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First published online November 1, 2006
Journal of Experimental Biology 209, 4429-4435 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02553

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Excitatory actions of GABA mediate severe-hypoxia-induced depression of neuronal activity in the pond snail (Lymnaea stagnalis)

Una Cheung, Mehrnoush Moghaddasi, Hannah L. Hall, J. J. B. Smith, Leslie T. Buck and Melanie A. Woodin^*

Department of Cell and Systems Biology, University of Toronto, Ontario, Canada

View larger version (29K): [in a new window]   Fig. 1. Electrophysiological recording from neurones of the Lymnaea pedal ganglia. (A) The central ring ganglia isolated from Lymnaea. Intracellular recordings were made from neurones in cluster F (white region) on the dorsal surface of either the left or right pedal ganglion (LPeDG or RPeDG). (B) Schematic of the Lymnaea central ring ganglia. Recordings were not obtained from the identified neurones L- or RPeD1. (C) An example trace of a recording from a cluster F neurone maintained entirely under normoxic conditions.

View larger version (12K): [in a new window]   Fig. 2. Severe hypoxia decreases neuronal activity. (A) No significant changes in the action potential (AP) frequency were observed in normoxic neurones throughout the entire recording period (black bars; N=9, P=0.935 paired t-test). After switching from normoxia to severe hypoxia, AP frequency decreased significantly (grey bars; N=9, P=0.001 paired t-test). (B) Example traces of AP frequency during normoxia and 10 min after the switch to severe hypoxia.

View larger version (9K): [in a new window]   Fig. 3. GABAA receptors mediate hypoxia-induced neuronal depression. (A) When neurones were recorded at rest under normoxic conditions action potentials (APs) (at I), inhibitory postsynaptic potential (IPSPs; at II) and excitatory postsynaptic potential (EPSPs; at III) were observed. (B) Addition of 100 µmol l-1 bicuculline to the perfusate induced a significant decrease in AP frequency (grey bars; N=7, P=0.003 paired t-test). When neurones underwent a normoxic to hypoxic transition in the presence of 100 µmol l-1 bicuculline, there was no significant change in AP frequency (white bars; N=6, P=0.235 paired t-test). The hypoxia-mediated decrease in AP frequency is not significantly different from the decrease observed during the normoxic application of bicuculline (black hypoxia bars vs grey normoxia+bicuculline bars; P=0.844 unpaired t-test). Data sets denoted by a white triangle were taken from Fig. 2A for direct visual comparison.

View larger version (38K): [in a new window]   Fig. 4. Severe hypoxia decreases excitatory GABAergic neurotransmission in the Lymnaea central ring ganglia. (A) Example traces demonstrating the change in action potential (AP) firing frequency produced by puffing 500 µmol l-1 GABA (at arrow) onto the central ring ganglia. In normoxia (top trace) GABA produced an increase in AP firing frequency. Switching from normoxia to hypoxia decreased the excitatory response to GABA (lower trace). (B) Bar graph summarizing the percentage change in AP firing frequency and postsynaptic potential amplitude induced by puffing 500 µmol l-1 GABA onto both normoxic and hypoxic central ring ganglia.

View larger version (12K): [in a new window]   Fig. 5. NKCC1 renders GABA excitatory in the Lymnaea CNS. (A) Addition of the NKCC1 antagonist bumetanide (100 µmol l-1) to the perfusate significantly decreases action potential (AP) firing frequency (grey bars; N=6, P=0.01 paired t-test). The normoxic decrease in AP frequency caused by bumetanide is not significantly different from the decrease observed in the normoxia to hypoxia switch (black bars vs grey bars; P=0.844 unpaired t-test). (B) Spontaneous firing of APs was prevented by the addition of 100 µmol l-1 bumetanide (at bar).