TY  - JOUR
A1  - Burnstock, G
JF  - Brazilian Journal of Medical and Biological Research
SN  - 0100-879X
UR  - http://www.scielo.br/scielo.php?script=sci_serial&pid=0100-879X&lng=en&nrm=iso
N1  - This work is published under a Creative Commons Attribution License (CC-BY). The authors retain ownership of the copyright for their article and can allow anyone to download, reuse, reprint, modify, distribute, and/or copy articles published in the BJMBR, as long as the original authors and source are cited. No permission is required from the authors or the publishers.
IS  - 1
SP  - 3
VL  - 42
KW  - Purinoceptors P1
KW  -  P2X
KW  -  P2Y
KW  -  ATP release and breakdown
KW  -  Purinergic neuropathology
KW  -  Pain
KW  -  Neurodegenerative diseases
KW  -  CENTRAL-NERVOUS-SYSTEM
KW  -  GATED ION CHANNELS
KW  -  GUINEA-PIG
KW  -  ATP RECEPTOR
KW  -  ADENOSINE TRIPHOSPHATE
KW  -  EXTRACELLULAR ATP
KW  -  TAENIA-COLI
KW  -  SYNAPTIC TRANSMISSION
KW  -  MAMMALIAN NEURONS
KW  -  STRUCTURAL MOTIF
PB  - ASSOC BRAS DIVULG CIENTIFICA
ID  - discovery1311081
N2  - The discovery of non-adrenergic, non-cholinergic neurotransmission in the gut and bladder in the early 1960's is described as well as the identification of adenosine 5'-triphosphate (ATP) as a transmitter in these nerves in the early 1970's. The concept of purinergic cotransmission was formulated in 1976 and it is now recognized that ATP is a cotransmitter in all nerves in the peripheral and central nervous systems. Two families of receptors to purines were recognized in 1978, P1 ( adenosine) receptors and P2 receptors sensitive to ATP and adenosine diphosphate ( ADP). Cloning of these receptors in the early 1990's was a turning point in the acceptance of the purinergic signalling hypothesis and there are currently 4 subtypes of P1 receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of G protein-coupled receptors. Both short-term purinergic signalling in neurotransmission, neuromodulation and neurosecretion and long-term ( trophic) purinergic signalling of cell proliferation, differentiation, motility, death in development and regeneration are recognized. There is now much known about the mechanisms underlying ATP release and extracellular breakdown by ecto-nucleotidases. The recent emphasis on purinergic neuropathology is discussed, including changes in purinergic cotransmission in development and ageing and in bladder diseases and hypertension. The involvement of neuron-glial cell interactions in various diseases of the central nervous system, including neuropathic pain, trauma and ischemia, neurodegenerative diseases, neuropsychiatric disorders and epilepsy are also considered.
EP  - 8
AV  - public
Y1  - 2009/01//
TI  - Purinergic signalling: past, present and future
ER  -