Construction and disruption of spatial memory networks during development

Abstract

Spatial memory, the aspect of memory involving encoding and retrieval of information regarding one's environment and spatial orientation, is a complex biological function incorporating multiple neuronal networks. Hippocampus-dependent spatial memory is not innate and emerges during development in both humans and rodents. In children, nonhippocampal dependent egocentric (self-to-object) memory develops before hippocampal-dependent allocentric (object-to-object) memory. The onset of allocentric spatial memory abilities in children around 22 mo of age occurs at an age-equivalent time in rodents when spatially tuned grid and place cells arise from patterned activity propagating through the entorhinal-hippocampal circuit. Neuronal activity, often driven by specific sensory signals, is critical for the normal maturation of brain circuits This patterned activity fine-tunes synaptic connectivity of the network and drives the emergence of specific firing necessary for spatial memory. Whereas normal activity patterns are required for circuit maturation, aberrant neuronal activity during development can have major adverse consequences, disrupting the development of spatial memory. Seizures during infancy, involving massive bursts of synchronized network activity, result in impaired spatial memory when animals are tested as adolescents or adults. This impaired spatial memory is accompanied by alterations in spatial and temporal coding of place cells. The molecular mechanisms by which early-life seizures lead to disruptions at the cellular and network levels are now becoming better understood, and provide a target for intervention, potentially leading to improved cognitive outcome in individuals experiencing early-life seizures.

Microcircuits for spatial coding in the medial entorhinal cortex

“…A full discussion of grid cell models is beyond the scope of this review [see e.g. (14,(46)(47)(48)(49)], in which we will focus on local excitatory and inhibitory microcircuits in the mature animal, and the extent to which they exhibit connectivity consistent with CAN dynamics. Although there is a large body of work on spatial coding and microcircuits in the MEC or its functional analogues in species ranging from the fly [e.g.…”

Changes in Representation of Thalamic Projection Neurons within Prefrontal-Thalamic-Hippocampal Circuitry in a Rat Model of Third Trimester Binge Drinking

“…Alcohol is widely recognized to have negative effects on wellbeing, with any amount of alcohol exposure (AE) ultimately having a net negative impact on health [ 1 ]. Considering the critical role that early life experiences have in shaping brain development throughout the lifespan [ 2 , 3 ], fetal AE poses substantial risk to the developing brain [ 4 ]. Exposure to alcohol in utero causes a spectrum of physiological, neurological, and behavioral outcomes [ 5 , 6 ], referred to as “Fetal Alcohol Spectrum Disorders” (FASD).…”

A Unique Mouse Model of Early Life Exercise Enables Hippocampal Memory and Synaptic Plasticity

“…In humans, neuronal differentiation and synaptogenesis within hippocampus reach adult levels around 3-5 years of age 27 , which is around the time children are able to reliably form long-term spatial memory 28 . In rodents, the hippocampus reaches milestones in synapse density and circuit refinement during the 3 rd to 4 th postnatal weeks (reviewed in 29,30 ) which coincides with development of stable long-term potentiation (LTP 31,32 ) and establishment of learning and memory functions 33,34 . A characteristic of postnatal brain maturation is synaptic overproduction and subsequent pruning 35 , thus rendering these developmental processes exquisitely sensitive to environmental experiences 36 .…”