DISTRIBUTION AND FUNCTIONAL-PROPERTIES OF GLUTAMATE RECEPTORS IN THE LEECH CENTRAL-NERVOUS-SYSTEM

1. The effect of kainate and other glutamatergic agonists on the membr ane potential (E(m)), the intracellular Na+ activity (aNa(i)), and the intracellular free Ca2+ concentration ([Ca2+](i)) of identified leech neurons and neuropile glial cells was measured with conventional and ion-sensitive microelectrodes, as well as with the use of the iontopho retically injected fluorescent indicators sodium-binding benzofuran is ophthalate and Fura-2. 2. In Retzius neurons, AE, L, 8, and 101 motone urons, and in the unclassified 50 neurons (Leydig cells) and AP neuron s, as well as in neuropile glial cells, bath application of 100 mu M k ainate evoked a marked membrane depolarization and an increase in aNa( i) and [Ca2+](i). The kainate-induced aNa(i) increase persisted in sol utions with high Mg2+ concentration in which synaptic transmission is blocked. 3. A membrane depolarization as well as an Increase in aNa(i) and [Ca2+](i) was also evoked by L-glutamate. quisqualate, and pha-am ino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). The agonist-induc ed [Ca2+](i) increase was inhibited by 6,7-dinitroquinoxaline-2,3-dion e (DNQX). 4. In Ca2+-free solution, the kainate-induced [Ca2+](i) incr ease was abolished in the neurons and in neuropile glial cells, wherea s membrane depolarization and aNa(i) increase were unchanged, In Na+-f ree solution, kainate had no effect on E(m), aNa(i), or [Ca2+](i) in t he neurons. 5. In the mechanosensory T, P, and N neurons, kainate indu ced considerably smaller membrane depolarizations than in the other ne urons or in neuropile glial cells, and it had no significant effect on aNa, or [Ca2+](i). 6. It is concluded that in leech segmental ganglia the majority of the neurons and the neuropile glial cells, but probab ly not th; mechanosensory neurons, possess glutamate receptors of the AMPA-kainate type. In the neurons, the [Ca2+](i) increase caused by gl utamatergic agonists is due to Ca2+ influx through voltage-dependent C a2+ channels that are activated by the agonist-induced membrane depola rization.