In everyday life, human cognitive systems meet a continuous stream of happenings. Confronted with this dynamic complexity, we parse the ongoing experience stream into units of meaningful events, which are punctuated with variable inter- and intra-event durations. Our ability in utilizing such temporal duration information enables us to organize and remember our personal past flexibly.
While the human hippocampus (a limbic brain structure involved in memory and spatial navigation) has been shown to be responsive to detecting the inter- and intra-event durations of episodic events, a recent collaborative effort by researchers at NYU Shanghai and Oxford University for the first time established this structure’s critical role in dealing with a changing temporal structure to meet memory demands.
“We set out to determine how this very specific temporal aspect of episodic memory may be impacted by hippocampal system damage in primates”, proclaimed Sze Chai Kwok, Associate Professor at East China Normal University, and member of the NYU-ECNU Institute of Brain and Cognitive Science at NYU Shanghai. Using rhesus macaques as an experimental model, Kwok and his colleagues surgically disconnected several monkeys’ fornical fibers, which contain the input/output pathways of the hippocampus, and then observed how these monkeys perform differently on a delayed-matching-to-position task in comparison to normal macaque monkeys.
The most critical aspect of this study is on manipulating the duration structure of inter- and intra-events. Each trial, separated by a fixed inter-event duration, comprised an encoding stage of a spatial position presented on a touch-sensitive monitor, and following a brief delay (intra-event duration), a retrieval memory test of this position. “Across two experiments, fornix-damaged monkeys were found to be impaired when, and only when, the memory task contained trials interspersed with changing, and unpredictable, delay intervals,” Kwok explained. Importantly, the researchers further ruled out differences in motor control, motivation, perception, or working memory deficits between the two groups as contributing factors to the deficit in a second experiment. They were thus able to attribute the memory deficit to the compromised ability in tracking changes in temporal structure, which could only be caused by the putative surgical disruption in the hippocampal system.
“The major contribution is that we provided the first ever piece of causal evidence in establishing the hippocampal role in meeting memory demands in the face of changes in temporal structure of episodic events, over and above the myriad findings in the neuroimaging literature”, said Kwok. “Intervention experiments like this provide crucial pieces of evidence for discerning the brain mechanisms of cognition as they remain the only way to determine causality in the brain and cannot be replaced by brain neuroimaging; animal models are necessary because the precise interventions need to be replicable across animals in ways that never occur in patients”, said Professor Buckley from Oxford University. “The animals we use receive appropriate anaesthesia and analgesia and live in social groups and were not food or water deprived at any time” added Professor Buckley. The study was published in the August issue of Learning & Memory, a journal dedicated to the study of the neurobiology of learning and memory.