Memory impairment is common following traumatic brain injury (TBI). In recent years, researchers have demonstrated that the processes underlying memory formation (working memory, encoding, consolidation, and retrieval) are interrelated but dissociable events.The following study was designed to determine how these processes contribute to memory impairment following experimental TBI in the rat. Experiment 1 indicated thatTBI induces severe working memory deficits in a delayed non-matching-to-place task.Although all animals displayed intact acquisition, only injured animals displayed poor performance as the delay between the sample and choice phases was increased.Experiment 2 was designed to determine if TBI produces a transient period of posttraumatic amnesia (PTA) following TBI. During the early post-injury period, injured animals displayed intact short-term (3min) object recognition memory but impaired long-term (1 and 24hrs) memory. However, during the chronic post-injury period (days 14-17), no recognition memory deficits were observed in injured animals, indicating thatPTA resolves by 14 days post-injury. Experiment 3 was designed to determine the mechanism of anterograde memory impairment following TBI. Animals were injured and then trained to a pre-determined criterion in a 1 -day water maze procedure.Although injured animals required more trials to reach criterion, the rate of forgetting was identical among sham and injured groups up to 24hrs post-training. This suggests that the amount of information encoded into long-term memory, not more rapid forgetting, is the primary mechanism of anterograde memory impairment following TBI. InExperiment 4, animals were trained in the water maze and then injured 1 (recent memory) or 14 (recent memory) days post-training. Fourteen days post-injury, animals were given a retention probe trial followed by a reminding procedure and a second probe trial. Injured animals in both the recent and remote memory conditions displayed impaired performance on the first probe trial. However, injured animals benefited from the reminding procedure, and animals in the remote memory group were identical to shams during the second probe trial. These results indicate that retrograde memory impairment following TBI is mediated primarily by retrieval deficits at the time of testing, while the quality of the memory trace remains largely intact.

A short wakeful rest immediately after new learning boosts verbal memory retention over several minutes. This memory boost is observed both in healthy people and in patients with amnesia, including patients with amnestic mild cognitive impairment (aMCI) and mild Alzheimer’s Disease (AD). Wakeful resting is hypothesized to boost memory by protecting the memory consolidation (strengthening) process from interfering sensory stimulation. The effect of a short wakeful rest immediately after new learning has, to this stage, been tested only over standard retention intervals (≤1 hour). The objectives of this PhD project were to: 1.) examine whether a short wakeful rest immediately after learning boosts memory over a longer retention interval (7 days) in healthy older adults (Experiment 1, Experiment 2) and aMCI/mild AD patients (Experiment 3) 2.) investigate whether intentional rehearsal is necessary and sufficient to boost memory during wakeful rest, over both short-term (15-minute) and long-term (7-day) delays (Experiment 4, 5 and 6) 3.) compare the effect of a short post-learning rest on retention as assessed via cued recall, free recall and recognition, both over short delays (15 minutes) and long delays (7 days and 4 weeks) (Experiments 4,5 and 7) 4.) examine whether a short wakeful rest immediately after learning boosts retention of real-life-like stimuli (face/name paired associates) in healthy older adults and aMCI/mild AD patients (Experiment 8, Experiment 9) In order to accomplish these aims, several samples of healthy adults and amnesic patients were tested, utilising a range of experimental designs. In all experiments, the learning of new material was followed immediately (i) by a brief wakeful rest, or (ii) by a cognitively demanding task. A delayed memory test took place after a range of intervals. The results demonstrate a pronounced memory enhancement over 15-30 minutes and 7 days in aMCI/mild AD patients via a short post-learning wakeful rest. A similar, albeit less pronounced 7-day memory benefit via post-learning wakeful rest was found in healthy older adults. Moreover, it was found that post-learning wakeful resting boosted 7-day recognition memory in healthy older adults, even when the learned material could not be rehearsed intentionally. Although intentional rehearsal did provide a 7-day memory improvement in healthy older adults, the present results indicate that it is not necessary in order to enhance long-term recognition memory via wakeful resting. The long-lived memory benefit gained via post-learning wakeful rest was shown to last at least 4 weeks in healthy adults, and free recall tests were more sensitive to the post-learning delay manipulation than cued recall tests. Finally, healthy controls and aMCI/mild AD patients who were able to learn face/name pairs showed enhanced 30-minute retention of these stimuli following wakeful rest conditions. The present findings demonstrate that both clinical and non-clinical populations are able to retain more new information over long periods, if the time interval immediately after new learning is devoid of further sensory stimulation. These results contribute to a growing body of literature stipulating that minimizing sensory stimulation frees early memory consolidation resources, allowing for superior offline consolidation of verbal material over a standard (≤1 hour) interval. The findings of this thesis extend this hypothesis over (i) a longer interval and (ii) to real-life-like stimuli, and these results are examined in light of memory consolidation theory. Implications of the premise of retroactive interference as a mechanism of longer-term forgetting are discussed.

Domoic acid (DA), a potent neurotoxin that has the potential to cause amnesic shellfish poisoning (ASP), is produced by members of the marine diatom genus Pseudo-nitzschia. Outbreaks of ASP in humans and of DA poisoning in birds and marine mammals have been reported across the United States and Canada since the late 1980's. Pseudo-nitzschia species can be extremely abundant in Florida waters, with densities often exceeding 106 cells/L, and sometimes exceeding 107 cells/L. Based on preliminary data, it is evident that at least nine species of Pseudo-nitzschia are found in Florida coastal waters. At least six of these species are known to produce DA in other parts of the world, and some are morphologically identical to some of the major toxin-producing species in Californian and Canadian waters. Despite the strong presence of Pseudo-nitzschia, there has never been a report of ASP or a DA-related animal mortality event from Florida. Data collected from 2004 to 2011 show maximum Pseudo-nitzschia abundances exceeded 4 x 107 cells/L. Six species of Pseudo-nitzschia were identified from central west and southwest Florida waters via light and electron microscopy. This is the first report of P. micropora from the Gulf of Mexico. Additionally P. calliantha, P. cuspidata, and P. pungens were identified as producers of DA in Florida coastal waters; although cell quotas of DA were low. Low levels of DA were detected in about one third of the water samples analyzed and DA concentrations measured in the majority of shellfish from the study area were at least an order of magnitude below the regulatory limit of 20 µg/g, suggesting that Pseudo-nitzschia currently poses little threat to human health in Florida. However, DA production in Pseudo-nitzschia species has been shown to be variable and dependent on nutrient conditions, indicating that the potential for DA-related events to occur in Florida warrants further investigation.