Biology subjects

Arieli, E.

Publications and source records attributed to Arieli, E..

3 recordsLinked to original sources

bioRxiv2021

Distinct progressions of neuronal activity changes underlie the formation and consolidation of a gustatory associative memory

Acquiring new memories is a multi-stage process. Ample of studies have convincingly demonstrated that initially acquired memories are labile, and only stabilized by later consolidation processes. These multiple phases of memory formation are known to involve modification of both cellular excitability and synaptic connectivity, which in turn change neuronal activity at both the single neuron and ensemble levels. However, the specific mapping between the known phases of memory and the observed changes in neuronal activity remains unknown. Here we address this unknown in the context of conditioned taste aversion learning by continuously tracking gustatory cortex (GC) neuronal taste responses from alert rats in the 24 hours following a taste-malaise pairing. We found that the progression of neuronal activity changes in the GC depend on the neuronal organizational level. The population response changed continuously; these changes, however, were only reflected in the population mean amplitude during the acquisition and consolidation phases, and in the known quickening of the ensemble state dynamics after the time of consolidation. Together our results demonstrate how complex dynamics in different representational level of cortical activity underlie the formation and stabilization of memory within the cortex. Significant StatementMemories are formed through a multi-phase process; an early initial acquired memory consolidates into a stable form over hours and days. While the underlying phase-specific molecular pathways are fairly known, the neuronal activity changes during these different phases remain elusive. Here we studied this unknown by tracking cortical neuronal activity over 24h as the taste becomes aversive following association with malaise. We found that that the progression of activity changes is organization-level dependent: The population response changed continuously; the population mean amplitude was time-locked to the acquisition and consolidation phases, and the quickening of the known ensemble state dynamics appear only after consolidation. Our results reveal the complex organizational-level neuronal interactions that underlie the progression of memory formation.

neuroscience↗

bioRxiv2021

ApoE4 attenuates cortical neuronal activity and impairs memory in young apoE4 rats

The E4 allele of apolipoprotein E (apoE4) is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, apoE4 may cause innate brain abnormalities before the appearance of AD related neuropathology. Understanding these primary dysfunctions is vital for early detection of AD and the development of therapeutic strategies for it. Recently we have shown impaired extra-hippocampal memory in young apoE4 mice - a deficit that was correlated with attenuated structural pre-synaptic plasticity in cortical and subcortical regions. Here we test the hypothesis that these early structural deficits impact learning via changes in basal and stimuli evoked neuronal activity. We recorded extracellular neuronal activity from the gustatory cortex (GC) of three-month-old humanized apoE4 and wildtype rats, before and after conditioned taste aversion (CTA) training. Despite normal sucrose drinking behavior before CTA, young apoE4 rats showed impaired CTA learning, consistent with our previous results in apoE4 mice. This behavioral deficit was correlated with decreased basal and taste-evoked firing rates in both putative excitatory and inhibitory GC neurons. Single neuron and ensemble analyses of taste coding demonstrated that apoE4 neurons could be used to correctly classify tastes, but were unable to undergo plasticity to support learning. Our results suggest that apoE4 impacts brain excitability and plasticity early in life and may act as an initiator for later AD pathologies. Significant statementThe ApoE4 allele is the strongest genetic risk-factor for late-onset Alzheimers disease (AD), yet the link between apoE4 and AD is still unclear. Recent molecular and in-vitro studies suggest that apoE4 interferes with normal brain functions decades before the development of its related AD neuropathology. Here we recorded the activity of cortical neurons from young apoE4 rats during extra-hippocampal learning to study early apoE4 neuronal activity abnormalities, and their effects over coding capacities. We show that apoE4 drastically reduces basal and stimuli-evoked cortical activity in both excitatory and inhibitory neurons. The apoE4-induced activity attenuation did not prevent coding of stimuli identity and valence, but impaired capacity to undergo activity changes to support learning. Our findings support the hypothesis that apoE4 interfere with normal neuronal plasticity early in life; a deficit that may lead to late-onset AD development.

neuroscience↗

bioRxiv2020

Temporally-precise basolateral amygdala activation is required for the formation of taste memories in the gustatory cortex

Learning to associate malaise with the intake of novel food is critical for survival. Since food poisoning may take hours to affect, animals developed brain circuits to transform the current novel taste experience into a taste memory trace (TMT) and bridge this time lag. Ample studies showed that the basolateral amygdala (BLA), the nucleus basalis magnocellularis (NBM) and the gustatory cortex (GC) are involved in TMT formation and taste-malaise association. However, how dynamic activity across these brain regions during novel taste experience promotes the formation of these memories is currently unknown. We used the conditioned taste aversion (CTA) learning paradigm in combination with short-term optogenetics and electrophysiological recording in rats to test the hypothesis that temporally specific activation of BLA projection neurons is essential for TMT formation in the GC, and consequently CTA. We found that late-epoch (LE, >800ms), but not the early epoch (EE, 200-700ms), BLA activation during novel taste experience is essential for normal CTA, for early c-Fos expression in the GC (a marker of TMT formation) and for the subsequent changes in GC ensemble palatability coding. Interestingly, BLA activity was not required for intact taste identity or palatability perceptions. We further show that BLA-LE information is transmitted to GC through the BLA[->]NBM pathway where it affects the formation of taste memories. These results expose the dependence of long-term memory formation on specific temporal windows during sensory responses and the distributed circuits supporting this dependence. SignificanceConsumption of a novel taste may result in malaise and poses a threat to animals. Since the effects of poisoning appear only hours after consumption, animals must store the novel tastes information in memory until they associate it with its value (nutritious or poisonous). Here we elucidate the neuronal activity patterns and circuits that support the processing and creation of novel-taste memories in rats. Our results show that specific patterns of temporal activation in the basolateral amygdala transmitted across brain areas are important for formation of taste memory and taste-malaise association. These findings may shed light on long-term activity-to-memory transformation in other sensory modalities.

neuroscience↗