Neural Signature of Taste Familiarity in the Gustatory Cortex of the Freely Behaving Rat

2004 ◽  
Vol 92 (6) ◽  
pp. 3298-3308 ◽  
Author(s):  
Amir Bahar ◽  
Yadin Dudai ◽  
Ehud Ahissar

Ample data indicate that the gustatory cortex (GC) subserves the processing, encoding, and storage of taste information. To further elucidate the neural processes involved, we recorded multi-unit activity in the GC of the freely behaving rat as it became familiar with a novel tastant. Exposure to the tastant was performed over three 40- to 50-min sessions, 24 h apart. In each session, the tastant was presented repeatedly, 1 s at a time, with 10- to 12-s inter-trial intervals. The neural response to the tastant typically lasted 7 s. Our results show that the average neuronal response to the tastant increased as this tastant became familiar, but this increase was detected only during the last 5 s of the response. The increased response was not generalized to another tastant. Furthermore, our analysis suggests that specific neuronal populations subserve the processing of familiarity of specific tastants. The signature of familiarity was not detected in the course of the familiarization session, but only on the subsequent day, suggesting that its development involves slow post-acquisition processes. Our data are in line with the notion that GC neurons process multiple taste attributes, familiarity included, during different temporal phases of their response. The data also suggest that by default the brain considers a taste stimulus as novel, unless proven otherwise.

1981 ◽  
Vol 213 (1191) ◽  
pp. 101-137 ◽  

Learning is a complex set of processes involving the acquisition and storage of information. Imprinting in the domestic chick was studied to analyse the neural basis of storage. The recently hatched chick learns the characteristics of a visually conspicuous object by being exposed to it. When a chick is trained in this way, biochemical changes can be detected in the dorsal part of the forebrain. Through a series of experiments it was shown that these changes are unlikely to be non-specific consequences of training, but more probably reflect some aspect of the storage process. By using a radioautographic technique to localize the brain region more precisely, part of the hyperstriatum ventrale was implicated in this process. Bilateral destruction of the region before imprinting prevented acquisition, and bilateral destruction after imprinting impaired retention. After exposure for 140 min to an imprinting stimulus there was an increase in the area of contact between presynaptic and postsynaptic elements in the region. This effect was found on the left side only. Sequential lesions to left and right sides confirmed that there is a hemispheric asymmetry in the role of the region in the storage of information. The area receives input from the visual pathways and possibly from other sensory pathways, and projects to regions that are thought to be involved in the control of locomotor and viscero-endocrine functions. The results afford an opportunity for the further analysis both of storage and of the whole set of neural processes that underlie imprinting in the domestic chick.


Author(s):  
Markus Heilig ◽  
James MacKillop ◽  
Diana Martinez ◽  
Jürgen Rehm ◽  
Lorenzo Leggio ◽  
...  

AbstractThe view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.


2014 ◽  
Vol 5 (5) ◽  
pp. 371-382 ◽  
Author(s):  
Suyan Li ◽  
Sampada Joshee ◽  
Anju Vasudevan

AbstractMidbrain GABA neurons, endowed with multiple morphological, physiological and molecular characteristics as well as projection patterns are key players interacting with diverse regions of the brain and capable of modulating several aspects of behavior. The diversity of these GABA neuronal populations based on their location and function in the dorsal, medial or ventral midbrain has challenged efforts to rapidly uncover their developmental regulation. Here we review recent developments that are beginning to illuminate transcriptional control of GABA neurons in the embryonic midbrain (mesencephalon) and discuss its implications for understanding and treatment of neurological and psychiatric illnesses.


Author(s):  
Anastasia O. Shabalina ◽  

The article considers the main arguments against the neurobiological theory of consciousness from the point of view of the enactivist approach within the philosophy of mind. The neurobiological theory of consciousness, which reduces consciousness to neural activity, is currently the dominant approach to the mind-body problem. The neurobiological theory emerged as a result of advances in research on the phenomena of consciousness and through the development of technologies for visualizing the internal processes of mind. However, at the very heart of this theory, there is a number of logical contradictions. The non-reductive enactivist approach to consciousness, introduced in this article, contributes to the existing argumentation against the reduction of consciousness to neural processes with remonstrations that take into account the modern neuroscientific data. The article analyzes the argumentation of the sensorimotor enactivism developed by A. Noe and offers the account of the teleosemantic approach to the concept of information provided by R. Cao. The key problems of the neurobiological theory of consciousness are highlighted, and the objections emerging within the framework of the enactivist approach are analyzed. Since the main concepts on which the neural theory is based are the concepts of neural substrate, cognition as representation, and information as a unit of cognition, the author of the article presents three key enactivist ideas that oppose them. First, the enactivist concept of cognition as action allows us to consider the first-person experience as a mode of action, and not as a state of the brain substrate. Second, the article deals with the “explanatory externalism” argument proposed by Noe, who refutes the image of cognition as a representation in the brain. Finally, in order to critically revise the concept of information as a unit of cognition, the author analyzes Cao’s idea, which represents a teleosemantic approach, but is in line with the general enactivist argumentation. Cao shows that the application of the concept “information” to neural processes is problematic: no naturalized information is found in the brain as a physical substrate. A critical revision of beliefs associated with the neural theory of consciousness leads us to recognize that there are not enough grounds for reducing consciousness to processes that take place in the brain. That is why Noe calls expectations that the visualization of processes taking place in the brain with the help of the modern equipment will be able to depict the experience of consciousness the “new phrenology”, thus indicating the naive character of neural reduction. The article concludes that natural science methods are insufficient for the study of consciousness.


2021 ◽  
Vol 11 ◽  
Author(s):  
Orestis Stylianou ◽  
Frigyes Samuel Racz ◽  
Andras Eke ◽  
Peter Mukli

While most connectivity studies investigate functional connectivity (FC) in a scale-dependent manner, coupled neural processes may also exhibit broadband dynamics, manifesting as power-law scaling of their measures of interdependence. Here we introduce the bivariate focus-based multifractal (BFMF) analysis as a robust tool for capturing such scale-free relations and use resting-state electroencephalography (EEG) recordings of 12 subjects to demonstrate its performance in reconstructing physiological networks. BFMF was employed to characterize broadband FC between 62 cortical regions in a pairwise manner, with all investigated connections being tested for true bivariate multifractality. EEG channels were also grouped to represent the activity of six resting-state networks (RSNs) in the brain, thus allowing for the analysis of within- and between- RSNs connectivity, separately. Most connections featured true bivariate multifractality, which could be attributed to the genuine scale-free coupling of neural dynamics. Bivariate multifractality showed a characteristic topology over the cortex that was highly concordant among subjects. Long-term autocorrelation was higher in within-RSNs, while the degree of multifractality was generally found stronger in between-RSNs connections. These results offer statistical evidence of the bivariate multifractal nature of functional coupling in the brain and validate BFMF as a robust method to capture such scale-independent coupled dynamics.


2020 ◽  
Author(s):  
Thomas L. Botch ◽  
Alina Spiegel ◽  
Catherine Ricciardi ◽  
Caroline E. Robertson

AbstractBumetanide has received much interest as a potential pharmacological modulator of the putative imbalance in excitatory/inhibitory (E/I) signaling that is thought to characterize autism spectrum conditions. Yet, currently, no studies of bumetanide efficacy have used an outcome measure that is modeled to depend on E/I balance in the brain. In this manuscript, we present the first causal study of the effect of bumetanide on an objective marker of E/I balance in the brain, binocular rivalry, which we have previously shown to be sensitive to pharmacological manipulation of GABA. Using a within-subjects placebo-control crossover design study, we show that, contrary to expectation, acute administration of bumetanide does not alter binocular rivalry dynamics in neurotypical adult individuals. Neither changes in response times nor response criteria can account for these results. These results raise important questions about the efficacy of acute bumetanide administration for altering E/I balance in the human brain, and highlight the importance of studies using objective markers of the underlying neural processes that drugs hope to target.


1969 ◽  
Vol 40 (1) ◽  
pp. 124-133
Author(s):  
Lina Vanessa Becerra ◽  
Hernán José Pimienta

Programmed cell death occurs as a physiological process during development. In the brain and spinal cord this event determines the number and location of the different cell types. In adulthood, programmed cell death or apoptosis is more restricted but it may play a major role in different acute and chronic pathological entities. However, in contrast to other tissues where apoptosis has been widely documented from a morphological point of view, in the central nervous system complete anatomical evidence of apoptosis is scanty. In spite of this there is consensus about the activation of different signal systems associated to programmed cell death. In the present article we attempt to summarize the main apoptotic pathways so far identified in nervous tissue. Considering that apoptotic pathways are multiple, the neuronal cell types are highly diverse and specialized and that neuronal response to injury and survival depends upon tissue context, (i.e., preservation of connectivity, glial integrity and cell matrix, blood supply and trophic factors availability) what is relevant for the apoptotic process in a sector of the brain may not be important in another.


2018 ◽  
Author(s):  
Andreea Lazar ◽  
Chris Lewis ◽  
Pascal Fries ◽  
Wolf Singer ◽  
Danko Nikolić

SummarySensory exposure alters the response properties of individual neurons in primary sensory cortices. However, it remains unclear how these changes affect stimulus encoding by populations of sensory cells. Here, recording from populations of neurons in cat primary visual cortex, we demonstrate that visual exposure enhances stimulus encoding and discrimination. We find that repeated presentation of brief, high-contrast shapes results in a stereotyped, biphasic population response consisting of a short-latency transient, followed by a late and extended period of reverberatory activity. Visual exposure selectively improves the stimulus specificity of the reverberatory activity, by increasing the magnitude and decreasing the trial-to-trial variability of the neuronal response. Critically, this improved stimulus encoding is distributed across the population and depends on precise temporal coordination. Our findings provide evidence for the existence of an exposure-driven optimization process that enhances the encoding power of neuronal populations in early visual cortex, thus potentially benefiting simple readouts at higher stages of visual processing.


2019 ◽  
Author(s):  
Faisal Mushtaq ◽  
Samuel D. McDougle ◽  
Matt P. Craddock ◽  
Darius E. Parvin ◽  
Jack Brookes ◽  
...  

AbstractLosing a point playing tennis may result from poor shot selection or poor stroke execution. To explore how the brain responds to these different types of errors, we examined EEG signatures of feedback-related processing while participants performed a simple decision-making task. In Experiment 1, we used a task in which unrewarded outcomes were framed as selection errors, similar to how feedback information is treated in most studies. Consistent with previous work, EEG differences between rewarded and unrewarded trials in the medial frontal negativity (MFN) correlated with behavioral adjustment. In Experiment 2, the task was modified such that unrewarded outcomes could arise from either poor execution or selection. For selection errors, the results replicated that observed in Experiment 1. However, unrewarded outcomes attributed to poor execution produced larger amplitude MFN, alongside an attenuation in activity preceding this component and a subsequent enhanced error positivity (Pe) response in posterior sites. In terms of behavioral correlates, only the degree of the early attenuation and amplitude of the Pe correlated with behavioral adjustment following execution errors relative to reward; the amplitude of the MFN did not correlate with behavioral changes related to execution errors. These results indicate the existence of distinct neural correlates of selection and execution error processing and are consistent with the hypothesis that execution errors can modulate action selection evaluation. More generally, they provide insight into how the brain responds to different classes of error that determine future action.Significance StatementTo learn from mistakes, we must resolve whether decisions that fail to produce rewards are due to poorly selected action plans or badly executed movements. EEG data were obtained to identify and compare the physiological correlates of selection and execution errors, and how these are related to behavioral changes. A neural signature associated with reinforcement learning, a medial frontal negative (MFN) ERP deflection, correlated with behavioral adjustment after selection errors relative to reward outcomes, but not motor execution errors. In contrast, activity preceding and following the MFN response correlated with behavioral adjustment after execution errors relative to reward. These results provide novel insight into how the brain responds to different classes of error that determine future action.


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