Premium
Spinal dorsal horn astrocytes release GABA in response to synaptic activation
Author(s) -
Christensen Rasmus Kordt,
DelgadoLezama Rodolfo,
Russo Raúl E.,
Lind Barbara Lykke,
Alcocer Emanuel Loeza,
Rath Martin Fredensborg,
Fabbiani Gabriela,
Schmitt Nicole,
Lauritzen Martin,
Petersen Anders Victor,
Carlsen Eva Meier,
Perrier JeanFrançois
Publication year - 2018
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp276562
Subject(s) - glutamate receptor , neuroscience , spinal cord , inhibitory postsynaptic potential , astrocyte , glutamatergic , postsynaptic potential , chemistry , tetrodotoxin , gamma aminobutyric acid , biology , central nervous system , biophysics , receptor , biochemistry
Key points GABA is an essential molecule for sensory information processing. It is usually assumed to be released by neurons. Here we show that in the dorsal horn of the spinal cord, astrocytes respond to glutamate by releasing GABA. Our findings suggest a novel role for astrocytes in somatosensory information processing.Abstract Astrocytes participate in neuronal signalling by releasing gliotransmitters in response to neurotransmitters. We investigated if astrocytes from the dorsal horn of the spinal cord of adult red‐eared turtles ( Trachemys scripta elegans ) release GABA in response to glutamatergic receptor activation. For this, we developed a GABA sensor consisting of HEK cells expressing GABA A receptors. By positioning the sensor recorded in the whole‐cell patch‐clamp configuration within the dorsal horn of a spinal cord slice, we could detect GABA in the extracellular space. Puff application of glutamate induced GABA release events with time courses that exceeded the duration of inhibitory postsynaptic currents by one order of magnitude. Because the events were neither affected by extracellular addition of nickel, cadmium and tetrodotoxin nor by removal of Ca 2+ , we concluded that they originated from non‐neuronal cells. Immunohistochemical staining allowed the detection of GABA in a fraction of dorsal horn astrocytes. The selective stimulation of A∂ and C fibres in a dorsal root filament induced a Ca 2+ increase in astrocytes loaded with Oregon Green BAPTA. Finally, chelating Ca 2+ in a single astrocyte was sufficient to prevent the GABA release evoked by glutamate. Our results indicate that glutamate triggers the release of GABA from dorsal horn astrocytes with a time course compatible with the integration of sensory inputs.