By utilizing new information from both clinical and
experimental (lesion, electrophysiological, and gene-activation)
studies with animals, the anatomy underlying anterograde amnesia
has been reformulated. The distinction between temporal lobe and
diencephalic amnesia is of limited value in that a common feature
of anterograde amnesia is damage to part of an “extended
hippocampal system” comprising the hippocampus, the fornix,
the mamillary bodies, and the anterior thalamic nuclei. This view,
which can be traced back to Delay and Brion (1969), differs from
other recent models in placing critical importance on the efferents
from the hippocampus via the fornix to the diencephalon. These
are necessary for the encoding and, hence, the effective subsequent
recall of episodic memory. An additional feature of this
hippocampal–anterior thalamic axis is the presence
of projections back from the diencephalon to the temporal
cortex and hippocampus that also support episodic memory.
In contrast, this hippocampal system is not required for tests
of item recognition that primarily tax familiarity judgements.
Familiarity judgements reflect an independent process that depends
on a distinct system involving the perirhinal cortex of the temporal
lobe and the medial dorsal nucleus of the thalamus. In the large
majority of amnesic cases both the hippocampal–anterior
thalamic and the perirhinal–medial dorsal thalamic systems
are compromised, leading to severe deficits in both recall and
recognition.
The hallmark of medial temporal lobe amnesia is a loss of episodic memory such that patients fail to remember new events that are set in an autobiographical context (an episode). A further symptom is a loss of recognition memory. The relationship between these two features has recently become contentious. Here, we focus on the central issue in this dispute--the relative contributions of the hippocampus and the perirhinal cortex to recognition memory. A resolution is vital not only for uncovering the neural substrates of these key aspects of memory, but also for understanding the processes disrupted in medial temporal lobe amnesia and the validity of animal models of this syndrome.
It is widely believed that long-term depression (LTD) and its counterpart, long-term potentiation (LTP), involve mechanisms that are crucial for learning and memory. However, LTD is difficult to induce in adult cortex for reasons that are not known. Here we show that LTD can be readily induced in adult cortex by the activation of NMDA receptors (NMDARs), after inhibition of glutamate uptake. Interestingly there is no need to activate synaptic NMDARs to induce this LTD, suggesting that LTD is triggered primarily by extrasynaptic NMDA receptors. We also find that de novo LTD requires the activation of NR2B-containing NMDAR, whereas LTP requires activation of NR2A-containing NMDARs. Surprisingly another form of LTD, depotentiation, requires activation of NR2A-containing NMDARs. Therefore, NMDARs with different synaptic locations and subunit compositions are involved in various forms of synaptic plasticity in adult cortex.
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