The Journal of Neurophysiology Vol. 87 No. 6 June 2002, pp. 3165-3168
Copyright ©2002 by the American Physiological Society

RAPID COMMUNICATION

Inhibitor of Glutamate Transport Alters Synaptic Transmission at Sensorimotor Synapses in Aplysia

 ¹Department of Neurobiology and Anatomy, W. M. Keck Center for the Neurobiology of Learning and Memory, University of Texas-Houston Medical School, Houston 77030; and  ²Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204

Chin, Jeannie, John A. Burdohan, Arnold Eskin, and John H. Byrne. Inhibitor of Glutamate Transport Alters Synaptic Transmission at Sensorimotor Synapses in Aplysia. J. Neurophysiol. 87: 3165-3168, 2002. Aplysia sensory neurons possess high-affinity glutamate uptake activity that is regulated by serotonin. To gain insight into the physiological role of glutamate uptake in sensory neurons, we examined whether blockade of glutamate transport altered synaptic transmission. We also examined whether glutamate transport affected homosynaptic depression and posttetanic potentiation (PTP). In the presence of DL-threo--hydroxyaspartic acid (THA), previously shown to block glutamate uptake in Aplysia, the duration of unitary excitatory postsynaptic potentials (EPSPs) was significantly increased and their amplitude was significantly reduced. Similar effects were observed in the properties of summated EPSPs. However, no effect on the induction of homosynaptic depression or PTP was observed. Although it is unclear whether THA exerted its effect by modulating neuronal and/or glial mechanisms, at least one target of THA was neuronal, as the duration of unitary EPSPs measured in cultured sensorimotor synapses was also increased in the presence of THA. These results support the hypotheses that glutamate is the transmitter released by the sensory neurons and that glutamate transport plays an important role in regulating features of synaptic transmission in Aplysia.