另见
Autoreceptor
Biological neuron model § Synaptic transmission
Electrophysiology
G protein-coupled receptor
Molecular neuropharmacology
Neuromuscular transmission
Neuropsychopharmacology
参考
Melis M, Pistis M (December 2007). "Endocannabinoid signaling in midbrain dopamine neurons: more than physiology?". Current Neuropharmacology. 5 (4): 268–77. 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.
Flores A, Maldonado R, Berrendero F (December 2013). "Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far". Frontiers in Neuroscience. 7: 256. 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).
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
Freund TF, Katona I, Piomelli D (July 2003). "Role of endogenous cannabinoids in synaptic signaling". Physiological Reviews. 83 (3): 1017–66. doi:10.1152/physrev.00004.2003. PMID 12843414.
Reggio PH (2010). "Endocannabinoid binding to the cannabinoid receptors: what is known and what remains unknown". Current Medicinal Chemistry. 17 (14): 1468–86. PMC 4120766. PMID 20166921.
Holden A, Winlow W (1984). The Neurobiology of Pain: Symposium of the Northern Neurobiology Group Held at Leeds on 18 April 1983 (1st ed.). Manchester Univ Pr. p. 111. ISBN 0719010616.
Kolb B, Whishaw IQ (2003). Fundamentals of Human Neuropsychology (5th ed.). Worth. pp. 102–104. ISBN 978-0-7167-5300-1. (reference for all five stages)
Squire L, Berg D, Bloom FE, du Lac S, Ghosh A, Spitzer NC (2013). Fundamental neuroscience (4th ed.). Amsterdam: Elsevier/Academic Press. pp. 133–181. ISBN 978-0-12-385870-2.
Purves D, Augustine GJ, Fitzpatrick D, et al., eds. (2001). Summation of Synaptic Potentials. Neuroscience (2nd ed.). Sunderland (MA): Sinauer Associates.
Wang JH, Wei J, Chen X, Yu J, Chen N, Shi J (September 2008). "Gain and fidelity of transmission patterns at cortical excitatory unitary synapses improve spike encoding". Journal of Cell Science. 121 (Pt 17): 2951–60. doi:10.1242/jcs.025684. PMID 18697836.
Yu J, Qian H, Chen N, Wang JH (2011). "Quantal glutamate release is essential for reliable neuronal encodings in cerebral networks". PLOS One. 6 (9): e25219. doi:10.1371/journal.pone.0025219. PMC 3176814. PMID 21949885.
Yu J, Qian H, Wang JH (August 2012). "Upregulation of transmitter release probability improves a conversion of synaptic analogue signals into neuronal digital spikes". Molecular Brain. 5 (26): 26. doi:10.1186/1756-6606-5-26. PMC 3497613. PMID 22852823.
Hevern VW. "PSY 340 Brain and Behavior". Archived from the original on February 19, 2006.
Anderson LL (2006). "Discovery of the 'porosome'; the universal secretory machinery in cells". Journal of Cellular and Molecular Medicine. 10 (1): 126–31. doi:10.1111/j.1582-4934.2006.tb00294.x. PMID 16563225.
Lee JS, Jeremic A, Shin L, Cho WJ, Chen X, Jena BP (July 2012). "Neuronal porosome proteome: Molecular dynamics and architecture". Journal of Proteomics. 75 (13): 3952–62. doi:10.1016/j.jprot.2012.05.017. PMC 4580231. PMID 22659300.
Trudeau LE, Gutiérrez R (June 2007). "On cotransmission & neurotransmitter phenotype plasticity". Molecular Interventions. 7 (3): 138–46. doi:10.1124/mi.7.3.5. PMID 17609520.
Thomas EA, Bornstein JC (2003). "Inhibitory cotransmission or after-hyperpolarizing potentials can regulate firing in recurrent networks with excitatory metabotropic transmission". Neuroscience. 120 (2): 333–51. doi:10.1016/S0306-4522(03)00039-3. PMID 12890506.
Pakdeechote P, Dunn WR, Ralevic V (November 2007). "Cannabinoids inhibit noradrenergic and purinergic sympathetic cotransmission in the rat isolated mesenteric arterial bed". British Journal of Pharmacology. 152 (5): 725–33. doi:10.1038/sj.bjp.0707397. PMC 2190027. PMID 17641668.
Adams HH, Hibar DP, Chouraki V, Stein JL, Nyquist PA, Rentería ME, et al. (December 2016). "Novel genetic loci underlying human intracranial volume identified through genome-wide association". Nature Neuroscience. 19 (12): 1569–1582. doi:10.1038/nn.4398. PMC 5227112. PMID 27694991.