Chloride conductance produces both presynaptic inhibition and antidromic spikes in primary afferents

Primary afferents from a crayfish leg proprioceptor display both primary afferent depolarizations (PADs) and antidromic spikes. PADs are generated by activation of GABA receptors and produce presynaptic inhibition, while the antidromic spikes do not elicit any synaptic effect in the postsynaptic neurons. The aim of the present study was to investigate the ionic mechanisms that allow PADs to produce antidromic spikes and to test whether GABA can produce similar effects. Intracellular recordings from the sensory axon terminals within the ganglion where PAD are produced were performed. Lowering the extracellular chloride concentration resulted in an increase in PAD amplitude, which was then capable of producing antidromic spikes. Local application of GABA close to the axon terminal also resulted in production of antidromic spikes. We conclude that antidromic spikes may result from the activation of a GABA-mediated increase in chloride conductance that also produces PADs. Therefore PADs and antidromic spikes may represent two aspects of the same GABAergic inhibitory mechanism that gate sensory transmission.

[1]  F. Clarac,et al.  Direct evidence for presynaptic inhibitory mechanisms in crayfish sensory afferents. , 1992, Journal of neurophysiology.

[2]  P. Kostyuk,et al.  Polarization of primary afferent terminals of lumbosacral cord elicited by the activity of spinal locomotor generator , 1982, Neuroscience.

[3]  E. Marder,et al.  Presynaptic control of modulatory fibers by their neural network targets , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[4]  S. Rossignol,et al.  An intracellular study of muscle primary afferents during fictive locomotion in the cat. , 1991, Journal of neurophysiology.

[5]  F. Clarac,et al.  Central control of the sensory afferent terminals from a leg chordotonal organ in crayfish in vitro preparation , 1990, Neuroscience Letters.

[6]  S Grillner,et al.  The involvement of GABAB receptors and coupled G-proteins in spinal GABAergic presynaptic inhibition , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[7]  F. Clarac,et al.  Presynaptic control as a mechanism of sensory-motor integration , 1992, Current Opinion in Neurobiology.

[8]  G E Loeb,et al.  Activity of spindle afferents from cat anterior thigh muscles. I. Identification and patterns during normal locomotion. , 1985, Journal of neurophysiology.

[9]  H. Higashi,et al.  Characterization and ionic basis of GABA‐induced depolarizations recorded in vitro from cat primary afferent neurones. , 1978, The Journal of physiology.

[10]  F Clarac,et al.  Presynaptic inhibition is mediated by histamine and GABA in the crustacean escape reaction. , 1994, Journal of neurophysiology.

[11]  E. Anderson,et al.  Non-GABA mediated primary afferent depolarization , 1976, Brain Research.

[12]  M. Burrows,et al.  A presynaptic gain control mechanism among sensory neurons of a locust leg proprioceptor , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[13]  F. Clarac,et al.  GABA‐Mediated Presynaptic Inhibition in Crayfish Primary Afferents by Non‐A, Non‐B GABA Receptors , 1991, The European journal of neuroscience.

[14]  Excitation of mouse motoneurones by GABA-mediated primary afferent depolarization , 1986, Brain Research.

[15]  F. Clarac,et al.  Monosynaptic Interjoint Reflexes and their Central Modulation During Fictive Locomotion in Crayfish , 1991, The European journal of neuroscience.

[16]  S. Rossignol,et al.  Rhythmic antidromic discharges of single primary afferents recorded in cut dorsal root filaments during locomotion in the cat , 1985, Brain Research.

[17]  S. Rossignol,et al.  Rhythmic fluctuations of dorsal root potentials and antidromic discharges of primary afferents during fictive locomotion in the cat. , 1988 .