Abstract
Cerebrospinal fluid-contacting (CSF-c) cells are found in all vertebrates but their function has remained elusive. We recently identified one type of laterally projecting CSF-c cell in lamprey spinal cord with neuronal properties that expresses GABA and somatostatin. We show here that these CSF-c neurons respond to both mechanical stimulation and to lowered pH. These effects are most likely mediated by ASIC3-channels, since APETx2, a specific antagonist of ASIC3, blocks them both. Furthermore, lowering of pH as well as application of somatostatin will reduce the locomotor burst rate. The somatostatin receptor antagonist counteracts the effects of both a decrease in pH and of somatostatin. Lateral bending movement imposed on the spinal cord, as would occur during natural swimming, activates CSF-c neurons. Taken together, we show that CSF-c neurons act both as mechanoreceptors and as chemoreceptors through ASIC3 channels, and their action may protect against pH-changes resulting from excessive neuronal activity.
Highlights
Cerebrospinal fluid-contacting (CSF-c) cells are found in all vertebrates but their function has remained elusive
The CSF-c neurons have bulb-like protrusions into the central canal[3], and when these neurons were retrogradely filled from the lateral margin of the spinal cord, a cilium-like structure was observed extending from the bulb-like ending (Fig. 1a, arrowhead)
To explore whether CSF-c neurons are capable of sensing fluid movements, brief pressure pulses were applied to a Ringer-filled micropipette positioned close to the CSF-c cells bulb-like protrusion into the central canal, while performing patch recordings of the same cell (Fig. 1c)
Summary
Cerebrospinal fluid-contacting (CSF-c) cells are found in all vertebrates but their function has remained elusive. Projecting CSF-c cells in the lamprey spinal cord extend processes into the grey matter, and even as far as the lateral margin, where they form a plexus around the stretch-sensitive dendrites of stretch receptor neurons[3,6,7] These CSF-c cells are of two types: (1) one with neuronal properties that displays action potentials, receives synaptic input (GABA- and glutamate-mediated), and expresses GABA and somatostatin; and (2) another with glia-like properties that displays no active currents or expression of neurotransmitters[3]. We show that both somatostatin and lowering of pH have a depressing effect on the fictive locomotor burst rate and that this effect was blocked by a somatostatin receptor antagonist These results suggest that the network effects of lowering of the pH are mediated by somatostatin expressing CSF-c neurons, through an activation of ASIC3
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