Adenosine A1 receptor activates background potassium channels and modulates information processing in olfactory bulb mitral cells

Abstract

Neuromodulation by adenosine is of critical importance in many brain regions, but the role of adenosine in olfactory information processing has not been studied so far. We investigated the effects of adenosine on mitral cells, which are projection neurons of the olfactory bulb. Significant expression of A₁ and A_2A receptors was found in mitral cells, as demonstrated by in situ hybridization. Application of adenosine in acute olfactory bulb slices hyperpolarized mitral cells in wild type, but not in adenosine A₁ receptor knockout mice. Adenosine-induced hyperpolarization was mediated by background K⁺ currents that were reduced by halothane and bupivacaine which are known to inhibit two-pore domain K⁺ (K2P) channels. In mitral cells, electrical stimulation of axons of olfactory sensory neurons evoked synaptic currents, which can be considered as input signal, while spontaneous firing independent of sensory input can be considered as noise. Synaptic currents were not affected by adenosine, while adenosine reduced spontaneous firing, leading to an increase in the signal-to-noise ratio of mitral cell firing. Our findings demonstrate that A₁ adenosine receptors activate two-pore domain K⁺ channels, which increases the signal-to-noise ratio of the input-output relationship in mitral cells and thereby modulates information processing in the olfactory bulb.

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