scholarly journals Beyond Labeled Lines: A population coding account of the Thermal Grill Illusion

2019 ◽  
Author(s):  
Francesca Fardo ◽  
Brianna Beck ◽  
Micah Allen ◽  
Nanna Brix Finnerup

Heat and pain illusions can be generated by simultaneous cold and warm stimulation on the skin, at temperatures that would normally be perceived as innocuous in isolation (e.g., ‘synthetic heat’ and the ‘thermal grill illusion’). Historically, two key questions have dominated the literature: Which specific pathway conveys the illusory perception of heat and pain? Where specifically does the illusory pain originate in the central nervous system? Two major theories – the addition and the disinhibition theories – have suggested distinct pathways, as well as specific spinal or supraspinal mechanisms. However, both theories fail to fully explain experimental findings on illusory heat and pain phenomena. We suggest that the disagreement between previous theories and experimental evidence can be solved by abandoning the assumption of one-to-one relations between pathways and perceived qualities. We argue that a population coding framework, based on distributed activity across non-nociceptive and nociceptive pathways, offers a more powerful explanation of illusory heat and pain. This framework offers new hypotheses regarding the neural mechanisms underlying temperature and pain perception.

Cephalalgia ◽  
2002 ◽  
Vol 22 (2) ◽  
pp. 117-124 ◽  
Author(s):  
PD Drummond

The aim of this study was to determine whether scalp tenderness and photophobia, two well-recognized symptoms of migraine, develop during the motion sickness induced by optokinetic stimulation. To investigate whether motion sickness has a general influence on pain perception, pain was also assessed in the fingertips. After optokinetic stimulation, nausea increased more and headache persisted longer in 21 migraine sufferers than in 15 non-headache controls. Scalp tenderness increased during optokinetic stimulation in nauseated subjects, and pain in the fingertips increased more and photophobia persisted longer in migraine sufferers than controls. These findings suggest that the disturbance responsible for nausea also sensitizes trigeminal nociceptive neurones or releases inhibitory controls on their discharge. A low nausea threshold and a propensity for sensitization to develop rapidly in nociceptive pathways may increase susceptibility to migraine.


2021 ◽  
Vol 12 ◽  
Author(s):  
Roberta Lattanzi ◽  
Cinzia Severini ◽  
Daniela Maftei ◽  
Luciano Saso ◽  
Aldo Badiani

The prokineticin (PK) family, prokineticin 1 and Bv8/prokineticin 2 (PROK2), initially discovered as regulators of gastrointestinal motility, interacts with two G protein-coupled receptors, PKR1 and PKR2, regulating important biological functions such as circadian rhythms, metabolism, angiogenesis, neurogenesis, muscle contractility, hematopoiesis, immune response, reproduction and pain perception. PROK2 and PK receptors, in particular PKR2, are widespread distributed in the central nervous system, in both neurons and glial cells. The PROK2 expression levels can be increased by a series of pathological insults, such as hypoxia, reactive oxygen species, beta amyloid and excitotoxic glutamate. This suggests that the PK system, participating in different cellular processes that cause neuronal death, can be a key mediator in neurological/neurodegenerative diseases. While many PROK2/PKRs effects in physiological processes have been documented, their role in neuropathological conditions is not fully clarified, since PROK2 can have a double function in the mechanisms underlying to neurodegeneration or neuroprotection. Here, we briefly outline the latest findings on the modulation of PROK2 and its cognate receptors following different pathological insults, providing information about their opposite neurotoxic and neuroprotective role in different pathological conditions.


Author(s):  
Michael J. Aminoff

In 1811, Bell had printed privately a monograph titled Idea of a New Anatomy of the Brain. In it, Bell correctly showed that the anterior but not the posterior roots had motor functions. François Magendie subsequently showed that the anterior roots were motor, and the posterior roots were sensory. This led to a dispute about priority during which Bell republished some of his early work with textual alterations to support his claims. Bell was involved in a similar dispute with Herbert Mayo concerning the separate functions of the fifth (sensory) and seventh (motor) cranial nerves, and Mayo today is a forgotten man. In both instances, Bell deserves credit for the concepts and initial experimental approach, and Magendie and Mayo deserve credit for obtaining and correctly interpreting the definitive experimental findings.


2018 ◽  
Vol 73 (Suppl. 5) ◽  
pp. 43-52 ◽  
Author(s):  
John D. Fernstrom

The non-essential amino acid glutamate participates in numerous metabolic pathways in the body. It also performs important physiologic functions, which include a sensory role as one of the basic tastes (as monosodium glutamate [MSG]), and a role in neuronal function as the dominant excitatory neurotransmitter in the central nervous system. Its pleasant taste (as MSG) has led to its inclusion as a flavoring agent in foods for centuries. Glutamate’s neurotransmitter role was discovered only in the last 60 years. Its inclusion in foods has necessitated its safety evaluation, which has raised concerns about its transfer into the blood ultimately increasing brain glutamate levels, thereby causing functional disruptions because it is a neurotransmitter. This concern, originally raised almost 50 years ago, has led to an extensive series of scientific studies to examine this issue, conducted primarily in rodents, non-human primates, and humans. The key findings have been that (a) the ingestion of MSG in the diet does not produce appreciable increases in glutamate concentrations in blood, except when given experimentally in amounts vastly in excess of normal intake levels; and (b) the blood-brain barrier effectively restricts the passage of glutamate from the blood into the brain, such that brain glutamate levels only rise when blood glutamate concentrations are raised experimentally via non-physiologic means. These and related discoveries explain why the ingestion of MSG in the diet does not lead to an increase in brain glutamate concentrations, and thus does not produce functional disruptions in brain. This article briefly summarizes key experimental findings that evaluate whether MSG in the diet poses a threat to brain function.


2019 ◽  
Vol 130 (4) ◽  
pp. 634-650 ◽  
Author(s):  
Heberto Suarez-Roca ◽  
Rebecca Y. Klinger ◽  
Mihai V. Podgoreanu ◽  
Ru-Rong Ji ◽  
Martin I. Sigurdsson ◽  
...  

Abstract Baroreceptors are mechanosensitive elements of the peripheral nervous system that maintain homeostasis by coordinating physiologic responses to external and internal stimuli. While it is recognized that carotid and cardiopulmonary baroreceptor reflexes modulate autonomic output to mitigate excessive fluctuations in arterial blood pressure and to maintain intravascular volume, increasing evidence suggests that baroreflex pathways also project to key regions of the central nervous system that regulate somatosensory, somatomotor, and central nervous system arousal. In addition to maintaining autonomic homeostasis, baroreceptor activity modulates the perception of pain, as well as neuroimmune, neuroendocrine, and cognitive responses to physical and psychologic stressors. This review summarizes the role that baroreceptor pathways play in modulating acute and chronic pain perception. The contribution of baroreceptor function to postoperative outcomes is also presented. Finally, methods that enhance baroreceptor function, which hold promise in improving postoperative and pain management outcomes, are presented.


2006 ◽  
Vol 18 (8) ◽  
pp. 1951-1986 ◽  
Author(s):  
Maoz Shamir ◽  
Haim Sompolinsky

In many cortical and subcortical areas, neurons are known to modulate their average firing rate in response to certain external stimulus features. It is widely believed that information about the stimulus features is coded by a weighted average of the neural responses. Recent theoretical studies have shown that the information capacity of such a coding scheme is very limited in the presence of the experimentally observed pairwise correlations. However, central to the analysis of these studies was the assumption of a homogeneous population of neurons. Experimental findings show a considerable measure of heterogeneity in the response properties of different neurons. In this study, we investigate the effect of neuronal heterogeneity on the information capacity of a correlated population of neurons. We show that information capacity of a heterogeneous network is not limited by the correlated noise, but scales linearly with the number of cells in the population. This information cannot be extracted by the population vector readout, whose accuracy is greatly suppressed by the correlated noise. On the other hand, we show that an optimal linear readout that takes into account the neuronal heterogeneity can extract most of this information. We study analytically the nature of the dependence of the optimal linear readout weights on the neuronal diversity. We show that simple online learning can generate readout weights with the appropriate dependence on the neuronal diversity, thereby yielding efficient readout.


2004 ◽  
Vol 286 (2) ◽  
pp. H584-H601 ◽  
Author(s):  
K. Lu ◽  
J. W. Clark ◽  
F. H. Ghorbel ◽  
C. S. Robertson ◽  
D. L. Ware ◽  
...  

The goal of this work is to study the cerebral autoregulation, brain gas exchange, and their interaction by means of a mathematical model. We have previously developed a model of the human cardiopulmonary (CP) system, which included the whole body circulatory system, lung and peripheral tissue gas exchange, and the central nervous system control of arterial pressure and ventilation. In this study, we added a more detailed description of cerebral circulation, cerebrospinal fluid (CSF) dynamics, brain gas exchange, and cerebral blood flow (CBF) autoregulation. Two CBF regulatory mechanisms are included: autoregulation and CO2 reactivity. Central chemoreceptor control of ventilation is also included. We first established nominal operating conditions for the cerebral model in an open-loop configuration using data generated by the CP model as inputs. The cerebral model was then integrated into the larger CP model to form a new integrated CP model, which was subsequently used to study cerebral hemodynamic and gas exchange responses to test protocols commonly used in the assessment of CBF autoregulation (e.g., carotid artery compression and the thigh-cuff deflation test). The model can closely mimic the experimental findings and provide biophysically based insights into the dynamics of cerebral autoregulation and brain tissue gas exchange as well as the mechanisms of their interaction during test protocols, which are aimed at assessing the degree of autoregulation. With further refinement, our CP model may be used on measured data associated with the clinical evaluation of the cerebral autoregulation and brain oxygenation in patients.


2016 ◽  
Vol 74 (8) ◽  
pp. 671-678 ◽  
Author(s):  
Roberto E. Sica ◽  
Roberto Caccuri ◽  
Cecilia Quarracino ◽  
Francisco Capani

ABSTRACT Experimental evidence suggests that astrocytes play a crucial role in the physiology of the central nervous system (CNS) by modulating synaptic activity and plasticity. Based on what is currently known we postulate that astrocytes are fundamental, along with neurons, for the information processing that takes place within the CNS. On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson’s disease, Alzheimer’s dementia, Huntington’s dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. This hypothesis is supported by observations that demonstrated that the killing of neurons by non-neural cells plays a major role in the pathogenesis of those diseases, at both their onset and their progression. Furthermore, recent findings suggest that astrocytes might be involved in the pathogenesis of some psychiatric disorders as well.


2021 ◽  
Author(s):  
Sofia Pimpinella ◽  
Niccolò Zampieri

AbstractSomatosensory neurons detect vital information about the environment and internal status of the body, such as temperature, touch, itch and proprioception. The circuit mechanisms controlling the coding of somatosensory information and the generation of appropriate behavioral responses are not clear yet. In order to address this issue, it is important to define the precise connectivity patterns between primary sensory afferents dedicated to the detection of different stimuli and recipient neurons in the central nervous system. In this study we used a rabies tracing approach for mapping spinal circuits receiving sensory input from distinct, genetically defined, modalities. We analyzed the anatomical organization of spinal circuits involved in coding of thermal and mechanical stimuli and showed that somatosensory information from distinct modalities is relayed to partially overlapping ensembles of interneurons displaying stereotyped laminar organization, thus highlighting the importance of positional features and population coding for the processing and integration of somatosensory information.


2021 ◽  
Vol 8 ◽  
Author(s):  
Nimesha Tadepalle ◽  
Elena I. Rugarli

Hereditary spastic paraplegias (HSPs) are genetically heterogeneous conditions caused by the progressive dying back of the longest axons in the central nervous system, the corticospinal axons. A wealth of data in the last decade has unraveled disturbances of lipid droplet (LD) biogenesis, maturation, turnover and contact sites in cellular and animal models with perturbed expression and function of HSP proteins. As ubiquitous organelles that segregate neutral lipid into a phospholipid monolayer, LDs are at the cross-road of several processes including lipid metabolism and trafficking, energy homeostasis, and stress signaling cascades. However, their role in brain cells, especially in neurons remains enigmatic. Here, we review experimental findings linking LD abnormalities to defective function of proteins encoded by HSP genes, and discuss arising questions in the context of the pathogenesis of HSP.


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