In the first part of three overviews on recognition memory in the rat,
we discussed the tasks employed to study recognition memory. In the s
econd part, we discussed the neuroanatomical systems thought to be of
importance for the mediation of recognition memory in the rat. In part
icular, we delineated two parallel-distributed neuronal networks, one
thai is essential for the processing of non-spatial/item recognition m
emory processes and incorporates the cortical association areas such a
s TE1, TE2 and TE3, the rhinal cortices, the mediodorsal thalamic nucl
eus and prefrontal cortical areas (Network 1), the other comprising of
the hippocampus, mamillary bodies, anterior thalamic nuclei and media
l prefrontal areas (Network 2), suggested to be pivotal for the proces
sing of spatial recognition memory. The next step will progress to the
level of the neurotransmitters thought to be involved. Current data s
uggest that the majority of drugs have non-specific, i.e. delay-indepe
ndent effects in tasks measuring recognition memory. This may be due t
o attentional, motivational or motoric changes. Alternatively, delay-i
ndependent effects may result from altered acquisition/encoding rather
than from altered retention. Furthermore, the neurotransmitter system
s affected by these drugs could be important as modulators rather than
as mediators of recognition memory pei se, It could, of course, also
be the case that systemic treatment induces non-specific effects which
overshadow any specific, delay-dependent, effect. This possibility re
ceives support from lesion experiments (For example, of the septohippo
campal cholinergic system) or studies employing local intracerebral in
fusion techniques. However, it is evident that those delay-dependent e
ffects are relatively subtle and more readily seen in delayed response
paradigms, which tax spatial recognition memory. One interpretation o
f these results could be that some neurotransmitter systems are more i
nvolved in spatial than in item recognition memory processes. However,
performance in delayed response tasks can be aided by mediating strat
egies. Drugs or lesions can alter those strategies, which could equall
y explain some of the (delay-dependent) drug effects on delayed respon
ding. Thus, it is evident that neither of the neurotransmitter systems
reviewed (glutamate, GABA, acetylcholine, serotonin, dopamine and nor
adrenaline) can be viewed as being directly and exclusively concerned
with storage/retention. Rather, our model of recognition memory sugges
ts that information about previously encountered items is differential
ly processed by distinct neural networks and is not mediated by a sing
le neuro transmitter type. (C) 1998 Elsevier Science Ltd.