How does the Hippocampus interface with Cortex? March 9, 2007Posted by Johan in Connectionism, Neural Networks, Neuroscience, Sleep.
Hahn, Sakmann & Meta report some intriguing results, for now only available in a press release, as PNAS apparently offers no ahead of print feature. A related paper by the same group (Hahn, Sakmann & Mehta, 2006) is available, however, which is where I got the micrograph of a cell in hippocampal area CA1 that you see above.
Hahn et al anesthetised rats to simulate deep sleep, while recording the activity of cells in the hippocampus and cortex simultaneously. They found that excitatory activity in the cortex produced an echo in hippocampal cells. The pattern of activity in the hippocampus was not uniform: cells in the dentate gyrus showed a strong response, CA3 region cells showed a weaker response, and CA1 region cells were seemingly inhibited by the cortical activity.
One reason why this is interesting is that a popular theory of memory consolidation makes the opposite prediction, that is, the hippocampus should largely drive cortical activation. In the connectionist model of McClelland, McNaughton and O’Reilly (1995), the hippocampus is positioned as the “trainer” of long-term memory structures in the cortex.
The “trainer” role for the hippocampus arose from the observation that while a single connectionist network can easily accommodate large amounts of information, incrementally adding new items causes catastrophic interference. Simply put, this occurs because when new memories are formed by changing the connection weights in the network, the older memory traces are disrupted, since they relied on the previous weightings. By positing a second network that uses more easily changeable connection weights to allow for rapid learning, interleaved learning is made possible.
In this view, then, the hippocampus acquires new information rapidly, after which it trains the larger and slower cortical network on the new information. The hippocampus interleaves this new information with re-activation of older memories, which allows the old and new memories to co-exist in the cortical network, without catastrophic interference. McClelland et al suggested that this consolidation process occurs during slow-wave sleep.
To tie this in with Hahn et al’s results, the cortex-driven hippocampal activation could be viewed speculatively as the re-activation of memory traces described in the McClelland et al model. But it’s hard to see how the hippocampus then “trains” the cortical network on new informaton, when no activity seems to go in this direction. This leaves us with the possibility that this hippocampus-driven training of the cortical network occurs at a different point in the circadian cycle, or with the more bleak possibility that there is something fundamentally wrong with the functional division that McClelland et al proposed.
In any case, the method used by Hahn et al is quite fascinating. Up until now, very little has been known about how the hippocampus interacts with the cortex to play its (disputed!) role in memory formation and consolidation. The paper in PNAS is definitely one to look out for.
The Mehta Lab’s publications at Brown
Hahn, T.G., Sakmann, B., & Mehta, M.R. (2006). Phase-locking of hippocampal interneurons’ membrane potential to neocortical up-down states. Nature Neuroscience, 9, 1359-1361.
McClelland, J.L., McNaughton, B.L., & O’Reilly, R.C. (1995). Why There are Complementary Learning Systems in the Hippocampus and Neocortex: Insights from the Successes and Failures of Connectionist Models of Learning and Memory. Psychological Review, 102, 419-457.