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'''Retrograde Signaling''' in biology is the process where a signal travels backwards from a target source to its original source. For example, the [[Cell nucleus|nucleus]] of a cell is the original source for creating signaling proteins. During retrograde signaling, instead of signals leaving the nucleus, they are sent to the nucleus. In [[cell biology]], this type of signaling typically occurs between the [[Mitochondrion|mitochondria]] or [[chloroplast]] and the nucleus. Signaling molecules from the mitochondria or chloroplast act on the nucleus to affect nuclear gene expression. In this regard, the chloroplast or mitochondria act as a a sensor for internal external stimuli which activate a signaling pathway<ref name=":4" />.
'''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 [[organelle]]s. A typical example in plants is retrograde signaling from the [[plastid]] to control [[cell nucleus|nuclear]] [[gene expression]].<ref name=Lagarias2013>{{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 }}</ref>


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 [[perikaryon|cell body]], and travels "backwards" across a [[chemical synapse]] to bind to the [[axon terminal]] of a presynaptic [[neuron]].<ref name="Regehr 2009">{{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}}</ref>
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 [[perikaryon|cell body]], and travels "backwards" across a [[chemical synapse]] to bind to the [[axon terminal]] of a presynaptic [[neuron]].<ref name="Regehr 2009">{{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}}</ref>


==In cell biology==
==In cell biology==
Retrograde signals are transmitted from [[plastid]]s to the nucleus in plants and [[eukaryotes|eukaryotic]] algae,<ref name=Lagarias2013/><ref>{{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}}</ref> and from [[mitochondria]] to the nucleus in most eukaryotes.<ref>{{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}}</ref> Retrograde signals are generally considered to convey intracellular signals related to stress and environmental sensing.<ref>Nott, Ajit, et al. "Plastid-to-nucleus retrograde signaling." Annu. Rev. Plant Biol. 57 (2006): 739–759
Retrograde signals are transmitted from [[plastid]]s to the nucleus in plants and [[eukaryotes|eukaryotic]] algae,<ref name="Lagarias2013">{{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|date=26 Feb 2013|title=Retrograde bilin signaling enables Chlamydomonas greening and phototrophic survival.|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=110|issue=9|pages=3621–3626|doi=10.1073/pnas.1222375110|pmc=3587268|pmid=23345435}}</ref><ref name=":4">{{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}}</ref> and from [[mitochondria]] to the nucleus in most eukaryotes.<ref>{{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}}</ref> Retrograde signals are generally considered to convey intracellular signals related to stress and environmental sensing<ref>Nott, Ajit, et al. "Plastid-to-nucleus retrograde signaling." Annu. Rev. Plant Biol. 57 (2006): 739–759
</ref>. Retrograde signals are generally considered to convey intracellular signals related to stress and environmental sensing. Many of the molecules associated with retrograde signaling act on modifying the [[Transcription (biology)|transcription]] or by directly binding and acting as a [[transcription factor]]. The outcomes of these signaling pathways vary by [[organism]] and by stimuli or stress<ref name="Lagarias2013" />.
</ref>

=== Evolution ===
Retrograde signaling is believe to have arisen after [[endocytosis]] of the mitochondria and chloroplast billions of years ago<ref>{{Citation|last=Bevan|first=Rachel B.|title=Mitochondrial genome evolution: the origin of mitochondria and of eukaryotes|date=2004|url=http://dx.doi.org/10.1007/b96830|work=Mitochondrial Function and Biogenesis|pages=1–35|publisher=Springer Berlin Heidelberg|isbn=978-3-540-21489-2|access-date=2019-11-21|last2=Lang|first2=B. Franz}}</ref>. Originally believed to be photosynthetic bacteria, the mitochondria and chloroplast transferred some of their DNA to the membrane protected nucleus<ref>{{Cite journal|last=da Cunha|first=Fernanda Marques|last2=Torelli|first2=Nicole Quesada|last3=Kowaltowski|first3=Alicia J.|date=2015|title=Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes|url=http://dx.doi.org/10.1155/2015/482582|journal=Oxidative Medicine and Cellular Longevity|volume=2015|pages=1–10|doi=10.1155/2015/482582|issn=1942-0900}}</ref>. Thus, some of the proteins required for the mitochondria or chloroplast are within the nucleus. This transfer of DNA further required a network of communication to properly respond to external and internal signals and produce requisite proteins<ref>{{Cite journal|last=Whelan|first=Sean P.|last2=Zuckerbraun|first2=Brian S.|date=2013|title=Mitochondrial Signaling: Forwards, Backwards, and In Between|url=http://dx.doi.org/10.1155/2013/351613|journal=Oxidative Medicine and Cellular Longevity|volume=2013|pages=1–10|doi=10.1155/2013/351613|issn=1942-0900}}</ref>.

=== In Yeast ===
The first retrograde signaling pathways discovered in [[yeast]] is the RTG pathway<ref>{{Cite journal|last=Parikh|first=V.|last2=Morgan|first2=M.|last3=Scott|first3=R|last4=Clements|first4=L.|last5=Butow|first5=R.|date=1987-01-30|title=The mitochondrial genotype can influence nuclear gene expression in yeast|url=http://dx.doi.org/10.1126/science.3027892|journal=Science|volume=235|issue=4788|pages=576–580|doi=10.1126/science.3027892|issn=0036-8075}}</ref><ref name=":02">{{Cite journal|last=Liu|first=Z.|date=2001-12-17|title=RTG-dependent mitochondria to nucleus signaling is negatively regulated by the seven WD-repeat protein Lst8p|url=http://dx.doi.org/10.1093/emboj/20.24.7209|journal=The EMBO Journal|volume=20|issue=24|pages=7209–7219|doi=10.1093/emboj/20.24.7209|issn=1460-2075}}</ref>. The RTG pathway plays an important role in maintain the metabolic homeostasis of yeast<ref name=":02" />. Under limited resources the mitochondria must maintain a balance of [[Glutamic acid|glutamate]] for the [[Citric acid cycle]]<ref>{{Cite journal|last=Jazwinski|first=S. Michal|last2=Kriete|first2=Andres|date=2012|title=The Yeast Retrograde Response as a Model of Intracellular Signaling of Mitochondrial Dysfunction|url=http://dx.doi.org/10.3389/fphys.2012.00139|journal=Frontiers in Physiology|volume=3|doi=10.3389/fphys.2012.00139|issn=1664-042X}}</ref>. Retrograde signaling form the mitochondria initiates production precursor molecules of glutamate to properly balance supplies within the mitochondria<ref name=":12">{{Cite journal|last=Liu|first=Zhengchang|last2=Butow|first2=Ronald A.|date=1999-10-01|title=A Transcriptional Switch in the Expression of Yeast Tricarboxylic Acid Cycle Genes in Response to a Reduction or Loss of Respiratory Function|url=https://mcb.asm.org/content/19/10/6720|journal=Molecular and Cellular Biology|language=en|volume=19|issue=10|pages=6720–6728|doi=10.1128/MCB.19.10.6720|issn=0270-7306|pmid=10490611}}</ref>. Retrograde signaling can also act to arrest growth if problems are encountered. In ''[[Saccharomyces cerevisiae]],'' if the mitochondria fails to develop properly, they will stop growing until the issue is addressed or cell death is induced<ref name=":12" />. These mechanism are vital to maintain homeostasis of the cell and ensure proper function of the mitochondria<ref name=":12" />.

=== In Plants ===
One of the most studied retrograde signaling molecules in plants are [[reactive oxygen species]] (ROS) <ref>{{Cite journal|last=Maruta|first=Takanori|last2=Noshi|first2=Masahiro|last3=Tanouchi|first3=Aoi|last4=Tamoi|first4=Masahiro|last5=Yabuta|first5=Yukinori|last6=Yoshimura|first6=Kazuya|last7=Ishikawa|first7=Takahiro|last8=Shigeoka|first8=Shigeru|date=2012-02-09|title=H2O2-triggered Retrograde Signaling from Chloroplasts to Nucleus Plays Specific Role in Response to Stress|url=http://dx.doi.org/10.1074/jbc.m111.292847|journal=Journal of Biological Chemistry|volume=287|issue=15|pages=11717–11729|doi=10.1074/jbc.m111.292847|issn=0021-9258}}</ref>. These compounds, previously believed to be damaging to the cell, have since been discovered to act as a signaling molecule<ref name=":22">{{Cite journal|last=Schieber|first=Michael|last2=Chandel|first2=Navdeep S.|date=2014-05|title=ROS Function in Redox Signaling and Oxidative Stress|url=http://dx.doi.org/10.1016/j.cub.2014.03.034|journal=Current Biology|volume=24|issue=10|pages=R453–R462|doi=10.1016/j.cub.2014.03.034|issn=0960-9822}}</ref>. Reactive oxygen species are created as a by-product of aerobic respiration and act on genes involved in the stress response<ref name=":22" />. Depending on the stress, reactive oxygen species can act on neighboring cells to initiate a local signal<ref name=":3">{{Cite journal|last=Shapiguzov|first=Alexey|last2=Vainonen|first2=Julia P.|last3=Wrzaczek|first3=Michael|last4=Kangasjärvi|first4=Jaakko|date=2012|title=ROS-talk – how the apoplast, the chloroplast, and the nucleus get the message through|url=http://dx.doi.org/10.3389/fpls.2012.00292|journal=Frontiers in Plant Science|volume=3|doi=10.3389/fpls.2012.00292|issn=1664-462X}}</ref>. By doing this, surrounding cells are "primed" to react to the stress because genes involved in stress response are initiated prior to encountering the stress<ref name=":3" />. The chloroplast can also act as a sensor for pathogen response and drought. Detection of these stresses in the cell will induce the formation of compounds that can then act on the nucleus to produce pathogen resistance genes or drought tolerance<ref>{{Cite journal|last=Estavillo|first=Gonzalo M.|last2=Chan|first2=Kai Xun|last3=Phua|first3=Su Yin|last4=Pogson|first4=Barry J.|date=2013|title=Reconsidering the nature and mode of action of metabolite retrograde signals from the chloroplast|url=http://dx.doi.org/10.3389/fpls.2012.00300|journal=Frontiers in Plant Science|volume=3|doi=10.3389/fpls.2012.00300|issn=1664-462X}}</ref>. 


==In neuroscience==
==In neuroscience==

Revision as of 01:29, 21 November 2019

Retrograde Signaling in biology is the process where a signal travels backwards from a target source to its original source. For example, the nucleus of a cell is the original source for creating signaling proteins. During retrograde signaling, instead of signals leaving the nucleus, they are sent to the nucleus. In cell biology, this type of signaling typically occurs between the mitochondria or chloroplast and the nucleus. Signaling molecules from the mitochondria or chloroplast act on the nucleus to affect nuclear gene expression. In this regard, the chloroplast or mitochondria act as a a sensor for internal external stimuli which activate a signaling pathway[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

Retrograde signals are transmitted from plastids to the nucleus in plants and eukaryotic algae,[3][1] and from mitochondria to the nucleus in most eukaryotes.[4] Retrograde signals are generally considered to convey intracellular signals related to stress and environmental sensing[5]. Retrograde signals are generally considered to convey intracellular signals related to stress and environmental sensing. Many of the molecules associated with retrograde signaling act on modifying the transcription or by directly binding and acting as a transcription factor. The outcomes of these signaling pathways vary by organism and by stimuli or stress[3].

Evolution

Retrograde signaling is believe to have arisen after endocytosis of the mitochondria and chloroplast billions of years ago[6]. Originally believed to be photosynthetic bacteria, the mitochondria and chloroplast transferred some of their DNA to the membrane protected nucleus[7]. Thus, some of the proteins required for the mitochondria or chloroplast are within the nucleus. This transfer of DNA further required a network of communication to properly respond to external and internal signals and produce requisite proteins[8].

In Yeast

The first retrograde signaling pathways discovered in yeast is the RTG pathway[9][10]. The RTG pathway plays an important role in maintain the metabolic homeostasis of yeast[10]. Under limited resources the mitochondria must maintain a balance of glutamate for the Citric acid cycle[11]. Retrograde signaling form the mitochondria initiates production precursor molecules of glutamate to properly balance supplies within the mitochondria[12]. Retrograde signaling can also act to arrest growth if problems are encountered. In Saccharomyces cerevisiae, if the mitochondria fails to develop properly, they will stop growing until the issue is addressed or cell death is induced[12]. These mechanism are vital to maintain homeostasis of the cell and ensure proper function of the mitochondria[12].

In Plants

One of the most studied retrograde signaling molecules in plants are reactive oxygen species (ROS) [13]. These compounds, previously believed to be damaging to the cell, have since been discovered to act as a signaling molecule[14]. Reactive oxygen species are created as a by-product of aerobic respiration and act on genes involved in the stress response[14]. Depending on the stress, reactive oxygen species can act on neighboring cells to initiate a local signal[15]. By doing this, surrounding cells are "primed" to react to the stress because genes involved in stress response are initiated prior to encountering the stress[15]. The chloroplast can also act as a sensor for pathogen response and drought. Detection of these stresses in the cell will induce the formation of compounds that can then act on the nucleus to produce pathogen resistance genes or drought tolerance[16]. 

In neuroscience

The 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,[17][18][19] as is nitric oxide.[20][21]

Retrograde signaling may also play a role in long-term potentiation, a proposed mechanism of learning and memory, although this is controversial.[22][23][24]

Formal definition of a retrograde neurotransmitter

In 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]

  • The appropriate machinery for synthesizing and releasing the retrograde messenger must be located in the postsynaptic neuron
  • Disrupting the synthesis and/or release of the messenger from the postsynaptic neuron must prevent retrograde signaling
  • The appropriate targets for the retrograde messenger must be located in the presynaptic bouton
  • Disrupting the targets for the retrograde messenger in the presynaptic boutons must eliminate retrograde signaling
  • Exposing the presynaptic bouton to the messenger should mimic retrograde signaling provided the presence of the retrograde messenger is sufficient for retrograde signaling to occur
  • In cases where the retrograde messenger is not sufficient, pairing the other factor(s) with the retrograde signal should mimic the phenomenon

Types of retrograde neurotransmitters

The most prevalent endogenous retrograde neurotransmitters are nitric oxide[20][21] and various cannabinoids.

Retrograde signaling in long-term potentiation

Main article: 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.[25]

Background

Long-term potentiation is the persistent increase in the strength of a chemical synapse that lasts from hours to days.[26] It is thought to occur via two temporally separated events, with induction occurring first, followed by expression.[26] Most LTP investigators agree that induction is entirely postsynaptic, whereas there is disagreement as to whether expression is principally a presynaptic or postsynaptic event.[23] Some researchers believe that both presynaptic and postsynaptic mechanisms play a role in LTP expression.[23]

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.[22]

Mechanism

The 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.[27][28] 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.[29]

Identity of the messenger

Of 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,[30] platelet-activating factor,[31][32] arachidonic acid,[33] 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.[29] The endocannabinoids anandamide and/or 2-AG, acting through G-protein coupled cannabinoid receptors, may play an important role in retrograde signaling in LTP.[17][18]

References

  1. ^ a b Nott, Ajit; Jung, Hou-Sung; Koussevitzky, Shai; Chory, Joanne (June 2006). "Plastid-to-nucleus retrograde signaling". Annual Review of Plant Biology. 57: 739–759. doi:10.1146/annurev.arplant.57.032905.105310. PMID 16669780.
  2. ^ a b c Regehr, Wade G.; Carey, Megan R.; Best, Aaron R. (30 July 2009). "Activity-Dependent Regulation of Synapses by Retrograde Messengers". Neuron. 63 (2): 154–170. doi:10.1016/j.neuron.2009.06.021. PMC 3251517. PMID 19640475.
  3. ^ a b Lagarias JC, Duanmu D; Casero D; Dent RM; Gallaher S; Yang W; Rockwell NC; Martin SS; Pellegrini M; Niyogi KK; Merchant SS; Grossman AR (26 Feb 2013). "Retrograde bilin signaling enables Chlamydomonas greening and phototrophic survival". Proceedings of the National Academy of Sciences of the United States of America. 110 (9): 3621–3626. doi:10.1073/pnas.1222375110. PMC 3587268. PMID 23345435.
  4. ^ Liu, Zhengchang; Butow, Ronald A. (December 2006). "Mitochondrial retrograde signaling". Annual Review of Genetics. 40: 159–185. doi:10.1146/annurev.genet.40.110405.090613. PMID 16771627.
  5. ^ Nott, Ajit, et al. "Plastid-to-nucleus retrograde signaling." Annu. Rev. Plant Biol. 57 (2006): 739–759
  6. ^ Bevan, Rachel B.; Lang, B. Franz (2004), "Mitochondrial genome evolution: the origin of mitochondria and of eukaryotes", Mitochondrial Function and Biogenesis, Springer Berlin Heidelberg, pp. 1–35, ISBN 978-3-540-21489-2, retrieved 2019-11-21
  7. ^ da Cunha, Fernanda Marques; Torelli, Nicole Quesada; Kowaltowski, Alicia J. (2015). "Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes". Oxidative Medicine and Cellular Longevity. 2015: 1–10. doi:10.1155/2015/482582. ISSN 1942-0900.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  8. ^ Whelan, Sean P.; Zuckerbraun, Brian S. (2013). "Mitochondrial Signaling: Forwards, Backwards, and In Between". Oxidative Medicine and Cellular Longevity. 2013: 1–10. doi:10.1155/2013/351613. ISSN 1942-0900.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ Parikh, V.; Morgan, M.; Scott, R; Clements, L.; Butow, R. (1987-01-30). "The mitochondrial genotype can influence nuclear gene expression in yeast". Science. 235 (4788): 576–580. doi:10.1126/science.3027892. ISSN 0036-8075.
  10. ^ a b Liu, Z. (2001-12-17). "RTG-dependent mitochondria to nucleus signaling is negatively regulated by the seven WD-repeat protein Lst8p". The EMBO Journal. 20 (24): 7209–7219. doi:10.1093/emboj/20.24.7209. ISSN 1460-2075.
  11. ^ Jazwinski, S. Michal; Kriete, Andres (2012). "The Yeast Retrograde Response as a Model of Intracellular Signaling of Mitochondrial Dysfunction". Frontiers in Physiology. 3. doi:10.3389/fphys.2012.00139. ISSN 1664-042X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ a b c Liu, Zhengchang; Butow, Ronald A. (1999-10-01). "A Transcriptional Switch in the Expression of Yeast Tricarboxylic Acid Cycle Genes in Response to a Reduction or Loss of Respiratory Function". Molecular and Cellular Biology. 19 (10): 6720–6728. doi:10.1128/MCB.19.10.6720. ISSN 0270-7306. PMID 10490611.
  13. ^ Maruta, Takanori; Noshi, Masahiro; Tanouchi, Aoi; Tamoi, Masahiro; Yabuta, Yukinori; Yoshimura, Kazuya; Ishikawa, Takahiro; Shigeoka, Shigeru (2012-02-09). "H2O2-triggered Retrograde Signaling from Chloroplasts to Nucleus Plays Specific Role in Response to Stress". Journal of Biological Chemistry. 287 (15): 11717–11729. doi:10.1074/jbc.m111.292847. ISSN 0021-9258.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ a b Schieber, Michael; Chandel, Navdeep S. (2014-05). "ROS Function in Redox Signaling and Oxidative Stress". Current Biology. 24 (10): R453–R462. doi:10.1016/j.cub.2014.03.034. ISSN 0960-9822. {{cite journal}}: Check date values in: |date= (help); no-break space character in |first2= at position 8 (help)
  15. ^ a b Shapiguzov, Alexey; Vainonen, Julia P.; Wrzaczek, Michael; Kangasjärvi, Jaakko (2012). "ROS-talk – how the apoplast, the chloroplast, and the nucleus get the message through". Frontiers in Plant Science. 3. doi:10.3389/fpls.2012.00292. ISSN 1664-462X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  16. ^ Estavillo, Gonzalo M.; Chan, Kai Xun; Phua, Su Yin; Pogson, Barry J. (2013). "Reconsidering the nature and mode of action of metabolite retrograde signals from the chloroplast". Frontiers in Plant Science. 3. doi:10.3389/fpls.2012.00300. ISSN 1664-462X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ a b Alger BE (2002). "Retrograde signaling in the regulation of synaptic transmission: focus on endocannabinoids". Prog. Neurobiol. 68 (4): 247–86. doi:10.1016/S0301-0082(02)00080-1. PMID 12498988.
  18. ^ a b Wilson RI, Nicoll RA (2001). "Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses". Nature. 410 (6828): 588–92. doi:10.1038/35069076. PMID 11279497.
  19. ^ Kreitzer, A.; Regehr, W. G. (2002). "Retrograde signaling by endocannabinoids". Current Opinion in Neurobiology. 12 (3): 324–330. doi:10.1016/S0959-4388(02)00328-8. PMID 12049940.
  20. ^ a b O'Dell, TJ; Hawkins, RD; Kandel, ER; Arancio, O (Dec 15, 1991). "Tests of the roles of two diffusible substances in long-term potentiation: evidence for nitric oxide as a possible early retrograde messenger". Proceedings of the National Academy of Sciences of the United States of America. 88 (24): 11285–9. doi:10.1073/pnas.88.24.11285. PMC 53119. PMID 1684863.
  21. ^ a b Malen, PL; Chapman, PF (Apr 1, 1997). "Nitric oxide facilitates long-term potentiation, but not long-term depression". The Journal of Neuroscience. 17 (7): 2645–51. doi:10.1523/JNEUROSCI.17-07-02645.1997. PMID 9065524.
  22. ^ a b Regehr, Wade G.; Carey, Megan R.; Best, Aaron R. (2009-07). "Activity-Dependent Regulation of Synapses by Retrograde Messengers". Neuron. 63 (2): 154–170. doi:10.1016/j.neuron.2009.06.021. ISSN 0896-6273. {{cite journal}}: Check date values in: |date= (help)
  23. ^ a b c Nicoll, Roger A.; Malenka, Robert C. (1995-09). "Contrasting properties of two forms of long-term potentiation in the hippocampus". Nature. 377 (6545): 115–118. doi:10.1038/377115a0. ISSN 0028-0836. {{cite journal}}: Check date values in: |date= (help)
  24. ^ Abraham, Wickliffe C.; Jones, Owen D.; Glanzman, David L. (2019-12). "Is plasticity of synapses the mechanism of long-term memory storage?". npj Science of Learning. 4 (1): 9. doi:10.1038/s41539-019-0048-y. ISSN 2056-7936. PMC 6606636. PMID 31285847. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
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