Synaptic long-term depression alters recovery from, and frequency dependency of, short-term depression in Helix pomatia.
Kinetic properties of synaptic depression were analysed for excitatory postsynaptic potentials in neuron number 3 in the right pallial ganglion of Helix pomatia. It was observed that long-term depression did not only suppress the amplitudes of excitatory postsynaptic potentials but also changed the kinetics of short-term depression. Early during each experiment (before the induction of long-term depression), the degree of short-term depression was inversely related to the frequency of excitatory postsynaptic potentials (contrary to most earlier reports). Later in the experiments, after the formation of long-term depression induced by four spaced excitatory postsynaptic potential series, the inverse frequency dependency had changed into a direct proportionality between short-term depression and frequency. This change was associated with, and could be at least partially explained by, an alternation of recovery from short-term depression induced by long-term depression: early in experiments, recovery showed a transient phase of large recovery between excitatory postsynaptic potentials separated by 3 to 45 s. After the induction of long-term depression, this large and transient recovery was absent. The relationship between the amount of long-term depression formed and the number of preceding excitatory postsynaptic potentials inducing the depression was analysed, and it was observed that a significant long-term depression was present 10 min after only six excitatory postsynaptic potentials. The results point towards the implication that many previous investigations of the kinetics of short-term depression observed in experiments involving a high number of excitatory postsynaptic potentials have been performed under the influence of variable degrees of long-term depression. Since long-term depression (at least in Helix) induced substantial alterations of the kinetic properties of short-term depression, such changes may have significantly influenced the conclusions of earlier reports.
Christoffersen
G R
GR
Neuroscience Centre for Cognition and Memory, August Krogh Institute, University of Copenhagen, Denmark.
Schilhab
T S
TS
D000818:Animals; D017952:Ganglia, Invertebrate / Q000166:cytology / Q000502:physiology; D006372:Helix, Snails; D017774:Long-Term Potentiation / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission