Adenosine is released during thalamic oscillations to provide negative feedback control

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dc.cclicenceCC-BY-NC-NDen
dc.contributor.authorWall, Mark J
dc.contributor.authorPuddefoot, Katie
dc.contributor.authorYin, Wencheng
dc.contributor.authorBingham, Chris
dc.contributor.authorSeifi, Mohsen
dc.contributor.authorSwinny, Jerome D
dc.contributor.authorNgomba, Richard Teke
dc.date.acceptance2023-06-23
dc.date.accessioned2022-07-13T09:49:52Z
dc.date.available2022-07-13T09:49:52Z
dc.date.issued2022-07-01
dc.descriptionThe file attached to this record is the author's final peer reviewed version. The Publisher's final version can be found by following the DOI link.en
dc.description.abstractPhysiological oscillations in the cortico-thalamo-cortical loop occur during processes such as sleep, but these can become dysfunctional in pathological conditions such as absence epilepsy. The purine neuromodulator adenosine can act as an endogenous anticonvulsant: it is released into the extracellular space during convulsive seizures to activate A1 receptors suppressing on-going activity and delaying the occurrence of the next seizure. However, the role of adenosine in thalamic physi- ological and epileptiform oscillations is less clear. Here we have combined immunohistochemistry, electrophysiology, and fixed potential amperometry (FPA) biosensor measurements to characterise the release and actions of adenosine in thalamic oscillations measured in rodent slices. In the thalamus, A1 receptors are highly expressed particularly in the ventral basal (VB) thalamus and reticular thalamic nucleus (nRT) supporting a role for adenosine signalling in controlling oscillations. In agreement with previous studies, both adenosine and adenosine A1 receptor agonists inhibited thalamic oscillations in control (spindle-like) and in epileptic conditions. Here we have shown for the first time that both control and epileptiform oscillations are enhanced (i.e., increased number of oscillatory cycles) by blocking A1 receptors consistent with adenosine release occurring during oscillations. Although increases in extracellular adenosine could not be directly detected during control oscillations, clear increases in adenosine concentration could be detected with a biosensor during epileptiform oscillation activity. Thus, adenosine is released during thalamic oscillations and acts via A1 receptors to feedback and reduce thalamic oscillatory activity.en
dc.funderOther external funder (please detail below)en
dc.funder.otherERUK pilot granten
dc.identifier.citationWall, M.J., Puddefoot, K., Yin, W., Bingham, C., Seifi, M., Swinny, J.D. and Ngomba, R.T. (2022) Adenosine is released during thalamic oscillations to provide negative feedback control. Neuropharmacology, 216, 109172en
dc.identifier.doihttps://doi.org/10.1016/j.neuropharm.2022.109172
dc.identifier.urihttps://hdl.handle.net/2086/22054
dc.language.isoenen
dc.peerreviewedYesen
dc.projectidPGE 1720en
dc.publisherElsevieren
dc.researchinstituteLeicester Institute for Pharmaceutical Innovation - From Molecules to Practice (LIPI)en
dc.titleAdenosine is released during thalamic oscillations to provide negative feedback controlen
dc.typeArticleen

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