SYNAPTIC INTERACTIONS UNDERLYING MEMORY INDUCTION

Project Details

Description

The biophysical events which serve as substrates for memory storage have
been well documented in Hermissenda B cells, and include a Ca2+-dependent
reduction of outward K+ currents and a resultant Increase in membrane
input resistance and light-elicited generator potentials. Nevertheless,
comparatively little is known about the synaptic events which culminate in
these biophysical modifications. In fact, many of the proposed mechanisms
thought to underlie the induction of the biophysical memory trace are
based on correlative evidence and in some cases are untested. Given that
the disparities between various cellular models of learning are most
pronounced with regard to the induction process, these assumptions must be
more closely examined. Only through such an examination will those
ubiquitous principles which govern memory formation be discerned. In the
present series of experiments, behavioral, biophysical, and biochemical
indices of memory will be employed during induction of an associative
memory trace. Hermissenda will serve in all experiments, and is well
suited for such an analysis in that its relatively simple nervous system
permits the identification and isolation of single cells involved in
memory storage.

Although both intracellular Ca2+ and specific neurotransmitters have been
proposed to participate in the induction of associative memory in
Hermissenda, the mechanism by which these cofactors interact to induce new
memories is vague. The experiments described here are intended to address
the role of these cofactors and the events that they regulate, via
behavioral indices of conditioning in conjunction with acute in vivo and
in vitro recording and stimulation of identified neurons in the animal's
visual-vestibular network. The role of specific transmitters, in
particular, GABA and 5-HT, and their effects on neuronal excitability as
a function of the physiological state of the postsynaptic neuron will be
examined. Mechanisms that underlie trial-by-trial induction of learning
will be explored (e.g.,transmitter release paired with postsynaptic Ca2+
elevation), and will be distinguished from the consolidation that takes
place both during and after the learning event. A major portion of the
present proposal concerns the role of transmitter-activated GTP-binding
proteins, both as mediators of Visual-vestibular interactions in
Hermissenda, as well as in their function as dual regulators of
postsynaptic second messengers which may contribute to the differential
modulation of K+ conductance on the postsynaptic membrane. The
identification and characterization of mechanisms which causally
contribute to Initial induction and subsequent storage of a simple
associative memory, and, which can account for a general form of synaptic
plasticity, are likely to contribute to the development of unifying
principles in the cellular analysis of memory, and may thus provide
insight Into specific interventions and treatments to benefit the
acquisition and subsequent retrieval of memories.
StatusFinished
Effective start/end date8/1/947/31/99

Funding

  • National Institute of Mental Health
  • National Institute of Mental Health
  • National Institute of Mental Health
  • National Institute of Mental Health
  • National Institute of Mental Health

ASJC

  • Biophysics
  • Physiology
  • Behavioral Neuroscience

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