658:
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).
267:
amplifies this process. Neurotransmitters containing vesicles cluster around active sites, and after they have been released may be recycled by one of three proposed mechanisms. The first proposed mechanism involves partial opening and then re-closing of the vesicle. The second two involve the full fusion of the vesicle with the membrane, followed by recycling, or recycling into the endosome. Vesicular fusion is driven largely by the concentration of calcium in micro domains located near calcium channels, allowing for only microseconds of neurotransmitter release, while returning to normal calcium concentration takes a couple of hundred of microseconds. The vesicle exocytosis is thought to be driven by a protein complex called
197:); instead, neurons interact at close contact points called synapses. A neuron transports its information by way of an action potential. When the nerve impulse arrives at the synapse, it may cause the release of neurotransmitters, which influence another (postsynaptic) neuron. The postsynaptic neuron may receive inputs from many additional neurons, both excitatory and inhibitory. The excitatory and inhibitory influences are summed, and if the net effect is inhibitory, the neuron will be less likely to "fire" (i.e., generate an action potential), and if the net effect is excitatory, the neuron will be more likely to fire. How likely a neuron is to fire depends on how far its
275:. Once released, a neurotransmitter enters the synapse and encounters receptors. Neurotransmitter receptors can either be ionotropic or g protein coupled. Ionotropic receptors allow for ions to pass through when agonized by a ligand. The main model involves a receptor composed of multiple subunits that allow for coordination of ion preference. G protein coupled receptors, also called metabotropic receptors, when bound to by a ligand undergo conformational changes yielding in intracellular response. Termination of neurotransmitter activity is usually done by a transporter, however enzymatic deactivation is also plausible.
63:
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Neurotransmission implies both a convergence and a divergence of information. First one neuron is influenced by many others, resulting in a convergence of input. When the neuron fires, the signal is sent to many other neurons, resulting in a divergence of output. Many other neurons are influenced by
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are activated so that the net inward sodium current exceeds all outward currents. Excitatory inputs bring a neuron closer to threshold, while inhibitory inputs bring the neuron farther from threshold. An action potential is an "all-or-none" event; neurons whose membranes have not reached threshold
147:
Neurotransmission is regulated by several different factors: the availability and rate-of-synthesis of the neurotransmitter, the release of that neurotransmitter, the baseline activity of the postsynaptic cell, the number of available postsynaptic receptors for the neurotransmitter to bind to, and
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is the adding together of these impulses at the axon hillock. If the neuron only gets excitatory impulses, it will generate an action potential. If instead the neuron gets as many inhibitory as excitatory impulses, the inhibition cancels out the excitation and the nerve impulse will stop there.
266:
Neurotransmitters are spontaneously packed in vesicles and released in individual quanta-packets independently of presynaptic action potentials. This slow release is detectable and produces micro-inhibitory or micro-excitatory effects on the postsynaptic neuron. An action potential briefly
657:
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
71:
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means that the effects of impulses received at the same place can add up if the impulses are received in close temporal succession. Thus the neuron may fire when multiple impulses are received, even if each impulse on its own would not be sufficient to cause firing.
600:
Thus, it is conceivable that low levels of CB1 receptors are located on glutamatergic and GABAergic terminals impinging on DA neurons , where they can fine-tune the release of inhibitory and excitatory neurotransmitter and regulate DA neuron
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means that the effects of impulses received at different places on the neuron add up, so that the neuron may fire when such impulses are received simultaneously, even if each impulse on its own would not be sufficient to cause firing.
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Some neurons can release at least two neurotransmitters at the same time, the other being a cotransmitter, in order to provide the stabilizing negative feedback required for meaningful encoding, in the absence of inhibitory
166:. The released neurotransmitter may then move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an
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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.
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Deactivation of the neurotransmitter. The neurotransmitter is either destroyed enzymatically, or taken back into the terminal from which it came, where it can be reused, or degraded and removed.
76:
1275:
Thomas EA, Bornstein JC (2003). "Inhibitory cotransmission or after-hyperpolarizing potentials can regulate firing in recurrent networks with excitatory metabotropic transmission".
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Recent studies in a myriad of systems have shown that most, if not all, neurons release several different chemical messengers. Cotransmission allows for more complex effects at
970:
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".
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Neurons form complex biological neural networks through which nerve impulses (action potentials) travel. Neurons do not touch each other (except in the case of an
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Action potential generation is proportionate to the probability and pattern of neurotransmitter release, and to postsynaptic receptor sensitization.
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way. The binding of neurotransmitters to receptors in the postsynaptic neuron can trigger either short term changes, such as changes in the
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One unusual pair of co-transmitters is GABA and glutamate which are released from the same axon terminals of neurons originating from the
339:. To release neurotransmitters, the synaptic vesicles transiently dock and fuse at the base of specialized 10–15 nm cup-shaped
1074:"Upregulation of transmitter release probability improves a conversion of synaptic analogue signals into neuronal digital spikes"
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In modern neuroscience, neurons are often classified by their cotransmitter. For example, striatal "GABAergic neurons" utilize
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The presynaptic neuron (top) releases a neurotransmitter, which activates receptors on the nearby postsynaptic cell (bottom).
1320:"Cannabinoids inhibit noradrenergic and purinergic sympathetic cotransmission in the rat isolated mesenteric arterial bed"
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Ayakannu, Thangesweran; Taylor, Anthony H.; Marczylo, Timothy H.; Willets, Jonathon M.; Konje, Justin C. (2013).
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levels) that signal through receptors that are located on the axon terminal of the presynaptic neuron, mainly at
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1372:"Selective Brain Distribution and Distinctive Synaptic Architecture of Dual Glutamatergic-GABAergic Neurons"
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Figure 1: Schematic of brain CB1 expression and orexinergic neurons expressing OX1 (HcrtR1) or OX2 (HcrtR2)
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At the nerve terminal, neurotransmitters are present within 35–50 nm membrane-encased vesicles called
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will not fire, while those that do must fire. Once the action potential is initiated (traditionally at the
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of different signaling pathways led to the discovery of a genetic association with intracranial volume.
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83:
Ligand-gated ion channel showing the binding of transmitter (Tr) and changing of membrane potential (Vm)
1240:
Trudeau LE, Gutiérrez R (June 2007). "On cotransmission & neurotransmitter phenotype plasticity".
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877:
The
Neurobiology of Pain: Symposium of the Northern Neurobiology Group Held at Leeds on 18 April 1983
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has been solved, providing the molecular architecture and the complete composition of the machinery.
1423:"Novel genetic loci underlying human intracranial volume identified through genome-wide association"
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the subsequent removal or deactivation of the neurotransmitter by enzymes or presynaptic reuptake.
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Dh, Root; S, Zhang; Dj, Barker; J, Miranda-Barrientos; B, Liu; Hl, Wang; M, Morales (2018-06-19).
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can modify the overall response to sympathetic nerve stimulation, and indicate that prejunctional
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After its release, the transmitter binds to and activates a receptor in the postsynaptic membrane.
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Neurotransmission is genetically associated with other characteristics or features. For example,
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Adams HH, Hibar DP, Chouraki V, Stein JL, Nyquist PA, Rentería ME, et al. (December 2016).
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of another neuron (the postsynaptic neuron) a short distance away. A similar process occurs in
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Williams SM, McNamara JO, Lamantia AS, Katz LC, Fitzpatrick D, Augustine GJ, Purves D (2001).
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1015:"Quantal glutamate release is essential for reliable neuronal encodings in cerebral networks"
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Each neuron connects with numerous other neurons, receiving numerous impulses from them.
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617:"Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far"
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Storage of the neurotransmitter in storage granules or vesicles in the axon terminal.
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whereas the projections from the supramammillary nucleus are known to target the
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562:"Endocannabinoid signaling in midbrain dopamine neurons: more than physiology?"
820:"The role of spontaneous neurotransmission in synapse and circuit development"
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463:-inhibitory action. Thus cannabinoids can inhibit both the noradrenergic and
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1144:"Discovery of the 'porosome'; the universal secretory machinery in cells"
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Figure 2: Synaptic signaling mechanisms in cannabinoid and orexin systems
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98:"send, let through") is the process by which signaling molecules called
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930:(4th ed.). Amsterdam: Elsevier/Academic Press. pp. 133–181.
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726:"The Endocannabinoid System and Sex Steroid Hormone-Dependent Cancers"
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Calcium enters the axon terminal during an action potential, causing
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is the release of several types of neurotransmitters from a single
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Squire L, Berg D, Bloom FE, du Lac S, Ghosh A, Spitzer NC (2013).
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Biological neuron model § Synaptic transmission (Koch & Segev)
61:
1193:"Neuronal porosome proteome: Molecular dynamics and architecture"
1191:
Lee JS, Jeremic A, Shin L, Cho WJ, Chen X, Jena BP (July 2012).
955:. In Purves D, Augustine GJ, Fitzpatrick D, et al. (eds.).
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Synthesis of the neurotransmitter. This can take place in the
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Figure 3: Schematic of brain pathways involved in food intake
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to pass along information to yet another adjacent neuron.
110:(the presynaptic neuron), and bind to and react with the
687:"Role of endogenous cannabinoids in synaptic signaling"
42:
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co-transmitters. It is found that the endocannabinoid
1473:
Historical evolution of the neurotransmission concept
615:
Flores A, Maldonado R, Berrendero F (December 2013).
1318:Pakdeechote P, Dunn WR, Ralevic V (November 2007).
959:(2nd ed.). Sunderland, MA: Sinauer Associates.
879:(1st ed.). Manchester Univ Pr. p. 111.
251:of the neurotransmitter into the synaptic cleft.
818:Andreae, Laura C.; Burrone, Juan (March 2018).
343:structures at the presynaptic membrane called
182:, or longer term changes by the activation of
685:Freund TF, Katona I, Piomelli D (July 2003).
467:components of sympathetic neurotransmission.
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1148:Journal of Cellular and Molecular Medicine
222:Stages in neurotransmission at the synapse
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904:(5th ed.). Worth. pp. 102–104.
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159:, a neurotransmitter is released at the
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32:This is an accepted version of this page
785:Rinsho Shinkeigaku = Clinical Neurology
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126:; synthesized in response to a rise in
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1013:Yu J, Qian H, Chen N, Wang JH (2011).
730:International Journal of Endocrinology
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1072:Yu J, Qian H, Wang JH (August 2012).
902:Fundamentals of Human Neuropsychology
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59:Impulse transmission between neurons
560:Melis M, Pistis M (December 2007).
1160:10.1111/j.1582-4934.2006.tb00294.x
953:"Summation of Synaptic Potentials"
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783:Nagatsu, T. (December 2000). "".
824:Journal of Neuroscience Research
482:. The former two project to the
369:as their primary cotransmitter.
1324:British Journal of Pharmacology
916:(reference for all five stages)
416:calcitonin gene-related peptide
1:
1289:10.1016/S0306-4522(03)00039-3
409:vasoactive intestinal peptide
1389:10.1016/j.celrep.2018.05.063
1125:"PSY 340 Brain and Behavior"
1040:10.1371/journal.pone.0025219
120:retrograde neurotransmission
1209:10.1016/j.jprot.2012.05.017
900:Kolb B, Whishaw IQ (2003).
875:Holden A, Winlow W (1984).
532:Molecular neuropharmacology
404:(ACh)–glutamate co-release.
285:Summation (neurophysiology)
157:graded electrical potential
151:In response to a threshold
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703:10.1152/physrev.00004.2003
578:10.2174/157015907782793612
537:Neuromuscular transmission
527:G protein-coupled receptor
312:Convergence and divergence
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621:Frontiers in Neuroscience
566:Current Neuropharmacology
271:, that is the target for
237:, in the axon, or in the
94:"passage, crossing" from
928:Fundamental neuroscience
634:10.3389/fnins.2013.00256
476:internal globus pallidus
347:. The neuronal porosome
39:latest accepted revision
1242:Molecular Interventions
972:Journal of Cell Science
542:Neuropsychopharmacology
480:supramammillary nucleus
180:postsynaptic potentials
1493:Molecular neuroscience
1336:10.1038/sj.bjp.0707397
1091:10.1186/1756-6606-5-26
472:ventral tegmental area
356:postsynaptic receptors
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1197:Journal of Proteomics
1131:on February 19, 2006.
691:Physiological Reviews
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18:Synaptic transmission
1142:Anderson LL (2006).
490:of the hippocampus.
377:. Examples include:
102:are released by the
1427:Nature Neuroscience
1031:2011PLoSO...625219Y
743:10.1155/2013/259676
500:enrichment analyses
494:Genetic association
262:General description
203:threshold potential
29:Page version status
984:10.1242/jcs.025684
978:(Pt 17): 2951–60.
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418:(CGRP) co-release.
305:Temporal summation
199:membrane potential
191:electrical synapse
184:signaling cascades
176:membrane potential
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791:(12): 1185–1188.
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411:(VIP) co-release.
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298:Spatial summation
100:neurotransmitters
88:Neurotransmission
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512:Autoreceptor
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459:mediate the
453:WIN 55,212-2
432:
375:interneurons
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212:axon hillock
201:is from the
195:gap junction
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96:transmittere
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37:This is the
31:
1123:Hevern VW.
450:cannabinoid
442:sympathetic
427:hippocampus
398:co-release.
388:co-release.
367:substance P
341:lipoprotein
161:presynaptic
92:transmissio
1482:Categories
1084:(26): 26.
736:: 259676.
548:References
465:purinergic
421:Glutamate–
193:through a
172:excitatory
168:inhibitory
844:0360-4012
797:0009-918X
752:1687-8337
446:anadamide
423:dynorphin
396:glutamate
345:porosomes
291:Summation
279:Summation
235:cell body
135:GABAergic
116:dendrites
112:receptors
1457:27694991
1408:29924991
1354:17641668
1305:26851745
1297:12890506
1262:17609520
1227:22659300
1178:16563225
1110:22852823
1059:21949885
1019:PLOS ONE
1000:31747181
992:18697836
862:29034487
805:11464453
770:24369462
711:12843414
653:24391536
596:19305743
506:See also
484:habenula
461:sympatho
448:and the
392:Dopamine
349:proteome
164:terminal
142:synapses
90:(Latin:
43:reviewed
1448:5227112
1399:7534802
1345:2190027
1218:4580231
1169:3933105
1101:3497613
1050:3176814
1027:Bibcode
853:5813191
761:3863507
644:3868890
627:: 256.
601:firing.
587:2644494
474:(VTA),
386:glycine
249:release
178:called
131:calcium
114:on the
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478:, and
108:neuron
1301:S2CID
996:S2CID
269:SNARE
106:of a
1453:PMID
1404:PMID
1350:PMID
1293:PMID
1258:PMID
1223:PMID
1174:PMID
1106:PMID
1055:PMID
988:PMID
932:ISBN
906:ISBN
881:ISBN
858:PMID
840:ISSN
801:PMID
793:ISSN
766:PMID
748:ISSN
734:2013
707:PMID
649:PMID
592:PMID
440:are
436:and
414:ACh–
407:ACh–
382:GABA
137:and
1443:PMC
1435:doi
1394:PMC
1384:doi
1340:PMC
1332:doi
1328:152
1285:doi
1281:120
1250:doi
1213:PMC
1205:doi
1164:PMC
1156:doi
1096:PMC
1086:doi
1045:PMC
1035:doi
980:doi
976:121
848:PMC
832:doi
756:PMC
738:doi
699:doi
639:PMC
629:doi
582:PMC
574:doi
438:ATP
365:or
170:or
155:or
45:on
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