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((more citations needed|date=November 2012))
((Infobox medical condition (new)
| name            = <!--((PAGENAME)) by default-->
| synonym         = 
| image           = File:Excitotoxicity Animation Speed 2.gif
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| caption         = A common cause of synaptopathy is glutamate [[excitotoxicity]]. As shown in the animation, the over-activation of [[NMDA|NMDA receptors]] leads to an increase in free intracellular calcium, which produces oxygen free-radicals and eventually neuronal dysfunction.<ref>((cite journal |last1= Mark |first1= Leighton P |last2= Prost |first2= Robert W |last3= Ulmer |first3= John L |last4= Smith |first4= Michelle M |last5= Daniels |first5= David L |last6= Strottmann |first6= James M |last7= Brown |first7=W Douglas |last8= Hacein-Bey |first8= Lotfi |date=November 2001 |title=Pictorial Review of glutamate excitotoxicity: fundamental concepts for neuroimaging |url=http://www.ajnr.org/content/22/10/1813 |journal=American Journal of Neuroradiology |volume=22 |issue=10 |pages=1813–1824 |pmid=11733308|pmc= 7973850 ))</ref>
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))

A '''synaptopathy''' is a disease of the [[brain]], [[spinal cord]] or [[peripheral nervous system]] relating to the dysfunction of [[synapses]]. This can arise as a result of a mutation in a gene encoding a synaptic protein such as an [[ion channel]], [[neurotransmitter receptor]], or a protein involved in [[neurotransmitter release]]. It can also arise as a result of an [[autoantibody]] targeting a synaptic protein. Synaptopathies caused by [[ion channel]] mutations are also known as synaptic [[channelopathies]]. An example is [[episodic ataxia]]. [[Myasthenia gravis]] is an example of an [[autoimmune]] synaptopathy. Some toxins also affect synaptic function. [[Tetanus toxin]] and [[botulinum toxin]] affect neurotransmitter release. Tetanus toxin can enter the body via a wound, and botulinum toxin can be  ingested or administered therapeutically to alleviate [[dystonia]] or as cosmetic treatment.

Another example of synaptopathy occurs in the auditory system. This cochlear synaptopathy has been seen after prolonged noise exposure in both primate and non-primate models.<ref>((cite journal |last1= Valero |first1= MD |last2= Burton |first2= JA |last3= Hauser |first3= SN |last4= Hackett |first4= TA |last5= Ramachandran |first5= R |last6= Liberman |first6=MC |date=September 2017 |title=Noise-induced cochlear synaptopathy in rhesus monkeys (Macaca mulatta) |journal=Hearing Research |volume=353 |pages= 213–223 |doi=10.1016/j.heares.2017.07.003 |pmid= 28712672|pmc= 5632522 ))</ref><ref>((cite journal |last1= Ruel |first1= Jérôme |last2= Wang |first2= Jing |last3= Rebillard |first3= Guy |last4= Eybalin |first4= Michel |last5= Lloyd |first5= Ruth |last6= Pujol |first6= Rémy |last7= Puel |first7= Jean-Luc |date=May 2007 |title=Physiology, pharmacology and plasticity at the inner hair cell synaptic complex |journal=Hearing Research |volume=227 |issue=1–2 |pages=19–27 |doi=10.1016/j.heares.2006.08.017 |pmid=17079104|s2cid= 21778893 ))</ref> Two possible reasons for this neuronal death are both glutamate-mediated [[excitotoxicity]] in the postsynaptic terminal, and presynaptic ribbon damage which occurs by an unknown mechanism.<ref>((cite journal |last1= Pujol |first1= Rémy |last2= Puel |first2= Jean‐Luc |date=November 1999|title=Excitotoxicity, synaptic repair, and functional recovery in the mammalian cochlea: a review of recent findings |journal=Annals of the New York Academy of Sciences |volume=884 |issue=1 |pages= 249–254 |doi=10.1111/j.1749-6632.1999.tb08646.x |pmid=10842598|bibcode= 1999NYASA.884..249P |s2cid= 25371542 |doi-access=free ))</ref>

Synaptopathies are attracting research interest because they provide an insight into fundamental mechanisms of [[synaptic transmission]] and because an improved understanding of disease mechanisms may lead to new treatments.

Some diseases of unknown etiology have been proposed to be synaptopathies. Examples include [[autism spectrum disorder]]<ref>((cite journal |last1=Wang |first1=Xinxing |last2=Kery |first2=Rachel |last3=Xiong |first3=Qiaojie |title=Synaptopathology in autism spectrum disorders: Complex effects of synaptic genes on neural circuits |journal=Progress in Neuro-Psychopharmacology and Biological Psychiatry |volume=84 |issue=Pt B |date=June 2018 |pages=398–415 |issn=0278-5846 |doi=10.1016/j.pnpbp.2017.09.026 |pmid= 28986278|s2cid=207411792 ))</ref> and [[schizophrenia]].<ref>((cite journal |last1=Hayashi-Takagi |first1=Akiko |title=Synapse pathology and translational applications for schizophrenia |journal=Neuroscience Research |volume=114 |date=January 2017 |pages=3–8 |doi=10.1016/j.neures.2016.09.001 |pmid= 27633835|s2cid=1806948 |doi-access=free ))</ref> Synaptic dysfunction can also occur in [[neurodegenerative]] disorders such as [[Alzheimer's disease|Alzheimer's]].<ref>((cite journal |last1=Jha |first1=Saurabh Kumar |last2=Jha |first2=Niraj Kumar |last3=Kumar |first3=Dhiraj |last4=Sharma |first4=Renu |last5=Shrivastava |first5=Abhishek |last6=Ambasta |first6=Rashmi K. |last7=Kumar |first7=Pravir |title=Stress-induced synaptic dysfunction and neurotransmitter release in Alzheimer's Disease: Can neurotransmitters and neuromodulators be potential therapeutic targets? |journal=Journal of Alzheimer's Disease |volume=57 |issue=4 |year=2017 |pages=1017–1039 |doi=10.3233/JAD-160623 |pmid=27662312))</ref> Immune-mediated cerebellar ataxias represent a group of disorders causing cerebellar ataxia induced by a dysfunction of synapses.<ref>((cite journal |last1=Mitoma |first1=H. |last2=Honnorat |first2=J. |last3=Yamaguchi |first3=K.|last4=Manto |first4=M.|title=Fundamental Mechanisms of Autoantibody-Induced Impairments on Ion Channels and Synapses in Immune-Mediated Cerebellar Ataxias|journal=Int J Mol Sci |volume=21 |date=2020 |issue=14 |pages=E4936 |doi=10.3390/ijms21144936|pmc=7404345  |pmid= 32668612|doi-access=free ))</ref> Increasing knowledge of the genetic basis of these diseases has linked proteins to the function of the synapse.  Age-related cochlear synaptic and neural degeneration has also been demonstrated in mice.<ref>((cite journal |last1=Sergeyenko |first1=Yevgeniya |last2=Lall |first2= Kumud |last3= Liberman |first3= M Charles |last4=Kujawa |first4=Sharon G |date=21 August 2013 |title=Age-related cochlear synaptopathy: an early-onset contributor to auditory functional decline |journal=The Journal of Neuroscience |volume=33 |issue=34 |pages=13686–13694 |doi=10.1523/JNEUROSCI.1783-13.2013 |pmc=3755715 |pmid=23966690))</ref>

Molecules such as [[FMR1|FMRP1]] act as translational repressor thus when ablated such as in [[fragile X syndrome|FXS]] result in varying degrees of cellular and behavioural abnormalities. Additional molecules thought to be involved include SynGAP and [[SHANK1]].<ref>((cite journal |last1=Brose |first1=Nils |last2=O'Connor |first2=Vincent |last3=Skehel |first3=Paul |date=April 2010 |title=Synaptopathy: dysfunction of synaptic function? |journal=Biochemical Society Transactions |volume=38 |issue=2 |pages=443–4 |doi=10.1042/bst0380443 |pmid=20298199))</ref>

==References==
((Reflist))

== External links ==
* https://www.ucl.ac.uk/ion/synaptopathies

[[Category:Neurological disorders]]

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