Possible functional role of diadenosine polyphosphates: Negative feedback for excitation in hippocampus
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The role of dinucleoside polyphosphates on the ocular surface and other eye structures
2016, Progress in Retinal and Eye ResearchCitation Excerpt :Moreover, it was possible to demonstrate that these dinucleotides were releasable in a Ca2+ dependent manner from brain synaptic terminals (Pintor et al., 1991, 1992) and also by the effect of drugs such as amphetamines (Pintor et al., 1993). The role of diadenosine polyphosphates, mainly Ap4A and Ap5A in the nervous system has been the modulation of the release of monoamines (Giraldez et al., 2001), glutamate (Gualix et al., 2003), or the inhibition of synaptic transmission in the hippocampus (Klishin et al., 1994). Extracellular actions of dinucleoside polyphosphates occurred by means of receptors on the cell surface termed P2 purinergic receptors.
Highly sensitive, selective and rapid LC-MS method for simultaneous quantification of diadenosine polyphosphates in human plasma
2014, Journal of Chromatography B: Analytical Technologies in the Biomedical and Life SciencesCitation Excerpt :Diadenosine polyphosphates (ApnAs) are endogenous mediators, isolated from e.g. blood platelets [1,2], adrenal medullary chromaffin granules [3,4], the central nervous system [4,5] and human plasma [6].
Dinucleoside polyphosphates in the eye: from physiology to therapeutics
2007, Progress in Retinal and Eye ResearchCharacterisation of ATP-induced facilitation of transmission in rat hippocampus
2000, European Journal of PharmacologyDiadenosine polyphosphates facilitate the evoked release of acetylcholine from rat hippocampal nerve terminals
2000, Brain ResearchCitation Excerpt :Thus, it is likely that the repetitive stimulation of nerve terminals may lead to a localised synaptic extracellular accumulation of ApnA similar to that estimated for adenine nucleotides (7–25 μM) [3,25]. In different systems, ApnA may activate ApnA receptors [15,16,19,21,22], some P2 receptor subtypes [20,26], or be extracellularly metabolised into adenosine [11], and activate adenosine receptors [14]. The facilitation by Ap5A of ACh release was strongly inhibited by Ip5I, a ApnA receptor antagonist [21], and only slightly attenuated by the P2 receptor antagonists, suramin and PPADS [23].