A three-enzyme microelectrode sensor for detecting purine release from central nervous system

Llaudet, Enrique; Botting, Nigel P.; Crayston, Joe A.; Dale, Nicholas

doi:10.1016/s0956-5663(02)00106-9

Cited by 137 publications

(169 citation statements)

References 20 publications

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“…Since epileptiform activity is followed by an increase in extracellular levels of adenosine ), we tested whether DHPG-induced bursting was associated with adenosine release by utilising enzyme-based microelectrode adenosine biosensors (Frenguelli et al, 2003;Llaudet et al, 2003). Adenosine release was detected from both areas CA1 and CA3 of hippocampal slices following challenge with DHPG: 0.74 ± 0.22 µM' (n = 6) for area CA1 (data not shown) and 2.2 ± 0.8 µM' (n = 6) for area CA3 ( Figure 1C).…”

Section: Activation Of Group I Metabotropic Glutamate Receptors Inducmentioning

confidence: 99%

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

2015

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The activation of Group I metabotropic glutamate receptors (GI mGluRs) in the hippocampus results in the appearance of persistent bursts of synchronised neuronal activity. Such activity is known to cause the release of the purines ATP and its neuroactive metabolite, adenosine.We have investigated the role of the purines in GI mGluR-induced oscillations in hippocampal areas CA3 and CA1 using pharmacological techniques and microelectrode biosensors for ATP and adenosine. The GI mGluR agonist DHPG induced both persistent oscillations in neuronal activity and the release of adenosine in areas CA1 and CA3. In contrast, the DHPG-induced release of ATP was only observed in area CA3. Whilst adenosine acting at adenosine A 1 receptors suppressed DHPG-induced burst activity, the activation of mGlu5 and P2Y 1 ATP receptors were necessary for the induction of DHPG-induced oscillations. Selective inhibition of pannexin-1 hemichannels with a low concentration of carbenoxolone (10 µM) or probenecid (1 mM) did not affect adenosine release in area CA3, but prevented both ATP release in area CA3 and DHPG-induced bursting. These data reveal key aspects of GI mGluR-dependent neuronal activity that are subject to bidirectional regulation by ATP and adenosine in the initiation and pacing of burst firing, respectively, and which have implications for the role of GI mGluRs in seizure activity and neurodevelopmental disorders.

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Section: Activation Of Group I Metabotropic Glutamate Receptors Inducmentioning

confidence: 99%

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

2015

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“…This ATP electrode was instrumental in demonstrating recently that ATP is an important central sensory transmitter in the medulla oblongata, stimulating breathing after elevation of peripheral pCO 2 [4]. Interestingly, in a very similar fashion, the same group has also produced an adenosine electrode [51]. This has the potential of recording the ATP breakdown product adenosine and detecting the temporospatial formation of ATP and adenosine in native tissues [51].…”

Section: The Amperometric Atp Biosensor Microelectrodementioning

confidence: 99%

“…Interestingly, in a very similar fashion, the same group has also produced an adenosine electrode [51]. This has the potential of recording the ATP breakdown product adenosine and detecting the temporospatial formation of ATP and adenosine in native tissues [51]. Adaptation of the ATP electrode to micromanipulator scanning devices or even an atomic force microscope cantilever is under technical development and may evolve into an electrode-based ATP imaging method applicable to physiological preparations [52,53].…”

Section: The Amperometric Atp Biosensor Microelectrodementioning

confidence: 99%

ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

205

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All cells release nucleotides and are in one way or another involved in local autocrine and paracrine regulation of organ function via stimulation of purinergic receptors. Significant technical advances have been made in recent years to quantify more precisely resting and stimulated adenosine triphosphate (ATP) concentrations in close proximity to the plasma membrane. These technical advances are reviewed here. However, the mechanisms by which cells release ATP continue to be enigmatic. The current state of knowledge on different suggested mechanisms is also reviewed. Current evidence suggests that two separate regulated modes of ATP release co-exist in nonexcitable cells: (1) a conductive pore which in several systems has been found to be the channel pannexin 1 and (2) vesicular release. Modes of stimulation of ATP release are reviewed and indicate that both subtle mechanical stimulation and agonist-triggered release play pivotal roles. The mechano-sensor for ATP release is not yet defined.

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“…Our particular approach has been to develop microelectrode biosensors for the purines [35,36]. While there are many ways biosensors can operate (indeed luciferase, patch sniffing, and recombinant receptors are all biosensing approaches for the detection of purines), we have developed electrochemical biosensors based around oxidases to provide a real-time signal for both ATP and adenosine and downstream purines.…”

Section: Microelectrode Biosensorsmentioning

confidence: 99%

“…For adenosine, we use a cascade of three enzymes: adenosine deaminase, nucleoside phosphorylase and xanthine oxidase (Fig. 1c) to produce an electrochemical signal proportional to adenosine concentration [35].…”

Section: Microelectrode Biosensorsmentioning

confidence: 99%

Measurement of purine release with microelectrode biosensors

Dale

Frenguelli

2011

Purinergic Signalling

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Purinergic signalling departs from traditional paradigms of neurotransmission in the variety of release mechanisms and routes of production of extracellular ATP and adenosine. Direct real-time measurements of these purinergic agents have been of great value in understanding the functional roles of this signalling system in a number of diverse contexts. Here, we review the methods for measuring purine release, introduce the concept of microelectrode biosensors for ATP and adenosine and explain how these have been used to provide new mechanistic insight in respiratory chemoreception, synaptic physiology, eye development and purine salvage. We finish by considering the association of purine release with pathological conditions and examine the possibilities that biosensors for purines may one day be a standard part of the clinical diagnostic tool chest.Keywords Biosensor . Real-time measurement . Epilepsy . Stroke . Chemosensory mechanisms . DevelopmentThe need for real-time purine measurementThe traditional paradigm of synaptic transmission involves exocytotic release of transmitter from a defined presynaptic structure into the narrow gap of the synaptic cleft where it diffuses to activate receptors on the closely apposed postsynaptic membrane. Release is time-locked to the presynaptic action potential and results in the predictable occurrence of postsynaptic events on defined time scales. While capturing the essence of synaptic transmission, this paradigm is an oversimplification. For example, transmitters such as GABA [1] and glutamate [2] can spill out of the synaptic cleft to have more diffuse and widespread actions than this classical model suggests. Under pathological conditions, transmitters and neurotransmitters, such as glutamate [3], can be released by the reversal of Na + -dependent concentrative transporters.The purines, ATP and adenosine, depart from this paradigm even more comprehensively. ATP can indeed be released at synapses [4,5]. However, in the CNS, it seems that it acts mainly as a cotransmitter [6,7], and there are very few synapses where it acts as the principal transmitter. ATP is also released by glial cells [8,9] for the most part via exocytosis [10,11] but see [12]. However, ATP can also be released via a variety of channel-mediated mechanisms (for example, via gap junction hemichannels [13][14][15] and volume-activated channels [16,17]). Receptors for ATP are widespread throughout the CNS; yet, the cellular sources of ATP release to activate these receptors are not immediately obvious. In addition, although ATP can be broken down to ADP and further to adenosine, these breakdown products are themselves active at particular receptor subtypes.The routes for adenosine release and the cellular sources seem to be even more mysterious than those for ATP. For example, there is abundant evidence that adenosine can arise from the breakdown of previously released ATP [18].

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A three-enzyme microelectrode sensor for detecting purine release from central nervous system

Cited by 137 publications

References 20 publications

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

ATP release from non-excitable cells

Measurement of purine release with microelectrode biosensors

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