| 词条 | Retrograde signaling |
| 释义 |
Retrograde signaling in biology is a process whereby the function of one part of a cell is controlled by feedback from another part of the cell, or where one cell sends reciprocal messages back to another cell that regulates it. In cell biology, retrograde signaling occurs between different subcellular organelles. A typical example in plants is retrograde signaling from the plastid to control nuclear gene expression.[1] In neuroscience, retrograde signaling (or retrograde neurotransmission) refers more specifically to the process by which a retrograde messenger, such as anandamide or nitric oxide, is released by a postsynaptic dendrite or cell body, and travels "backwards" across a chemical synapse to bind to the axon terminal of a presynaptic neuron.[2] In cell biology{{Expand section|date=May 2014}}Retrograde signalling can go from plastids to the nucleus in plants,[1][3] or from mitochondria to the nucleus in yeast.[4] In neuroscienceThe primary purpose of retrograde neurotransmission is regulation of chemical neurotransmission.[2] For this reason, retrograde neurotransmission allows neural circuits to create feedback loops. In the sense that retrograde neurotransmission mainly serves to regulate typical, anterograde neurotransmission, rather than to actually distribute any information, it is similar to electrical neurotransmission. In contrast to conventional (anterograde) neurotransmitters, retrograde neurotransmitters are synthesized in the postsynaptic neuron, and bind to receptors on the axon terminal of the presynaptic neuron. Endocannabinoids like anandamide are known to act as retrograde messengers,[5][6][7] as is nitric oxide.[8][9]Retrograde signaling may also play a role in long-term potentiation, a proposed mechanism of learning and memory, although this is controversial. Formal definition of a retrograde neurotransmitterIn 2009, Regehr et al. proposed criteria for defining retrograde neurotransmitters. According to their work, a signaling molecule can be considered a retrograde neurotransmitter if it satisfies all of the following criteria:[2]
Types of retrograde neurotransmittersThe most prevalent endogenous retrograde neurotransmitters are nitric oxide and various cannabinoids. Retrograde signaling in long-term potentiation{{main|Long-term potentiation}}As it pertains to long-term potentiation (LTP), retrograde signaling is a hypothesis describing how events underlying LTP may begin in the postsynaptic neuron but be propagated to the presynaptic neuron, even though normal communication across a chemical synapse occurs in a presynaptic to postsynaptic direction. It is used most commonly by those who argue that presynaptic neurons contribute significantly to the expression of LTP. BackgroundLong-term potentiation is the persistent increase in the strength of a chemical synapse that lasts from hours to days. It is thought to occur via two temporally separated events, with induction occurring first, followed by expression. Most LTP investigators agree that induction is entirely postsynaptic, whereas there is disagreement as to whether expression is principally a presynaptic or postsynaptic event. Some researchers believe that both presynaptic and postsynaptic mechanisms play a role in LTP expression. Were LTP entirely induced and expressed postsynaptically, there would be no need for the postsynaptic cell to communicate with the presynaptic cell following LTP induction. However, postsynaptic induction combined with presynaptic expression requires that, following induction, the postsynaptic cell must communicate with the presynaptic cell. Because normal synaptic transmission occurs in a presynaptic to postsynaptic direction, postsynaptic to presynaptic communication is considered a form of retrograde transmission. MechanismThe retrograde signaling hypothesis proposes that during the early stages of LTP expression, the postsynaptic cell "sends a message" to the presynaptic cell to notify it that an LTP-inducing stimulus has been received postsynaptically. The general hypothesis of retrograde signaling does not propose a precise mechanism by which this message is sent and received. One mechanism may be that the postsynaptic cell synthesizes and releases a retrograde messenger upon receipt of LTP-inducing stimulation.[10][11] Another is that it releases a preformed retrograde messenger upon such activation. Yet another mechanism is that synapse-spanning proteins may be altered by LTP-inducing stimuli in the postsynaptic cell, and that changes in conformation of these proteins propagates this information across the synapse and to the presynaptic cell.[12] Identity of the messengerOf these mechanisms, the retrograde messenger hypothesis has received the most attention. Among proponents of the model, there is disagreement over the identity of the retrograde messenger. A flurry of work in the early 1990s to demonstrate the existence of a retrograde messenger and to determine its identity generated a list of candidates including carbon monoxide,[13] platelet-activating factor,[14][15] arachidonic acid,[16] and nitric oxide. Nitric oxide has received a great deal of attention in the past, but has recently been superseded by adhesion proteins that span the synaptic cleft to join the presynaptic and postsynaptic cells.[12] The endocannabinoids anandamide and/or 2-AG, acting through G-protein coupled cannabinoid receptors, may play an important role in retrograde signaling in LTP.[5][6] References1. ^1 {{cite journal|last=Lagarias JC|first=Duanmu D |author2=Casero D |author3=Dent RM |author4=Gallaher S |author5=Yang W |author6=Rockwell NC |author7=Martin SS |author8=Pellegrini M |author9=Niyogi KK |author10=Merchant SS |author11=Grossman AR|title=Retrograde bilin signaling enables Chlamydomonas greening and phototrophic survival.|journal=Proceedings of the National Academy of Sciences of the United States of America|date=26 Feb 2013|volume=110|issue=9|pages=3621–3626|doi=10.1073/pnas.1222375110|pmid=23345435 | pmc=3587268 }} 2. ^1 2 {{cite journal|last=Regehr|first=Wade G.|author2=Carey, Megan R. |author3=Best, Aaron R. |title=Activity-Dependent Regulation of Synapses by Retrograde Messengers|journal=Neuron|date=30 July 2009|volume=63|issue=2|pages=154–170|doi=10.1016/j.neuron.2009.06.021|pmid=19640475|pmc=3251517}} 3. ^{{Cite journal|title=Plastid-to-nucleus retrograde signaling|first1=Ajit|last1=Nott|first2=Hou-Sung|last2=Jung|first3=Shai|last3=Koussevitzky|first4=Joanne|last4=Chory|journal=Annual Review of Plant Biology|date=June 2006|volume=57|pages=739–759|doi=10.1146/annurev.arplant.57.032905.105310|pmid = 16669780}} 4. ^{{Cite journal|title=Mitochondrial retrograde signaling|first1=Zhengchang|last1=Liu|first2=Ronald A.|last2=Butow|journal=Annual Review of Genetics|date=December 2006|volume=40|pages=159–185|doi=10.1146/annurev.genet.40.110405.090613|pmid = 16771627}} 5. ^1 {{cite journal |author=Alger BE |title=Retrograde signaling in the regulation of synaptic transmission: focus on endocannabinoids |journal=Prog. Neurobiol. |volume=68 |issue=4 |pages=247–86 |year=2002 |pmid=12498988 |doi=10.1016/S0301-0082(02)00080-1}} 6. ^1 {{cite journal |vauthors=Wilson RI, Nicoll RA |title=Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses |journal=Nature |volume=410 |issue=6828 |pages=588–92 |year=2001 |pmid=11279497 |doi=10.1038/35069076}} 7. ^{{Cite journal | last1 = Kreitzer | first1 = A. | last2 = Regehr | first2 = W. G. | title = Retrograde signaling by endocannabinoids | doi = 10.1016/S0959-4388(02)00328-8 | journal = Current Opinion in Neurobiology | volume = 12 | issue = 3 | pages = 324–330 | year = 2002 | pmid = 12049940| pmc = }} 8. ^{{cite journal|last=O'Dell|first=TJ|author2=Hawkins, RD |author3=Kandel, ER |author4= Arancio, O |title=Tests of the roles of two diffusible substances in long-term potentiation: evidence for nitric oxide as a possible early retrograde messenger.|journal=Proceedings of the National Academy of Sciences of the United States of America|date=Dec 15, 1991|volume=88|issue=24|pages=11285–9|doi=10.1073/pnas.88.24.11285|pmid=1684863 |pmc=53119}} 9. ^{{cite journal|last=Malen|first=PL|author2=Chapman, PF |title=Nitric oxide facilitates long-term potentiation, but not long-term depression.|journal=The Journal of Neuroscience|date=Apr 1, 1997|volume=17|issue=7|pages=2645–51|pmid=9065524|doi=10.1523/JNEUROSCI.17-07-02645.1997}} 10. ^{{cite journal|last=Garthwaite|first=J|title=Glutamate, nitric oxide and cell-cell signalling in the nervous system.|journal=Trends in Neurosciences|date=Feb 1991|volume=14|issue=2|pages=60–7|doi=10.1016/0166-2236(91)90022-M|pmid=1708538}} 11. ^{{cite journal|last=Lei|first=S|author2=Jackson, MF |author3=Jia, Z |author4=Roder, J |author5=Bai, D |author6=Orser, BA |author7= MacDonald, JF |title=Cyclic GMP-dependent feedback inhibition of AMPA receptors is independent of PKG.|journal=Nature Neuroscience|date=Jun 2000|volume=3|issue=6|pages=559–65|doi=10.1038/75729|pmid=10816311}} 12. ^1 {{cite journal |vauthors=Malenka R, Bear M |title=LTP and LTD: an embarrassment of riches |journal=Neuron |volume=44 |issue=1 |pages=5–21 |year=2004|pmid=15450156 |doi=10.1016/j.neuron.2004.09.012}} 13. ^{{cite journal |vauthors=Alkadhi K, Al-Hijailan R, Malik K, Hogan Y |title=Retrograde carbon monoxide is required for induction of long-term potentiation in rat superior cervical ganglion |journal=J Neurosci |volume=21 |issue=10 |pages=3515–20 |year=2001 |pmid=11331380|doi=10.1523/JNEUROSCI.21-10-03515.2001 }} 14. ^{{cite journal |vauthors=Kato K, Zorumski C |title=Platelet-activating factor as a potential retrograde messenger |journal=J Lipid Mediat Cell Signal |volume=14 |issue=1–3 |pages=341–8 |year=1996 |pmid=8906580 |doi=10.1016/0929-7855(96)00543-3}} 15. ^{{cite journal |vauthors=Kato K, Clark G, Bazan N, Zorumski C |title=Platelet-activating factor as a potential retrograde messenger in CA1 hippocampal long-term potentiation |journal=Nature |volume=367 |issue=6459 |pages=175–9 |year=1994 |pmid=8114914 |doi=10.1038/367175a0}} 16. ^{{cite journal|last=Carta|first=Mario|title=Membrane Lipids Tune Synaptic Transmission by Direct Modulation of Presynaptic Potassium Channels|journal=Neuron|year=2014|doi=10.1016/j.neuron.2013.12.028|volume=81|issue=4|pages=787–799|pmid=24486086}} 2 : Cell signaling|Neurophysiology |
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