Characterisation of rebound depolarisation in mice deep dorsal horn neurons in vitro

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCB096

Poster Communications: Characterisation of rebound depolarisation in mice deep dorsal horn neurons in vitro

I. Rivera-Arconada1, J. A. Lopez-Garcia1

1. Physiology, University of Alcala, Alcala de Henares, Madrid, Spain.

View other abstracts by:


The differential array of ionic conductances expressed by a single neuron determines its intrinsic excitability and how it integrates synaptic inputs to generate adequate responses in accordance with its role. Dorsal horn neurons constitute the first relay of somatosensory information participating in sensory and motor processing. Here we show the presence of rebound depolarisation due to the presence of H and T-like currents in these neurons. Rebound behaviour has been related to neuronal plasticity and coding properties of several neuronal types. Spinal cords were removed from 7-12 day-old c57/CBA mice under urethane anaesthesia (2 g/kg; i.p.), hemisected, transferred to a recording chamber and superfused with oxygenated artificial cerebrospinal fluid (ACSF). Whole cell voltage and current-clamp recordings of deep dorsal horn neurons were performed with 5-9 MΩ pipettes. Tetrodotoxin, CsCl, mibefradil, NiCl and NNC 55-0396 were employed to unravel the nature of the ionic currents responsible of rebound behaviour. Rebound behaviour was observed in 78% of neurons studied (122 out of 156). In 60 neurons rebound presented fast kinetics and high amplitude and was usually accompanied by spike firing. When more than 1 action potential occurred instantaneous firing frequency was very high (79 ± 4 Hz, range 20-128 Hz, n=43). In these neurons the presence of a low threshold, transient inward current was documented. This current and its related rebound were partially sensitive to blockade with mibefradil, NNC 55-0396 and low concentrations of NiCl. Calcium-free ACSF and higher concentrations of NiCl completely abolished the current and the rebound. Pharmacologic and kinetics analysis suggest that the T-type calcium current underlies this fast rebound. The rebound observed in the remaining 62 neurons was slow and of low amplitude and was rarely associated with spike firing (35%). When more than 1 action potential was fired, instantaneous frequency was low (8 ± 1 Hz, range 5-15 Hz, n=11). In this subset of neurons T-like currents were absent but presented hyperpolarization activated current (IH). This slow rebound and the IH were fully blocked by 4 mM CsCl. We conclude that the existence of T- and/or H-like currents in deep dorsal horn neurons determines the presence of rebound behaviour at end of hyperpolarization pulses. T-type calcium currents were associated to a strong and fast rebound with high frequency firing. H currents were associated to small rebound, normally without spiking. Rebound depolarization and firing may constitute a mechanism to integrate somatosensory information in the spinal cord.



Where applicable, experiments conform with Society ethical requirements.

Site search

Filter

Content Type