scholarly journals Nanoconnectomic upper bound on the variability of synaptic plasticity

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Thomas M Bartol ◽  
Cailey Bromer ◽  
Justin Kinney ◽  
Michael A Chirillo ◽  
Jennifer N Bourne ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Upper Bound ◽  
Strong Correlation ◽  
Synaptic Activity ◽  
Synaptic Activation ◽  
Synaptic Contacts ◽  
Postsynaptic Activity ◽  
History Of ◽  
The Brain

Information in a computer is quantified by the number of bits that can be stored and recovered. An important question about the brain is how much information can be stored at a synapse through synaptic plasticity, which depends on the history of probabilistic synaptic activity. The strong correlation between size and efficacy of a synapse allowed us to estimate the variability of synaptic plasticity. In an EM reconstruction of hippocampal neuropil we found single axons making two or more synaptic contacts onto the same dendrites, having shared histories of presynaptic and postsynaptic activity. The spine heads and neck diameters, but not neck lengths, of these pairs were nearly identical in size. We found that there is a minimum of 26 distinguishable synaptic strengths, corresponding to storing 4.7 bits of information at each synapse. Because of stochastic variability of synaptic activation the observed precision requires averaging activity over several minutes.

scholarly journals Hippocampal Spine Head Sizes are Highly Precise

2015 ◽  
Author(s):  
Thomas M Bartol ◽  
Cailey Bromer ◽  
Justin P Kinney ◽  
Michael A Chirillo ◽  
Jennifer N Bourne ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Strong Correlation ◽  
Time Window ◽  
Synaptic Activity ◽  
Electron Microscopic ◽  
Synaptic Contacts ◽  
Amount Of Information ◽  
Spine Head ◽  
Postsynaptic Activity

Hippocampal synaptic activity is probabilistic and because synaptic plasticity depends on its history, the amount of information that can be stored at a synapse is limited. The strong correlation between the size and efficacy of a synapse allowed us to estimate the precision of synaptic plasticity. In an electron microscopic reconstruction of hippocampal neuropil we found single axons making two or more synaptic contacts onto the same dendrites which would have shared histories of presynaptic and postsynaptic activity. The postsynaptic spine heads, but not the spine necks, of these pairs were nearly identical in size. The precision is much greater than previous estimates and requires postsynaptic averaging over a time window many seconds to minutes in duration depending on the rate of input spikes and probability of release.

Priming-Induced Shift in Synaptic Plasticity in the Rat Hippocampus

1999 ◽  
Vol 82 (4) ◽  
pp. 2024-2028 ◽  
Author(s):  
Hongyan Wang ◽  
John J. Wagner
Keyword(s):  
Synaptic Plasticity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Crossover Point ◽  
Term Potentiation ◽  
Before And After ◽  
History Of ◽  
The Brain ◽  
Dependent Mechanism

The activity history of a given neuron has been suggested to influence its future responses to synaptic input in one prominent model of experience-dependent synaptic plasticity proposed by Bienenstock, Cooper, and Munro (BCM theory). Because plasticity of synaptic plasticity (i.e., metaplasticity) is similar in concept to aspects of the BCM proposal, we have tested the possibility that a form of metaplasticity induced by a priming stimulation protocol might exhibit BCM-like characteristics. CA1 field excitatory postsynaptic potentials (EPSPs) obtained from rat hippocampal slices were used to monitor synaptic responses before and after conditioning stimuli (3–100 Hz) of the Schaffer collateral inputs. A substantial rightward shift (>5-fold) in the frequency threshold between long-term depression (LTD) and long-term potentiation (LTP) was observed <1 h after priming. This change in the LTD/P crossover point occurred at both primed and unprimed synaptic pathways. These results provide new support for the existence of a rapid, heterosynaptic, experience-dependent mechanism that is capable of modifying the synaptic plasticity phenomena that are commonly proposed to be important for developmental and learning/memory processes in the brain.

scholarly journals Synaptic plasticity is predicted by spatiotemporal firing rate patterns and robust to in vivo-like variability

2021 ◽  
Author(s):  
Dan B Dorman ◽  
Kim T Blackwell
Keyword(s):  
Synaptic Plasticity ◽  
Firing Rate ◽  
Dendritic Tree ◽  
Spike Timing ◽  
Synaptic Activity ◽  
Data Driven ◽  
Synaptic Inputs ◽  
The Brain

Synaptic plasticity, the experience-induced change in connections between neurons, underlies learning and memory in the brain. Most of our understanding of synaptic plasticity derives from in vitro experiments with precisely repeated stimulus patterns; however, neurons exhibit significant variability in vivo during repeated experiences. Further, the spatial pattern of synaptic inputs to the dendritic tree influences synaptic plasticity, yet is not considered in most synaptic plasticity rules. Here, we address the sensitivity of plasticity to trial-to-trial variability and delineate how spatiotemporal synaptic input patterns produce plasticity with in vivo-like conditions using a data-driven computational model with a calcium-based plasticity rule. Using in vivo spike train recordings as inputs, we show that plasticity is strongly robust to trial-to-trial variability of spike timing, and derive general synaptic plasticity rules describing how spatiotemporal patterns of synaptic inputs control the magnitude and direction of plasticity. Specifically, a high temporal input firing rate to a synapse late in a trial correlated with neighboring synaptic activity produces potentiation, while an earlier, moderate firing rate that is negatively correlated with neighboring synaptic activity produces depression. Together, our results reveal that calcium dynamics can unify diverse plasticity rules and reveal how spatiotemporal firing rate patterns control synaptic plasticity.

Vitamin A and Retinoic Acid in Cognition and Cognitive Disease

2020 ◽  
Vol 40 (1) ◽  
pp. 247-272 ◽  
Author(s):  
Marta U. Wołoszynowska-Fraser ◽  
Azita Kouchmeshky ◽  
Peter McCaffery
Keyword(s):  
Retinoic Acid ◽  
Synaptic Plasticity ◽  
Vitamin A ◽  
Cognitive Decline ◽  
Developmental Disorders ◽  
Vitamin A Deficiency ◽  
Retinoic Acid Receptors ◽  
Controlled Synthesis ◽  
History Of ◽  
The Brain

The history of vitamin A goes back over one hundred years, but our realization of its importance for the brain and cognition is much more recent. The brain is more efficient than other target tissues at converting vitamin A to retinoic acid (RA), which activates retinoic acid receptors (RARs). RARs regulate transcription, but their function in the cytoplasm to control nongenomic actions is also crucial. Controlled synthesis of RA is essential for regulating synaptic plasticity in regions of the brain involved in learning and memory, such as the hippocampus. Vitamin A deficiency results in a deterioration of these functions, and failure of RA signaling is perhaps associated with normal cognitive decline with age as well as with Alzheimer's disease. Further, several psychiatric and developmental disorders that disrupt cognition are also linked with vitamin A and point to their possible treatment with vitamin A or RA.

scholarly journals Numerical Simulation: Fluctuation in Background Synaptic Activity Regulates Synaptic Plasticity

2021 ◽  
Vol 15 ◽  
Author(s):  
Yuto Takeda ◽  
Katsuhiko Hata ◽  
Tokio Yamazaki ◽  
Masaki Kaneko ◽  
Osamu Yokoi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Statistical Fluctuation ◽  
Noisy Environment ◽  
Term Potentiation ◽  
Synapse Model ◽  
The Brain

Synaptic plasticity is vital for learning and memory in the brain. It consists of long-term potentiation (LTP) and long-term depression (LTD). Spike frequency is one of the major components of synaptic plasticity in the brain, a noisy environment. Recently, we mathematically analyzed the frequency-dependent synaptic plasticity (FDP) in vivo and found that LTP is more likely to occur with an increase in the frequency of background synaptic activity. Meanwhile, previous studies suggest statistical fluctuation in the amplitude of background synaptic activity. Little is understood, however, about its contribution to synaptic plasticity. To address this issue, we performed numerical simulations of a calcium-based synapse model. Then, we found attenuation of the tendency to become LTD due to an increase in the fluctuation of background synaptic activity, leading to an enhancement of synaptic weight. Our result suggests that the fluctuation affects synaptic plasticity in the brain.

How the brain learns to listen: deafness and the bionic ear

e-Neuroforum ◽  
2015 ◽  
Vol 21 (1) ◽  
Author(s):  
A. Kral ◽  
Thomas Lenarz
Keyword(s):  
Synaptic Plasticity ◽  
Animal Models ◽  
Cochlear Implant ◽  
Auditory System ◽  
Clinical Success ◽  
Auditory Neuroscience ◽  
Neuronal Mechanisms ◽  
History Of ◽  
First Time ◽  
The Brain

AbstractFor the first time in the history of neuroscience, hearing allows to systematically investigate brain development with and without sensory experience in humans. This is given by the clinical success of the cochlear implant, a neuroprosthesis that can replace the non-functional inner ear. In recent years, auditory neuroscience investigated the neuronal mechanisms of learning, sensitive developmental periods and cross-modal reorganization in parallel in humans and animal models, with highly consistent outcomes. We learned that the brain undergoes a complex adaptation to deafness, both within and outside the auditory system. These adaptations reorganize the brain optimally to cope with deafness, but they negatively interfere with a later prosthetic therapy of hearing. They eventually close the sensitive developmental periods. The critical nature of sensitive periods is not only a consequence of a developmentally reduced synaptic plasticity but also the consequence of changes in central integrative functions and cognitive adaptations to deafness.

scholarly journals L2HGDH Missense Variant in a Cat with L-2-Hydroxyglutaric Aciduria

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 682
Author(s):  
Matthias Christen ◽  
Nils Janzen ◽  
Anne Fraser ◽  
Adrian C. Sewell ◽  
Vidhya Jagannathan ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Missense Variant ◽  
Microcytic Anemia ◽  
Abnormal Behavior ◽  
Functional Candidate Gene ◽  
History Of ◽  
The Brain ◽  
Hydroxyglutaric Acid

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.

scholarly journals Molecular evolutionary analysis of human primary microcephaly genes

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Nashaiman Pervaiz ◽  
Hongen Kang ◽  
Yiming Bao ◽  
Amir Ali Abbasi
Keyword(s):  
Evolutionary History ◽  
Genetic Basis ◽  
Brain Size ◽  
Primate Species ◽  
Evolutionary Analysis ◽  
Australopithecus Afarensis ◽  
Primary Microcephaly ◽  
Modern Humans ◽  
History Of ◽  
The Brain

Abstract Background There has been a rapid increase in the brain size relative to body size during mammalian evolutionary history. In particular, the enlarged and globular brain is the most distinctive anatomical feature of modern humans that set us apart from other extinct and extant primate species. Genetic basis of large brain size in modern humans has largely remained enigmatic. Genes associated with the pathological reduction of brain size (primary microcephaly-MCPH) have the characteristics and functions to be considered ideal candidates to unravel the genetic basis of evolutionary enlargement of human brain size. For instance, the brain size of microcephaly patients is similar to the brain size of Pan troglodyte and the very early hominids like the Sahelanthropus tchadensis and Australopithecus afarensis. Results The present study investigates the molecular evolutionary history of subset of autosomal recessive primary microcephaly (MCPH) genes; CEP135, ZNF335, PHC1, SASS6, CDK6, MFSD2A, CIT, and KIF14 across 48 mammalian species. Codon based substitutions site analysis indicated that ZNF335, SASS6, CIT, and KIF14 have experienced positive selection in eutherian evolutionary history. Estimation of divergent selection pressure revealed that almost all of the MCPH genes analyzed in the present study have maintained their functions throughout the history of placental mammals. Contrary to our expectations, human-specific adoptive evolution was not detected for any of the MCPH genes analyzed in the present study. Conclusion Based on these data it can be inferred that protein-coding sequence of MCPH genes might not be the sole determinant of increase in relative brain size during primate evolutionary history.

Streptococcus pluranimalium meningoencephalitis in a horse

2021 ◽  
pp. 104063872110234
Author(s):  
Dah-Jiun Fu ◽  
Akhilesh Ramachandran ◽  
Craig Miller
Keyword(s):  
Ribosomal Rna ◽  
Cross Sections ◽  
Nucleotide Sequencing ◽  
Formalin Fixed Paraffin ◽  
Quarter Horse ◽  
Formalin Fixed Paraffin Embedded ◽  
History Of ◽  
The Brain ◽  
Gram Positive Cocci ◽  
Formalin Fixed

A 3-y-old, female Quarter Horse with a history of acute neurologic signs was found dead and was submitted for postmortem examination. Areas of petechial and ecchymotic hemorrhage were present on cross-sections of the cerebrum, cerebellum, and brainstem. Histologic examination of the brain revealed severe, purulent meningoencephalitis and vasculitis with a myriad of intralesional gram-positive cocci. Streptococcus pluranimalium was identified from formalin-fixed, paraffin-embedded tissue obtained from sites with active lesions by PCR and nucleotide sequencing of bacterial 16S ribosomal RNA. S. pluranimalium should be considered as a cause of meningoencephalitis in a horse.

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