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McNaughton, B.

Publications and source records attributed to McNaughton, B..

3 recordsLinked to original sources

Reversible inhibition of medial septum interneurons abolishes initial acquisition of new place-reward associations and reveals a progressive reduction in dependence on medial septal function

Hippocampal place cells encode spatial information within a theta-organized temporal framework paced by the medial septum (MS). Lesions or inactivation of the MS impair spatial learning and disrupt hippocampal theta rhythmicity, long-term potentiation, and plasticity-related gene expression, while often sparing spatially selective firing of CA1 neurons (but not CA3 neurons). Although many rodent studies argue against classical systems consolidation by showing persistent hippocampal dependence of spatial memories, other work has suggested that training structure, spaced vs. massed trials, can influence this dependence. To investigate this possibility, we used DREADD-based, reversible, inhibition of MS GABAergic neurons, some of which are known to project to hippocampus. DREADD activation reduced hippocampal theta power and spatial information encoded by hippocampal neurons while largely preserving overall neuronal firing. We then examined the effect of inhibition of medial septal GABAergic neurons on learning the correct goal arm in an 8-arm maze when the correct arm was randomly changed each day. On each day, the mice were given two forced-choice trials indicating the correct arm and then 5 free-choice trials (without correction) and were always started from an opaque cylinder in the maze center, in a random orientation, to eliminate possible use of a simple response strategy. When the correct goal arm varied randomly daily, MS cell inhibition severely and repeatedly impaired acquisition. In contrast, when the correct goal arm was subsequently fixed across days, performance was initially impaired but became resistant to DREADD activation over time. Once performance reached asymptote, the goal arm was switched to a new (random) position. In this case, learning was no longer impaired by DREADD activation. This generalization suggests that repeated fixed-goal training in the same environment induces a broader reorganization of the neural systems supporting spatial behaviour. One possibility is that mice develop a septal-independent task-solving strategy that supports both retrieval of established goal locations and acquisition of new ones within a stable environment. This transition could reflect the gradual adoption of a non-spatial strategy such as visual pattern recognition, or the use of a directional cue. Moving the most salient distal cue in the environment (a single room light) produced a substantial change in the visual configurations seen from the arm entry points, and disrupted performance; however, it did not produce a consistent directional shift relative to the cue, suggesting that the light contributed to an integrated visuo-spatial representation rather than serving as the reference frame origin. We conclude that the mice switched from a hippocampus/MS-dependent spatial strategy to a non-hippocampus-dependent visual pattern matching solution.

neuroscience↗

Cell Surface β-Lactamase Recruitment: A Facile Selection to Identify Protein-Protein Interactions

Protein-protein interactions are central to many cellular processes, and the identification of novel protein-protein interactions is a critical step in the discovery of protein therapeutics. Simple methods to identify naturally existing or laboratory evolved protein-protein interactions are therefore valuable research tools. We have developed a facile selection that links protein-protein interaction-dependent {beta}-lactamase recruitment on the surface of E. coli with resistance to ampicillin. Bacteria displaying a protein which form a complex with a specific protein-{beta}-lactamase fusion are protected from ampicillin-dependent cell death. In contrast, bacteria that do not recruit {beta}-lactamase to the cell surface are killed by ampicillin. Given its simplicity and tunability, we anticipate this selection will be a valuable addition to the palette of methods for illuminating and interrogating protein-protein interactions.

biochemistry↗

Impaired Hippocampal-cortical interactions during sleep and memory reactivation without consolidation in a mouse model of Alzheimer’s disease

Spatial learning is impaired in preclinical Alzheimers disease (AD). We reported similar impairments in 3xTg-AD mice learning a spatial reorientation task. Memory reactivation during sleep is critical for learning related plasticity, and memory consolidation is correlated with hippocampal sharp wave ripple (SWR) density, cortical delta waves (DWs), and their temporal coupling - postulated as a physiological substrate of memory consolidation. Finally, hippocampal-cortical dyscoordination is prevalent in individuals with AD. Thus, we hypothesized impaired memory consolidation mechanisms in hippocampal-cortical networks could account for spatial memory deficits. We assessed sleep architecture, SWR/DW dynamics and memory reactivation in a mouse model of tauopathy and amyloidosis implanted with a recording array targeting isocortex and hippocampus. Mice underwent daily recording sessions of rest-task-rest while learning the spatial reorientation task. We assessed memory reactivation by matching activity patterns from the approach to the unmarked reward zone to patterns during slow wave sleep (SWS). AD mice had more SWS, but reduced SWR density. The increased SWS compensated for reduced SWR density so there was no reduction in SWR number. Conversely, DW density was not reduced so the number of DWs was increased. In control mice hippocampal SWR-cortical DW coupling was strengthened in post-task-sleep and was correlated with performance on the spatial reorientation task the following day. However, in AD mice SWR-DW coupling was reduced and not correlated with behavior, suggesting behavioral decoupling. Thus, reduced SWR-DW coupling may cause impaired learning in AD and may serve as a biomarker for early AD related changes.\n\nSignificance StatementUnderstanding the relationship between network dynamics and cognition early in Alzheimers disease progression is critical for identifying therapeutic targets for earlier treatment. We assessed hippocampal-cortical interactions during sleep in AD mice as a potential cause of early spatial learning and memory deficits. We identified compensatory sleep changes in AD mice, that ameliorated some brain dysfunction. Despite the compensatory changes, impaired spatial navigation and impaired hippocampal-cortical (sharp wave ripple-delta wave) interactions were apparent in AD mice. In control but not AD mice hippocampal-cortical interactions were correlated with performance on the spatial task, the following day, suggesting a potential mechanism of impaired consolidation in AD mice. Thus, changes in hippocampal-cortical brain dynamics during sleep may underlie early memory deficits in AD.

neuroscience↗