed when CB1 and HcrtR1 were co-expressed ...  In this study, a higher potency of hypocretin-1 to regulate CB1-HcrtR1 heteromer compared with the HcrtR1-HcrtR1 homomer was reported (Ward et al., 2011b). These data provide unambiguous identification of CB1-HcrtR1 heteromerization, which has a substantial functional impact. ... The existence of a cross-talk between the hypocretinergic and endocannabinoid systems is strongly supported by their partially overlapping anatomical distribution and common role in several physiological and pathological processes. However, little is known about the mechanisms underlying this interaction. ... Acting as a retrograde messenger, endocannabinoids modulate the glutamatergic excitatory and GABAergic inhibitory synaptic inputs into the dopaminergic neurons of the VTA and the glutamate transmission in the NAc. Thus, the activation of CB1 receptors present on axon terminals of GABAergic neurons in the VTA inhibits GABA transmission, removing this inhibitory input on dopaminergic neurons (Riegel and Lupica, 2004). Glutamate synaptic transmission in the VTA and NAc, mainly from neurons of the PFC, is similarly modulated by the activation of CB1 receptors (Melis et al., 2004).{{استشهاد بدورية محكمة}}:  صيانة الاستشهاد: دوي مجاني غير معلم (link)

 · Figure 1: Schematic of brain CB1 expression and orexinergic neurons expressing OX1 (HcrtR1) or OX2 (HcrtR2)

 · Figure 2: Synaptic signaling mechanisms in cannabinoid and orexin systems

 · Figure 3: Schematic of brain pathways involved in food intake
↑  "Role of endogenous cannabinoids in synaptic signaling". Physiological Reviews. ج. 83 ع. 3: 1017–66. يوليو 2003. DOI:10.1152/physrev.00004.2003. PMID:12843414.
↑  Holden، Arun؛ Winlow، William (1984). The Neurobiology of Pain: Symposium of the Northern Neurobiology Group Held at Leeds on 18 April 1983 (ط. 1st). Manchester Univ Pr. ص. 111. ISBN:978-0719010613. {{استشهاد بكتاب}}: الوسيط غير المعروف |name-list-format= تم تجاهله يقترح استخدام |name-list-style= (مساعدة)
↑  Kolb، Bryan؛ Whishaw، Ian Q. (2003). Fundamentals of Human Neuropsychology (ط. 5th). Worth. ص. 102–104. ISBN:978-0-7167-5300-1. {{استشهاد بكتاب}}: الوسيط غير المعروف |name-list-format= تم تجاهله يقترح استخدام |name-list-style= (مساعدة) (reference for all five stages)
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