Abstract
Adenosine 5′-triphosphate (ATP) is an ubiquitous co-transmitter in the vertebrate brain. ATP itself, as well as its breakdown products ADP and adenosine are involved in synaptic transmission and plasticity, neuron-glia communication and neural development. Although purinoceptors have been demonstrated in the vertebrate olfactory system by means of histological techniques for many years, detailed insights into physiological properties and functional significance of purinergic signaling in olfaction have been published only recently. We review the current literature on purinergic neuromodulation, neuron-glia interactions and neurogenesis in the vertebrate olfactory system.
Highlights
Since the discovery of adenosine 5 -triphosphate (ATP) release from sensory nerve terminals (Holton, 1959) and peripheral purinergic neurotransmission (Burnstock et al, 1970), adenosine -triphosphate (ATP) has been described as atransmitter in most if not all parts of the vertebrate nervous system
P1 receptors are activated by adenosine, which is usually derived from extracellular degradation of ATP, adenosine -diphosphate (ADP) and AMP by ecto-nucleotidases (CD39/NTPDases, E-NPP, CD73) and alkaline phosphatase (Abbracchio et al, 2009; Zimmermann et al, 2012)
We summarize recent data on the role of purinergic signaling in cell physiology, adult neurogenesis and odor information processing in the vertebrate olfactory system
Summary
Since the discovery of adenosine 5 -triphosphate (ATP) release from sensory nerve terminals (Holton, 1959) and peripheral purinergic neurotransmission (Burnstock et al, 1970), ATP has been described as a (co-)transmitter in most if not all parts of the vertebrate nervous system. Physiological experiments in acute olfactory bulb slices provide additional evidence for the importance of tissue non-specific alkaline phosphatase, since its inhibition suppresses the A2A receptor-dependent calcium response in periglomerular astrocytes upon application of ATP, while inhibition of ecto-nucleotidases with ARL 67156 had no effect (Doengi et al, 2008).
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