Publications by authors named "Tomas Hromadka"

16 Publications

  • Page 1 of 1

Impact of rs243865 and rs3025058 Polymorphisms on Clinical Findings in Alzheimer's Disease Patients.

Mediators Inflamm 2021 19;2021:5573642. Epub 2021 Apr 19.

Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovakia.

Alzheimer's disease (AD) is a chronic neurodegenerative disease of the central nervous system with higher prevalence in elderly people. Despite numerous research studies, the etiopathogenesis of AD remains unclear. Matrix metalloproteinases (MMPs) are endopeptidases involved in the cleavage of extracellular matrix proteins and basement membrane compounds. In the brain, the pathological role of MMPs includes the disruption of the blood-brain barrier leading to the induction of neuroinflammation. Among various MMPs, MMP-2 and MMP-3 belong to candidate molecules related to AD pathology. In our study, we aimed to evaluate the association of rs243865 and rs3025058 polymorphisms with AD susceptibility and their influence on age at onset and MoCA score in patients from Slovakia. Both MMP gene promoter polymorphisms were genotyped in 171 AD patients and 308 controls by the PCR-RFLP method. No statistically significant differences in the distribution of rs243865 (-1306 C>T) and rs3025058 (-1171 5A>6A) alleles/genotypes were found between AD patients and the control group. However, correlation with clinical findings revealed later age at disease onset in rs243865 CC carriers in the dominant model as compared to T allele carriers (CC vs. CT+TT: 78.44 ± 6.28 vs. 76.36 ± 6.39, = 0.036). The results of rs3025058 analysis revealed that 5A/6A carriers in the overdominant model tended to have earlier age at disease onset as compared to other genotype carriers (5A/6A vs. 5A/5A+6A/6A: 76.61 ± 5.88 vs. 78.57 ± 6.79, = 0.045). In conclusion, our results suggest that rs243865 and rs3025058 promoter polymorphisms may have influence on age at onset in AD patients.
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http://dx.doi.org/10.1155/2021/5573642DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079184PMC
April 2021

Viral Delivery of Non-Mutated Human Truncated Tau to Neurons Recapitulates Key Features of Human Tauopathy in Wild-Type Mice.

J Alzheimers Dis 2020 ;77(2):551-568

Axon Neuroscience R & D Services SE, Bratislava, Slovakia.

Background: Neuronal accumulation of hyperphosphorylated and truncated tau aggregates is one of the major defining factors and key drivers of neurodegeneration in Alzheimer's disease and other tauopathies.

Objective: We developed an AAV-induced model of tauopathy mediated by human truncated tau protein without familial frontotemporal dementia-related mutations to study tau propagation and the functional consequences of tau pathology.

Methods: We performed targeted transductions of the hippocampus or entorhinal cortex in adult mice followed by histological analysis to study the progression of hippocampal tau pathology and tau spreading. We performed behavioral analysis of mice with AAV-induced hippocampal tau pathology.

Results: AAV-induced hippocampal tau pathology was characterized by tau hyperphosphorylation (AT8 positivity), sarkosyl insolubility, and the presence of neurofibrillary tangles. AAV-induced tau pathology was associated with microgliosis and hypertrophic astrocytes in the absence of cognitive deficits. Additionally, the co-expression of mCherry fluorescent protein and human truncated tau enabled us to detect both local spreading of human tau and spreading from the entorhinal cortex to the synaptically connected dentate gyrus.

Conclusion: Targeted delivery of AAV with truncated tau protein into subcortical and cortical structures of mammalian brains represents an efficient approach for creating temporally and spatially well-defined tau pathology suitable for in vivo studies of tau propagation and neuronal circuit deficits in Alzheimer's disease.
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http://dx.doi.org/10.3233/JAD-200047DOI Listing
September 2021

Humanized tau antibodies promote tau uptake by human microglia without any increase of inflammation.

Acta Neuropathol Commun 2020 05 29;8(1):74. Epub 2020 May 29.

Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Pathology, Amsterdam Neuroscience, De Boelelaan, 1117, Amsterdam, The Netherlands.

Immunotherapies targeting pathological tau have recently emerged as a promising approach for treatment of neurodegenerative disorders. We have previously showed that the mouse antibody DC8E8 discriminates between healthy and pathological tau, reduces tau pathology in murine tauopathy models and inhibits neuronal internalization of AD tau species in vitro.Here we show, that DC8E8 and antibodies elicited against the first-in-man tau vaccine, AADvac1, which is based on the DC8E8 epitope peptide, both promote uptake of pathological tau by mouse primary microglia. IgG1 and IgG4 isotypes of AX004, the humanized versions of DC8E8, accelerate tau uptake by human primary microglia isolated from post-mortem aged and diseased brains. This promoting activity requires the presence of the Fc-domain of the antibodies.The IgG1 isotype of AX004 showed greater ability to promote tau uptake compared to the IgG4 isotype, while none of the antibody-tau complexes provoked increased pro-inflammatory activity of microglia. Our data suggest that IgG1 has better suitability for therapeutic development.
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http://dx.doi.org/10.1186/s40478-020-00948-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7257136PMC
May 2020

Association of CD33 rs3865444:C˃A polymorphism with a reduced risk of late-onset Alzheimer's disease in Slovaks is limited to subjects carrying the APOE ε4 allele.

Int J Immunogenet 2020 Oct 24;47(5):397-405. Epub 2020 Apr 24.

Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovakia.

CD33 rs3865444:C>A single nucleotide polymorphism (SNP) has been previously associated with the risk of late-onset Alzheimer's disease (LOAD); however, the results have been inconsistent across different populations. CD33 is a transmembrane receptor that plays an important role in AD pathogenesis by inhibiting amyloid β42 uptake by microglial cells. In this study, we aimed to validate the association between rs3865444 and LOAD risk in the Slovak population and to evaluate whether it was affected by the carrier status of the major LOAD risk allele apolipoprotein (APOE) ε4. CD33 rs3865444 and APOE variants were genotyped in 206 LOAD patients and 487 control subjects using the polymerase chain reaction-restriction fragment length polymorphism method and direct sequencing, respectively. Logistic regression analysis revealed a significant association of rs3865444 A allele with a reduced LOAD risk that was only present in APOE ε4 allele carriers (AA + CA versus CC: p = .0085; OR = 0.45; 95% CI = 0.25-0.82). On the other hand, no such association was found in subjects without the APOE ε4 (p = .75; OR = 0.93; 95% CI = 0.61-1.42). Moreover, regression analysis detected a significant interaction between CD33 rs3865444 A and APOE ε4 alleles (p = .021 for APOE ε4 allele dosage and p = .051 for APOE ε4 carriage status), with synergy factor (SF) value of 0.49 indicating an antagonistic effect between the two alleles in LOAD risk. In conclusion, our results suggest that CD33 rs3865444:C˃A substitution may reduce the risk of LOAD in Slovaks by antagonizing the effect conferred by the major susceptibility allele APOE ε4.
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http://dx.doi.org/10.1111/iji.12489DOI Listing
October 2020

Propagation of Tau Pathology: Integrating Insights From Postmortem and In Vivo Studies.

Biol Psychiatry 2020 05 3;87(9):808-818. Epub 2019 Oct 3.

Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Clinical Memory Research Unit, Lund University, Malmö, Sweden; Dementia Research Centre, Department of Neurodegenerative Disease, Queen Square Institute of Neurology, University College London, London, United Kingdom. Electronic address:

Cellular accumulation of aggregated forms of the protein tau is a defining feature of so-called tauopathies such as Alzheimer's disease, progressive supranuclear palsy, and chronic traumatic encephalopathy. A growing body of literature suggests that conformational characteristics of tau filaments, along with regional vulnerability to tau pathology, account for the distinct histopathological morphologies, biochemical composition, and affected cell types seen across these disorders. In this review, we describe and discuss recent evidence from human postmortem and clinical biomarker studies addressing the differential vulnerability of brain areas to tau pathology, its cell-to-cell transmission, and characteristics of the different strains that tau aggregates can adopt. Cellular biosensor assays are increasingly used in human tissue to detect the earliest forms of tau pathology, before overt histopathological lesions (i.e., neurofibrillary tangles) are apparent. Animal models with localized tau expression are used to uncover the mechanisms that influence spreading of tau aggregates. Further, studies of human postmortem-derived tau filaments from different tauopathies injected in rodents have led to striking findings that recapitulate neuropathology-based staging of tau. Furthermore, the recent advent of tau positron emission tomography and novel fluid-based biomarkers render it possible to study the temporal progression of tau pathology in vivo. Ultimately, evidence from these approaches must be integrated to better understand the onset and progression of tau pathology across tauopathies. This will lead to improved methods for the detection and monitoring of disease progression and, hopefully, to the development and refinement of tau-based therapeutics.
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http://dx.doi.org/10.1016/j.biopsych.2019.09.019DOI Listing
May 2020

Intersection of pathological tau and microglia at the synapse.

Acta Neuropathol Commun 2019 07 5;7(1):109. Epub 2019 Jul 5.

Axon Neuroscience R&D Services SE, Bratislava, Slovak Republic.

Tauopathies are a heterogenous class of diseases characterized by cellular accumulation of aggregated tau and include diseases such as Alzheimer's disease (AD), progressive supranuclear palsy and chronic traumatic encephalopathy. Tau pathology is strongly linked to neurodegeneration and clinical symptoms in tauopathy patients. Furthermore, synapse loss is an early pathological event in tauopathies and is the strongest correlate of cognitive decline. Tau pathology is additionally associated with chronic neuroinflammatory processes, such as reactive microglia, astrocytes, and increased levels of pro-inflammatory molecules (e.g. complement proteins, cytokines). Recent studies show that as the principal immune cells of the brain, microglia play a particularly important role in the initiation and progression of tau pathology and associated neurodegeneration. Furthermore, AD risk genes such as Triggering receptor expressed on myeloid cells 2 (TREM2) and Apolipoprotein E (APOE) are enriched in the innate immune system and modulate the neuroinflammatory response of microglia to tau pathology. Microglia can play an active role in synaptic dysfunction by abnormally phagocytosing synaptic compartments of neurons with tau pathology. Furthermore, microglia are involved in synaptic spreading of tau - a process which is thought to underlie the progressive nature of tau pathology propagation through the brain. Spreading of pathological tau is also the predominant target for tau-based immunotherapy. Active tau vaccines, therapeutic tau antibodies and other approaches targeting the immune system are actively explored as treatment options for AD and other tauopathies. This review describes the role of microglia in the pathobiology of tauopathies and the mechanism of action of potential therapeutics targeting the immune system in tauopathies.
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http://dx.doi.org/10.1186/s40478-019-0754-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612163PMC
July 2019

Human Truncated Tau Induces Mature Neurofibrillary Pathology in a Mouse Model of Human Tauopathy.

J Alzheimers Dis 2016 09;54(2):831-43

Institute of Neuroimmunology, Slovak Academy of Sciences, AD Centre, Bratislava, Slovak Republic.

Alzheimer's disease (AD) represents the most common neurodegenerative disorder. Several animal models have been developed in order to test pathophysiological mechanisms of the disease and to predict effects of pharmacological interventions. Here we examine the molecular and behavioral features of R3m/4 transgenic mice expressing human non-mutated truncated tau protein (3R tau, aa151-391) that were previously used for efficacy testing of passive tau vaccine. The mouse model reliably recapitulated crucial histopathological features of human AD, such as pre-tangles, neurofibrillary tangles, and neuropil threads. The pathology was predominantly located in the brain stem. Transgenic mice developed mature sarkosyl insoluble tau complexes consisting of mouse endogenous and human truncated and hyperphosphorylated forms of tau protein. The histopathological and biochemical features were accompanied by significant sensorimotor impairment and reduced lifespan. The sensorimotor impairment was monitored by a highly sensitive, fully-automated tool that allowed us to assess early deficit in gait and locomotion. We suggest that the novel transgenic mouse model can serve as a valuable tool for analysis of the therapeutic efficacy of tau vaccines for AD therapy.
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http://dx.doi.org/10.3233/JAD-160347DOI Listing
September 2016

Immediate manifestation of acoustic trauma in the auditory cortex is layer specific and cell type dependent.

J Neurophysiol 2016 Apr 28;115(4):1860-74. Epub 2016 Jan 28.

Department of Auditory Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic.

Exposure to loud sounds damages the auditory periphery and induces maladaptive changes in central parts of the auditory system. Diminished peripheral afferentation and altered inhibition influence the processing of sounds in the auditory cortex. It is unclear, however, which types of inhibitory interneurons are affected by acoustic trauma. Here we used single-unit electrophysiological recording and two-photon calcium imaging in anesthetized mice to evaluate the effects of acute acoustic trauma (125 dB SPL, white noise, 5 min) on the response properties of neurons in the core auditory cortex. Electrophysiological measurements suggested the selective impact of acoustic trauma on inhibitory interneurons in the auditory cortex. To further investigate which interneuronal types were affected, we used two-photon calcium imaging to record the activity of neurons in cortical layers 2/3 and 4, specifically focusing on parvalbumin-positive (PV+) and somatostatin-positive (SST+) interneurons. Spontaneous and pure-tone-evoked firing rates of SST+ interneurons increased in layer 4 immediately after acoustic trauma and remained almost unchanged in layer 2/3. Furthermore, PV+ interneurons with high best frequencies increased their evoked-to-spontaneous firing rate ratios only in layer 2/3 and did not change in layer 4. Finally, acoustic trauma unmasked low-frequency excitatory inputs only in layer 2/3. Our results demonstrate layer-specific changes in the activity of auditory cortical inhibitory interneurons within minutes after acoustic trauma.
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http://dx.doi.org/10.1152/jn.00810.2015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869484PMC
April 2016

Up states are rare in awake auditory cortex.

J Neurophysiol 2013 Apr 23;109(8):1989-95. Epub 2013 Jan 23.

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.

The dynamics of subthreshold membrane potential provide insight into the organization of activity in neural circuits. In many brain areas, membrane potential is bistable, transiting between a relatively hyperpolarized down state and a depolarized up state. These up and down states, which have been proposed to play a number of computational roles, have mainly been studied in anesthetized and in vitro preparations. Here, we have used intracellular recordings to characterize the dynamics of membrane potential in the auditory cortex of awake rats. We find that long up states are rare in the awake auditory cortex, with only 0.4% of up states >500 ms. Most neurons displayed only brief up states (bumps) and spent on average ∼1% of recording time in up states >500 ms. We suggest that the near absence of long up states in awake auditory cortex may reflect an adaptation to the rapid processing of auditory stimuli.
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http://dx.doi.org/10.1152/jn.00600.2012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628040PMC
April 2013

Representations in auditory cortex.

Curr Opin Neurobiol 2009 Aug 10;19(4):430-3. Epub 2009 Aug 10.

Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.

How does auditory cortex represent auditory stimuli, and how do these representations contribute to behavior? Recent experimental evidence suggests that activity in auditory cortex consists of sparse and highly synchronized volleys of activity, observed both in anesthetized and awake animals. Many neurons are capable of remarkably precise activity with very low jitter or spike count variability. Most importantly, animals are capable of exploiting such precise neuronal activity in making sensory decisions. Whether the ability of auditory cortex to exploit fine temporal differences in cortical activity is unique to auditory modality, or represents a general strategy used by cortical circuits remains an open question.
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http://dx.doi.org/10.1016/j.conb.2009.07.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757052PMC
August 2009

PINP: a new method of tagging neuronal populations for identification during in vivo electrophysiological recording.

PLoS One 2009 Jul 7;4(7):e6099. Epub 2009 Jul 7.

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.

Neural circuits are exquisitely organized, consisting of many different neuronal subpopulations. However, it is difficult to assess the functional roles of these subpopulations using conventional extracellular recording techniques because these techniques do not easily distinguish spikes from different neuronal populations. To overcome this limitation, we have developed PINP (Photostimulation-assisted Identification of Neuronal Populations), a method of tagging neuronal populations for identification during in vivo electrophysiological recording. The method is based on expressing the light-activated channel channelrhodopsin-2 (ChR2) to restricted neuronal subpopulations. ChR2-tagged neurons can be detected electrophysiologically in vivo since illumination of these neurons with a brief flash of blue light triggers a short latency reliable action potential. We demonstrate the feasibility of this technique by expressing ChR2 in distinct populations of cortical neurons using two different strategies. First, we labeled a subpopulation of cortical neurons-mainly fast-spiking interneurons-by using adeno-associated virus (AAV) to deliver ChR2 in a transgenic mouse line in which the expression of Cre recombinase was driven by the parvalbumin promoter. Second, we labeled subpopulations of excitatory neurons in the rat auditory cortex with ChR2 based on projection target by using herpes simplex virus 1 (HSV1), which is efficiently taken up by axons and transported retrogradely; we find that this latter population responds to acoustic stimulation differently from unlabeled neurons. Tagging neurons is a novel application of ChR2, used in this case to monitor activity instead of manipulating it. PINP can be readily extended to other populations of genetically identifiable neurons, and will provide a useful method for probing the functional role of different neuronal populations in vivo.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006099PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702752PMC
July 2009

Correlated connectivity and the distribution of firing rates in the neocortex.

J Neurosci 2009 Mar;29(12):3685-94

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.

Two recent experimental observations pose a challenge to many cortical models. First, the activity in the auditory cortex is sparse, and firing rates can be described by a lognormal distribution. Second, the distribution of nonzero synaptic strengths between nearby cortical neurons can also be described by a lognormal distribution. Here we use a simple model of cortical activity to reconcile these observations. The model makes the experimentally testable prediction that synaptic efficacies onto a given cortical neuron are statistically correlated, i.e., it predicts that some neurons receive stronger synapses than other neurons. We propose a simple Hebb-like learning rule that gives rise to such correlations and yields both lognormal firing rates and synaptic efficacies. Our results represent a first step toward reconciling sparse activity and sparse connectivity in cortical networks.
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http://dx.doi.org/10.1523/JNEUROSCI.4500-08.2009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784918PMC
March 2009

Sparse representation of sounds in the unanesthetized auditory cortex.

PLoS Biol 2008 Jan;6(1):e16

Cold Spring Harbor Laboratory, Watson School of Biological Sciences, Cold Spring Harbor, New York, United States of America.

How do neuronal populations in the auditory cortex represent acoustic stimuli? Although sound-evoked neural responses in the anesthetized auditory cortex are mainly transient, recent experiments in the unanesthetized preparation have emphasized subpopulations with other response properties. To quantify the relative contributions of these different subpopulations in the awake preparation, we have estimated the representation of sounds across the neuronal population using a representative ensemble of stimuli. We used cell-attached recording with a glass electrode, a method for which single-unit isolation does not depend on neuronal activity, to quantify the fraction of neurons engaged by acoustic stimuli (tones, frequency modulated sweeps, white-noise bursts, and natural stimuli) in the primary auditory cortex of awake head-fixed rats. We find that the population response is sparse, with stimuli typically eliciting high firing rates (>20 spikes/second) in less than 5% of neurons at any instant. Some neurons had very low spontaneous firing rates (<0.01 spikes/second). At the other extreme, some neurons had driven rates in excess of 50 spikes/second. Interestingly, the overall population response was well described by a lognormal distribution, rather than the exponential distribution that is often reported. Our results represent, to our knowledge, the first quantitative evidence for sparse representations of sounds in the unanesthetized auditory cortex. Our results are compatible with a model in which most neurons are silent much of the time, and in which representations are composed of small dynamic subsets of highly active neurons.
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http://dx.doi.org/10.1371/journal.pbio.0060016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214813PMC
January 2008

Sparse optical microstimulation in barrel cortex drives learned behaviour in freely moving mice.

Nature 2008 Jan;451(7174):61-4

Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147, USA.

Electrical microstimulation can establish causal links between the activity of groups of neurons and perceptual and cognitive functions. However, the number and identities of neurons microstimulated, as well as the number of action potentials evoked, are difficult to ascertain. To address these issues we introduced the light-gated algal channel channelrhodopsin-2 (ChR2) specifically into a small fraction of layer 2/3 neurons of the mouse primary somatosensory cortex. ChR2 photostimulation in vivo reliably generated stimulus-locked action potentials at frequencies up to 50 Hz. Here we show that naive mice readily learned to detect brief trains of action potentials (five light pulses, 1 ms, 20 Hz). After training, mice could detect a photostimulus firing a single action potential in approximately 300 neurons. Even fewer neurons (approximately 60) were required for longer stimuli (five action potentials, 250 ms). Our results show that perceptual decisions and learning can be driven by extremely brief epochs of cortical activity in a sparse subset of supragranular cortical pyramidal neurons.
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http://dx.doi.org/10.1038/nature06445DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425380PMC
January 2008

Toward the mechanisms of auditory attention.

Hear Res 2007 Jul 17;229(1-2):180-5. Epub 2007 Jan 17.

Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

Since the earliest studies of auditory cortex, it has been clear that an animal's behavioral or attentional state can play a crucial role in shaping the response characteristics of single neurons. Much of what has been learned about attention has been made using human and animal models, but little is known about the cellular and synaptic mechanisms by which attentional modulation of neuronal responses occurs. The use of rodent experimental models allows us to exploit the full armamentarium of modern cellular and molecular neuroscience techniques. Here we present our program for studying auditory attention, specifically for development of rodent models of attention and finding the neural correlates of attention.
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http://dx.doi.org/10.1016/j.heares.2007.01.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042581PMC
July 2007

Reliability and representational bandwidth in the auditory cortex.

Neuron 2005 Nov;48(3):479-88

Cold Spring Harbor Laboratory, Watson School of Biological Sciences, Cold Spring Harbor, New York 11724, USA.

It is unclear why there are so many more neurons in sensory cortex than in the sensory periphery. One possibility is that these "extra" neurons are used to overcome cortical noise and faithfully represent the acoustic stimulus. Another possibility is that even after overcoming cortical noise, there is "excess representational bandwidth" available and that this bandwidth is used to represent conjunctions of auditory and nonauditory information for computation. Here, we discuss recent data about neuronal reliability in auditory cortex showing that cortical noise may not be as high as was previously believed. Although at present, the data suggest that auditory cortex neurons can be more reliable than those in the visual cortex, we speculate that the principles governing cortical computation are universal and that visual and other cortical areas can also exploit strategies based on similarly high-fidelity activity.
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http://dx.doi.org/10.1016/j.neuron.2005.10.016DOI Listing
November 2005
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