An astrocytic signaling loop for frequency-dependent control of dendritic integration and spatial learning

Kirsten Bohmbach, Nicola Masala, Eva M. Schönhense, Katharina Hill, André N. Haubrich, Andreas Zimmer, Thoralf Opitz, Heinz Beck and Christian Henneberger ()
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Kirsten Bohmbach: University of Bonn
Nicola Masala: University of Bonn
Eva M. Schönhense: University of Bonn
Katharina Hill: University of Bonn
André N. Haubrich: University of Bonn
Andreas Zimmer: University of Bonn
Thoralf Opitz: University of Bonn
Heinz Beck: University of Bonn
Christian Henneberger: University of Bonn

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Dendrites of hippocampal CA1 pyramidal cells amplify clustered glutamatergic input by activation of voltage-gated sodium channels and N-methyl-D-aspartate receptors (NMDARs). NMDAR activity depends on the presence of NMDAR co-agonists such as D-serine, but how co-agonists influence dendritic integration is not well understood. Using combinations of whole-cell patch clamp, iontophoretic glutamate application, two-photon excitation fluorescence microscopy and glutamate uncaging in acute rat and mouse brain slices we found that exogenous D-serine reduced the threshold of dendritic spikes and increased their amplitude. Triggering an astrocytic mechanism controlling endogenous D-serine supply via endocannabinoid receptors (CBRs) also increased dendritic spiking. Unexpectedly, this pathway was activated by pyramidal cell activity primarily in the theta range, which required HCN channels and astrocytic CB1Rs. Therefore, astrocytes close a positive and frequency-dependent feedback loop between pyramidal cell activity and their integration of dendritic input. Its disruption in mice led to an impairment of spatial memory, which demonstrated its behavioral relevance.

Date: 2022
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DOI: 10.1038/s41467-022-35620-8

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