Abstract
Hippocampal long-term potentiation (LTP) and long-term depression (LTD) are the most widely studied forms of synaptic plasticity thought to underlie spatial learning and memory. We report here that RARbeta deficiency in mice virtually eliminates hippocampal CA1 LTP and LTD. It also results in substantial performance deficits in spatial learning and memory tasks. Surprisingly, RXRgamma null mice exhibit a distinct phenotype in which LTD is lost whereas LTP is normal. Thus, while retinoid receptors contribute to both LTP and LTD, they do so in different ways. These findings not only genetically uncouple LTP and LTD but also reveal a novel and unexpected role for vitamin A in higher cognitive functions.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Excitatory Postsynaptic Potentials
-
Hippocampus / physiology*
-
Long-Term Potentiation / physiology*
-
Maze Learning / physiology*
-
Mice
-
Mice, Knockout
-
Neuronal Plasticity / physiology*
-
Phenotype
-
Receptors, Retinoic Acid / deficiency
-
Receptors, Retinoic Acid / genetics
-
Receptors, Retinoic Acid / physiology*
-
Retinoid X Receptors
-
Space Perception
-
Synapses / physiology*
-
Synaptic Transmission
-
Transcription Factors / deficiency
-
Transcription Factors / genetics
-
Transcription Factors / physiology*
Substances
-
Receptors, Retinoic Acid
-
Retinoid X Receptors
-
Transcription Factors
-
retinoic acid receptor beta