Synaptic plasticity and learning II: Do different kinds of plasticity underlie different kinds of learning?

Abstract

This paper discusses certain issues connected with the question of whether synaptic plasticity is involved in information storage by the brain. We begin by contrasting two well documented types of synaptic plasticity—activity-dependent modulation of presynaptic facilitation (“Kandel synapses”) and NMDA receptor triggered alterations in excitatory amino acid transmission (“Hebb synapses”). We then propose that, embedded-into appropriate circuitry, these different forms of plasticity might underlie different kinds of learning. In partial support of this idea, we show that, in freely moving rats, intrahippocampal microinfusion of the NMDA-receptor antagonist D,L-AP5 causes a dose-dependent impairment of a type of spatial learning known to be sensitive to disruption by hippocampal lesions (water-maze place-navigation). In a second experiment, the same drug infusion protocol is shown to cause a blockade of hippocampal long-term potentiation in vivo across a comparable dose range. Finally, third, autoradiographic experiments indicate that diffusion of the drug was largely restricted to the hippocampus. Together, these results (1) suggest that blockade of hippocampal NMDA receptors, under conditions which leave baseline synaptic transmission relatively unaffected, blocks a type of learning with which the vertebrate hippocampus has been implicated on the basis of neuropsychological work; and (2) supports Abrams and Kandel's Trends Neurosci. 11 (1988) recent proposal that there may be several logically distinct forms of synaptic plasticity.