Abstract
Memory formation involves dynamic interactions among many brain structures and their
linking pathways. The noradrenaline (NA) system in the CNS plays an important role
in a wide variety of neurological and psychological functions. Alteration in the NA
system is implicated in the pathological states of some neuropsychiatric disorders.
Tyrosine hydroxylase (TH) is the initial and rate-limiting enzyme for the biosynthesis
of catecholamines. The regulatory mechanism of the TH reaction is generally considered
to play a key role in controlling the catecholaminergic actions. Mice heterozygous
for the mutation of the gene encoding TH exhibit the reduced TH activity in tissues.
These mice have a moderate reduction in NA accumulation and release in brain regions.
The mutant mice exhibit deficits in the water-finding task associated with latent
learning performance, suggesting the impairment in memory formation. Spatial learning
performance measured by the water maze task is normal in the mutants. However, they
display deficits in long-term memory formation of conditioned learning evaluated with
three distinct behavioral paradigms, including active avoidance, cued fear conditioning,
and conditioned taste aversion, without affecting short-term memory. These memory
deficits are restored by the drug-induced stimulation of NA activity at the postconditioning
phase. Analysis of the mutant mice indicates that the central NA system is essential
for the consolidation process in long-term memory of conditioned learning. The process
appears to be implicated in the NA activity in the cerebral cortex and/or amygdaloid
complex.
Keywords
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© 2001 Elsevier Science B.V. Published by Elsevier Inc. All rights reserved.
