Abstract
We examined the effect of adenosine and of adenosine A1 receptor blockage on short‐term synaptic plasticity in slices of adult mouse anterior piriform cortex maintained in vitro in an in vivo‐like ACSF. Extracellular recording of postsynaptic responses was performed in layer 1a while repeated electrical stimulation (5‐pulse‐trains, frequency between 3.125 and 100 Hz) was applied to the lateral olfactory tract. Our stimulation protocol was aimed at covering the frequency range of oscillatory activities observed in the olfactory bulb in vivo. In control condition, postsynaptic response amplitude showed a large enhancement for stimulation frequencies in the beta and gamma frequency range. A phenomenological model of short‐term synaptic plasticity fitted to the data suggests that this frequency‐dependent enhancement can be explained by the interplay between a short‐term facilitation mechanism and two short‐term depression mechanisms, with fast and slow recovery time constants. In the presence of adenosine, response amplitude evoked by low‐frequency stimulation decreased in a dose‐dependent manner (IC50 = 70 μmol/L). Yet short‐term plasticity became more dominated by facilitation and less influenced by depression. Both changes compensated for the initial decrease in response amplitude in a way that depended on stimulation frequency: compensation was strongest at high frequency, up to restoring response amplitudes to values similar to those measured in control condition. The model suggested that the main effects of adenosine were to decrease neurotransmitter release probability and to attenuate short‐term depression mechanisms. Overall, these results suggest that adenosine does not merely inhibit neuronal activity but acts in a more subtle, frequency‐dependent manner.
Highlights
Neuronal activity in the brain is associated with various oscillatory phenomena
Previous studies established that adenosine inhibits synaptic transmission at the lateral olfactory tract (LOT)-layer 1a synapse of the piriform cortex (Kuroda et al 1976; Scholfield 1978; Okada and Saito 1979; Collins and Anson 1985; McCabe and Scholfield 1985; Yang et al 2007) and that this inhibitory action is mediated by presynaptic adenosine A1 receptor activation (Collins and Anson 1985; McCabe and Scholfield 1985; Yang et al 2007)
We first wished to confirm and quantify adenosine inhibitory effect by recording Local field potentials (LFPs) in layer 1a of the anterior piriform cortex while the LOT was stimulated at 0.5 Hz, a stimulation frequency that minimally recruited synaptic plasticity (STP) mechanisms – Gleizes et al (2017) reported a 3% difference in amplitude between responses evoked at the beginning and at the end of a 5 min long stimulation train at 0.5 Hz
Summary
Different kinds of oscillations have been categorized with respect to their frequency ranges and to their associations with vegetative, perceptive or cognitive processes. Beta oscillations (13–35 Hz) are mainly associated with motor preparation (Jasper and Penfield 1949; reviewed in: Kilavik et al 2013). Gamma band fluctuations (>35 Hz) have been abundantly studied in sensory integration domain (Chatrian et al 1960; reviewed in: Engel et al 1997; Gray 1999) and are associated with a variety of cognitive processes (reviewed in: Tallon-Baudry 2012; Bosman et al 2014). Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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