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Schizophr Res. 2018 Aug 30. pii: S0920-9964(18)30517-6. doi: 10.1016/j.schres.2018.08.025. [Epub ahead of print]

Synaptic plasticity/dysplasticity, process memory and item memory in rodent models of mental dysfunction.

Author information

1
Center for Neural Science, New York University, New York, NY 10003, USA. Electronic address: kally.sparks@nyspi.columbia.edu.
2
Center for Neural Science, New York University, New York, NY 10003, USA.
3
Center for Neural Science, New York University, New York, NY 10003, USA; Neuroscience Institute at the New York University Langone Medical Center, New York, NY 10016, USA; Department of Physiology & Pharmacology, Robert F. Furchgott Center for Neuroscience, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA. Electronic address: afenton@nyu.edu.

Abstract

Activity-dependent changes in the effective connection strength of synapses are a fundamental feature of a nervous system. This so-called synaptic plasticity is thought to underlie storage of information in memory and has been hypothesized to be crucial for the effects of cognitive behavioral therapy. Synaptic plasticity stores information in a neural network, creating a trace of neural activity from past experience. The plasticity can also change the behavior of the network so the network can differentially transform/compute information in future activations. We discuss these two related but separable functions of synaptic plasticity; one we call "item memory" as it represents and stores items of information in memory, the other we call "process memory" as it encodes and stores functions such as computations to modify network information processing capabilities. We review evidence of item and process memory operations in behavior and evidence that experience modifies the brain's functional networks. We discuss neurodevelopmental rodent models relevant for understanding mental illness and compare two models in which one model, neonatal ventral hippocampal lesion (NVHL) has beneficial adult outcomes after being exposed to an adolescent cognitive experience that is potentially similar to cognitive behavioral therapy. The other model, gestational day 17 methylazoxymethanol acetate (GD17-MAM), does not benefit from the same adolescent cognitive experience. We propose that process memory is altered by early cognitive experience in NVHL rats but not in GD17-MAM rats, and discuss how dysplasticity factors may contribute to the differential adult outcomes after early cognitive experience in the NVHL and MAM models.

KEYWORDS:

Cognitive behavioral therapy; Dysplasticity; Hippocampus; Neurodevelopment; Schizophrenia; Synaptic function

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