784 research outputs found
Neural systems underlying episodic memory: insights from animal research
No full textTwo strategies used to uncover neural systems for episodic–like memory in animals are discussed: (i) an attribute of episodic memory (what? when? where?) is examined in order to reveal the neuronal interactions supporting that component of memory; and (ii) the connections of a structure thought to be central to episodic memory in humans are studied at a level of detail not feasible in humans. By focusing on spatial memory (where?) and the hippocampus, it has proved possible to bring the strategies together. A review of lesion, disconnection and immediate early–gene studies in animals reveals the importance of interactions between the hippocampus and specific nuclei in the diencephalon (most notably the anterior thalamic nuclei) for spatial memory. Other parts of this extended hippocampal system include the mammillary bodies and the posterior cingulate (retrosplenial) cortex. Furthermore, by combining lesion and immediate early–gene studies it is possible to show how the loss of one component structure or tract can influence the remaining regions in this group of structures. The validity of this convergent approach is supported by new findings showing that the same set of regions is implicated in anterograde amnesia in humans
Intact negative patterning in rats with fornix or combined perirhinal and postrhinal cortex lesions
No full textIt has been proposed that the hippocampal formation is necessary for the acquisition of tasks that require the use of configural representations for their solution, including spatial learning and negative patterning. Tests of this influential view have, however, yielded conflicting results. For example fornix or hippocampal lesions, which reliably impair spatial learning, do not reliably impair negative patterning. A problem in interpreting these results has been the lack of controls for factors such as over-responding, excitatory effects of reward, and the possibility of non-configural solutions. At the same time, other studies have pointed to a role in configural learning for parahippocampal regions such as the perirhinal cortex. The present experiments controlled for the above factors and revealed that neither lesions of the fornix nor of the perirhinal/postrhinal cortex in the rat had any effect on negative patterning, although subsequent tests of object and spatial memory demonstrated the functional efficacy of the lesions
Stable Encoding of Visual Cues in the Mouse Retrosplenial Cortex
No full textAltres ajuts: This work was supported by a Biotechnology and Biological Sciences Research Council research grant awarded to JA, AN, SV and FS (BB/L021005/1), a Sêr Cymru fellowship (80762-CU-080) to AR, a Wellcome Trust Strategic Award (100202/z/12/z) to Michael J. Owen, J.H., Lawrence Wilkinson, Adrian Harwood, Meng Li, David Linden, John Aggleton, Vincenzo Crunelli, and Derek Jones, and a Wellcome Trust ISSF Seedcorn Award (105613/Z/14/Z) to A.R. S.V. is funded by a Wellcome Trust Senior Research Fellowship (212273/Z/18/Z).The rodent retrosplenial cortex (RSC) functions as an integrative hub for sensory and motor signals, serving roles in both navigation and memory. While RSC is reciprocally connected with the sensory cortex, the form in which sensory information is represented in the RSC and how it interacts with motor feedback is unclear and likely to be critical to computations involved in navigation such as path integration. Here, we used 2-photon cellular imaging of neural activity of putative excitatory (CaMKII expressing) and inhibitory (parvalbumin expressing) neurons to measure visual and locomotion evoked activity in RSC and compare it to primary visual cortex (V1). We observed stimulus position and orientation tuning, and a retinotopic organization. Locomotion modulation of activity of single neurons, both in darkness and light, was more pronounced in RSC than V1, and while locomotion modulation was strongest in RSC parvalbumin-positive neurons, visual-locomotion integration was found to be more supralinear in CaMKII neurons. Longitudinal measurements showed that response properties were stably maintained over many weeks. These data provide evidence for stable representations of visual cues in RSC that are spatially selective. These may provide sensory data to contribute to the formation of memories of spatial information
Intersex:cultural and social perspectives
No full textIntersex has been a topic of much discussion in courses on sex and gender in the academy. Much of this discourse has centred on the nature of intersex and how far it challenges the categories of sex and gender. As Emi Koyama and Lisa Weasel pointed out in 2002, this form of academic appropriation risks diverting attention from important social justice issues towards trivial or reductive theorising about social construction
An attempt to overcome the problem of motor mediation by rats in the delayed non matching-to-position task
No full textThis report describes the performance of rats in a delayed non matching-to-position task using an automated visual memory apparatus. A new testing procedure has been used to restrict the problem of motor mediation. In this procedure the rat must first activate a sample stimulus (either the right or left visual display panel). It has then to respond to one of three retractable levers that were extended throughout the retention delay before it can receive a reinforcer (reward pellet vs. nothing) for a response made to either one of the two visual stimulus display panels. A response on the levers was independent from a response on the stimulus display panels. These retractable levers were set in a compartment that protruded 15 cm from the back wall below the display panels, forming a platform which the rat needed to climb in order to reach the stimulus display panels. By requiring the rat to respond to one of these levers the rat could not linger by the correct display panel. Furthermore, as the rat could not anticipate the location of the response lever which would permitted the trial to continue nor the duration of the retention delays before a lever press allow access to the choice stimuli, the rat could not position itself by the correct panel during the retention delay. Rats were able to learn this task readily and perform above chance over delays of up to 16 sec, even though the task demands were likely to restrict any motor mediation strategies
Catechol O-methyltransferase gene variant and birth weight predict early-onset antisocial behavior in children with attention-deficit/hyperactivity disorder
No full textContext: Early-onset antisocial behavior accompanied by attention-deficit/hyperactivity disorder is a clinically severe variant of antisocial behavior that is associated with a particularly poor outcome. Identifying early predictors is thus important. Genetic and prenatal environmental risk factors and prefrontal cortical function are thought to contribute. Recent evidence suggests that prefrontal cortical function is influenced by a valine/methionine variant in the catechol O-methyltransferase (COMT) gene. Objective: To test the a priori hypothesis that this genetic variant predicts early-onset antisocial behavior in a high-risk sample and further examine the effects of birth weight, an environmentally influenced index of prenatal adversity previously linked to childhood disruptive behaviors and genotype x birth weight interaction. Design, Setting, and Participants: A family-based genetic study was undertaken between 1997 and 2003. Participants were prospectively recruited from child and adolescent psychiatry and child health clinics in the United Kingdom and included 240 clinic children who met diagnostic criteria for attention-deficit/hyperactivity disorder or hyperkinetic disorder. Participants underwent comprehensive standardized assessments including measures of antisocial behavior and IQ. Main Outcome Measure: DSM-IV symptoms of childhood-onset conduct disorder rated by trained interviewers using a standard diagnostic interview. Results: The results show main effects of the COMT gene variant (P = .002), birth weight (P = .002), and a significant gene x environment (COMT x birth weight) interaction (P = .006). Conclusions: Early-onset antisocial behavior in a high-risk clinical group is predicted by a specific COMT gene variant previously linked with prefrontal cortical function and birth weight, and those possessing the val/val genotype are more susceptible to the adverse effects of prenatal risk as indexed by lower birth weight. <br/
Mapping recognition memory in the primate brain: why it’s sometimes right to be wrong
No full textIt has been acerbically observed that the importance of a piece of research can be measured by the length of time that it holds up progress in that field. Although the comment was supposed to be sardonic, it does hold a grain of truth. This is because being wrong can be enormously helpful in advancing a field, just as long as the ideas are clearly formulated and testable. My ‘Twentieth Century Highlight’ is a study [4] where the findings were correct but their interpretation was utterly wrong.
By the 1960s it was accepted that the temporal lobes contain at least one structure vital for episodic memory, and that the hippocampus was the most probable candidate. Much of the evidence came from amnesic patients with damage in the temporal lobes, including the famous case H.M [9]. Unfortunately, the neuropathological data could not resolve the issue and it became apparent that lesion studies with nonhuman primates might offer a more direct approach. A series of studies in the 1960s and 1970s studied the cognitive effects of hippocampal lesions in monkeys but the impairments on tasks like visual discriminations and delayed response seemed very mild when compared to the clinical condition, and it seemed impossible to model anterograde amnesia.
The breakthrough came in 1978 with a paper by Mortimer Mishkin who reported that separate removals of the hippocampus and amygdala led to very mild deficits on a test of recognition memory, yet joint removal of the two structures had a devastating effect [4]. Parallel findings were reported for tests of associative memory [7] and tactile recognition [8], so strengthening the case that joint limbic pathology was responsible for temporal lobe global amnesia. This was a totally new concept, yet it seemed to make sense of a great deal of the neuropathological data and rapidly became the dominant viewpoint.
The 1978 study was a landmark because it not only showed that animal studies could model aspects of anterograde amnesia but it also highlighted the importance of selecting the right behavioural test for a given question. Thus a behavioural assay for amnesia did not simply consist of any task involving learning—what was needed was a test that measured a function severely disrupted in anterograde amnesia, and such a test became possible with the development of a behavioural test of visual recognition [2] , [5] and [6] . Recognition memory is typically lost in amnesia and this study was one of the first to examine this aspect of memory in animals. Nowadays, so much more is known about spared forms of learning in amnesia that the need to tailor behavioural tests more precisely seems obvious but this was not always so.
There is, however, a twist in the tale. As researchers pioneered ways of making more and more selective cortical and subcortical lesions in the temporal lobes a quite extraordinary fact emerged. Painstaking work by Murray and Mishkin at NIH and by Zola and Squire in San Diego [10] and [11] showed that circumscribed lesions of the amygdala and hippocampus alone had little, if any, additive effect contrary to the interpretation by Mishkin [4]. In fact, the critical regions for recognition proved to be not the hippocampus and amygdala but the perirhinal cortex and, to a lesser extent, the entorhinal cortex [3]. These rhinal regions, which lie just ventral to the amygdala and hippocampus, had been completely overlooked when interpreting the original study even though they had been removed. This was because almost all of the previous evidence had pointed to the hippocampus itself and next to nothing was known about any independent functions of the rhinal cortices. Since then the perirhinal cortex has proved to be critical for more than one mnemonic function, indicating that the amnesic syndrome can be further fractionated [1]. The discovery that the hippocampus and amygdala need not be critical for recognition in monkeys reaffirms one of Sherlock Holmes’ most famous maxims that “when you have eliminated all which is impossible, then whatever remains, however improbable, must be the truth”
Delayed non matching to sample in a novel automated visual memory apparatus using mixed retention intervals
No full textNine naive rats of the PVG strain were trained to non-match to sample in a visual automated apparatus using repeated stimuli. Their memory was then tested at different retention delays (0, 2, 4, 8, 12 sec) presented in mixed order within a session. The duration of the intertrial intervals (ITI= 30 sec) was adjusted to the duration of the next retention interval (RT) in order to equilibrate proactive interference across the different delays (ITI= 30 sec + next RT). The rats learned quickly to non-match to sample and performed the memory task well above the chance level at different retention intervals (in every session each rat achieved a score of 69% or more for at least one delay). However, their memory performance was independent of the duration of the retention interval. In the present paper, we describe the conditions under which these rats were trained and their memory tested
- …
