scholarly journals Short-term synaptic plasticity makes neurons sensitive to the distribution of presynaptic population firing rates

2019 ◽  
Author(s):  
Luiz Tauffer ◽  
Arvind Kumar
Keyword(s):  
Discrimination Problem ◽  
Background Activity ◽  
Strong Relationship ◽  
Sparse Signals ◽  
Population Code ◽  
Short Term ◽  
Short Term Plasticity ◽  
Rate Analysis ◽  
The Brain ◽  
Latent Function

AbstractThe ability to discriminate spikes that encode a particular stimulus from spikes produced by background activity is essential for reliable information processing in the brain. We describe how synaptic short-term plasticity (STP) modulates the output of presynaptic populations as a function of the distribution of the spiking activity and find a strong relationship between STP features and sparseness of the population code, which could solve the discrimination problem. Furthermore, we show that feedforward excitation followed by inhibition (FF-EI), combined with target-dependent STP, promote substantial increase in the signal gain even for considerable deviations from the optimal conditions, granting robustness to this mechanism. A simulated neuron driven by a spiking FF-EI network is reliably modulated as predicted by a rate analysis and inherits the ability to differentiate sparse signals from dense background activity changes of the same magnitude, even at very low signal-to-noise conditions. We propose that the STP-based distribution discrimination is likely a latent function in several regions such as the cerebellum and the hippocampus.

scholarly journals Short-term plasticity at Purkinje to deep cerebellar nuclear neuron synapses supports a slow gain-control mechanism enabling scaled linear encoding over second-long time windows

2019 ◽  
Author(s):  
Christine M. Pedroarena
Keyword(s):  
Control Mechanism ◽  
Background Activity ◽  
Time Windows ◽  
Gain Control ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Gain Adaptation ◽  
Long Time ◽  
The Brain

ABSTRACTModifications in the sensitivity of neural elements allow the brain to adapt its functions to varying demands. Frequency-dependent short-term synaptic depression (STD) provides a dynamic gain-control mechanism enabling adaptation to different background conditions alongside enhanced sensitivity to input-driven changes in activity. In contrast, synapses displaying frequency-invariant transmission can faithfully transfer ongoing presynaptic rates enabling linear processing, deemed critical for many functions. However, rigid frequency-invariant transmission may lead to runaway dynamics and low sensitivity to changes in rate. Here, I investigated the Purkinje cell to deep cerebellar nuclei neuron synapses (PC_DCNs), which display frequency-invariance, and yet, PCs maintain background-activity at disparate rates, even at rest. Using protracted PC_DCNs activation (120s) in cerebellar slices to mimic background-activity, I identified a previously unrecognized frequency-dependent, slow STD (S_STD) of PC_DCN inhibitory postsynaptic currents. S_STD supports a novel form of gain-control that enabled—over second-long time windows—scaled linear encoding of PC rate changes mimicking behavior-driven/learned PC-signals, alongside adaptation to background-activity. Cell-attached DCN recordings confirmed these results. Experimental and computational modeling results suggest S_STD-gain-control may emerge through a slow depression factor combined with balanced fast-short-term plasticity. Finally, evidence from opto-genetic experiments, statistical analysis and computer simulations pointed to a presynaptic, input-specific and possibly activity-dependent decrease in active synaptic release-sites as the basis for S_STD. This study demonstrates a novel slow gain-control mechanism, which could explain efficient and comprehensive PC_DCN linear transfer of input-driven/learned PC rates over behavioral-relevant time windows despite disparate background-activity, and furthermore, provides an alternative pathway to hone PCs output via background-activity control.SIGNIFICANCE STATEMENTThe brain can adapt to varying demands by dynamically changing the gain of its synapses; however, some tasks require linear transfer of presynaptic rates over extended periods, seemingly incompatible with non-linear gain adaptation. Here, I report a novel gain-adaptation mechanism, which enables scaled linear encoding of changes in presynaptic rates over second-long time windows and adaptation to background-activity at longer time-scales at the Purkinje to deep cerebellar nuclear neurons synapses (PC_DCNs). A previously unrecognized PC_DCN slow and frequency-dependent short-term synaptic depression (S_STD), together with frequency-invariant transmission at faster time scales likely explains this process. This slow-gain-control/modulation mechanism may enable efficient linear encoding of second-long presynaptic signals under diverse synaptic background-activity conditions, and flexible fine-tuning of synaptic gains by background-activity modulation.

Music Changes the Brain

2018 ◽  
pp. 98-111
Author(s):  
Paul Lennard
Keyword(s):  
Brain Development ◽  
Language Processing ◽  
Cerebral Hemisphere ◽  
Critical Periods ◽  
Short Term ◽  
Music Training ◽  
Short Term Plasticity ◽  
Process Music ◽  
The Brain

This chapter examines ways in which listening to or making music changes our brains morphologically and functionally. Evidence for short-term plasticity in response to music is reviewed. Critical periods early in life, when exposure to music and music training can alter brain development, are summarized. Evidence that the brains of musicians and nonmusicians differ is presented. It is shown that nonmusicians process music primarily in the nondominant cerebral hemisphere, while musicians have structural and functional shifts of lateralization to the dominant cerebral hemisphere. This shift is discussed in terms of a theory that nonmusicians process music holistically in the nondominant cerebral hemisphere, while trained musicians tend to apply syntax to music, using language-processing circuitry in the dominant cerebral hemisphere.

scholarly journals Coincident glutamatergic depolarizations enhance GABAA receptor-dependent Cl- influx in mature and suppress Cl- efflux in immature neurons

2020 ◽  
Author(s):  
Aniello Lombardi ◽  
Peter Jedlicka ◽  
Heiko J. Luhmann ◽  
Werner Kilb
Keyword(s):  
Gaba Receptors ◽  
Temporal Correlation ◽  
Gabaergic Inhibition ◽  
Relevant Factor ◽  
Decay Kinetics ◽  
Short Term ◽  
Substantial Impact ◽  
Short Term Plasticity ◽  
The Impact ◽  
The Brain

AbstractThe impact of GABAergic transmission on neuronal excitability depends on the Cl−-gradient across membranes. However, the Cl−-fluxes through GABAA receptors alter the intracellular Cl− concentration ([Cl−]i) and in turn attenuate GABAergic responses, a process termed ionic plasticity. Recently it has been shown that coincident glutamatergic inputs significantly affect ionic plasticity. Yet how the [Cl−]i changes depend on the properties of glutamatergic inputs and their spatiotemporal relation to GABAergic stimuli is unknown. To investigate this issue, we used compartmental biophysical models of Cl− dynamics simulating either a simple ball-and-stick topology or a reconstructed immature CA3 neuron. These computational experiments demonstrated that glutamatergic co-stimulation enhances GABA receptor-mediated Cl− influx at low and attenuates or reverses the Cl− efflux at high initial [Cl−]i. The size of glutamatergic influence on GABAergic Cl−-fluxes depends on the conductance, decay kinetics, and localization of glutamatergic inputs. Surprisingly, the glutamatergic shift in GABAergic Cl−-fluxes is invariant to latencies between GABAergic and glutamatergic inputs over a substantial interval. In agreement with experimental data, simulations in a reconstructed CA3 pyramidal neuron with physiological patterns of correlated activity revealed that coincident glutamatergic synaptic inputs contribute significantly to the activity-dependent [Cl−]i changes. Whereas the influence of spatial correlation between distributed glutamatergic and GABAergic inputs was negligible, their temporal correlation played a significant role. In summary, our results demonstrate that glutamatergic co-stimulation had a substantial impact on ionic plasticity of GABAergic responses, enhancing the destabilization of GABAergic inhibition in the mature nervous systems, but suppressing GABAergic [Cl−]i changes in the immature brain. Therefore, glutamatergic shift in GABAergic Cl−-fluxes should be considered as a relevant factor of short term plasticity.Author SummaryInformation processing in the brain requires that excitation and inhibition are balanced. The main inhibitory neurotransmitter in the brain is gamma-amino-butyric acid (GABA). GABA actions depend on the Cl−-gradient, but activation of ionotropic GABA receptors causes Cl−-fluxes and thus reduces GABAergic inhibition. Here, we investigated how a coincident membrane depolarization by excitatory, glutamatergic synapses influences GABA-induced Cl−-fluxes using a biophysical compartmental model of Cl− dynamics, simulating either simple or realistic neuron topologies. We demonstrate that glutamatergic co-stimulation directly affects GABA-induced Cl−-fluxes, with the size of glutamatergic effects depending on the conductance, the decay kinetics, and localization of glutamatergic inputs. We also show that the glutamatergic shift in GABAergic Cl−-fluxes is surprisingly stable over a substantial range of latencies between glutamatergic and GABAergic inputs. We conclude from these results that glutamatergic co-stimulation alters GABAergic Cl−-fluxes and in turn affects the strength of GABAergic inhibition. These coincidence-dependent ionic changes should be considered as a relevant factor of short term plasticity in the CNS.

The Cochlear Nuclei

2018 ◽  
pp. 94-122 ◽  
Author(s):  
Donata Oertel ◽  
Xiao-Jie Cao ◽  
Alberto Recio-Spinoso
Keyword(s):  
Sensory Information ◽  
Short Term ◽  
Temporal Precision ◽  
Short Term Plasticity ◽  
Ventral Cochlear Nucleus ◽  
Cochlear Nuclei ◽  
Electrophysiological Studies ◽  
The Face ◽  
The Brain

Plasticity in neuronal circuits is essential for optimizing connections as animals develop and for adapting to injuries and aging, but it can also distort the processing, as well as compromise the conveyance of ongoing sensory information. This chapter summarizes evidence from electrophysiological studies in slices and in vivo that shows how remarkably robust signaling is in principal cells of the ventral cochlear nucleus. Even in the face of short-term plasticity, these neurons signal rapidly and with temporal precision. They can relay ongoing acoustic information from the cochlea to the brain largely independently of sounds to which they were exposed previously.

scholarly journals How synaptic strength, short-term plasticity, and temporal factors contribute to neuronal spike output

2021 ◽  
Author(s):  
Alexandra Gastone Guilabert ◽  
Benjamin Ehret ◽  
Moritz O. Buchholz ◽  
Gregor F.P. Schuhknecht
Keyword(s):  
Background Activity ◽  
Synaptic Strength ◽  
Temporal Coding ◽  
Excitatory Postsynaptic Potential ◽  
Short Term ◽  
Paired Pulse ◽  
Temporal Synchrony ◽  
Short Term Plasticity ◽  
Firing Rates

To compute spiking responses, neurons integrate inputs from thousands of synapses whose strengths span an order of magnitude. Intriguingly, in mouse neocortex, the small minority of 'strong' synapses is found predominantly between similarly tuned cells, suggesting they are the synapses that determine a neuron's spike output. This raises the question of how other computational primitives, such as 'background' activity from the majority of synapses, which are 'weak', short-term plasticity, and temporal synchrony contribute to spiking. First, we combined extracellular stimulation and whole-cell recordings in mouse barrel cortex to map the distribution of excitatory postsynaptic potential (EPSP) amplitudes and paired-pulse ratios of excitatory synaptic connections converging onto individual layer 2/3 (L2/3) neurons. While generally net short-term plasticity was weak, connections with EPSPs > 2 mV displayed pronounced paired-pulse depression. EPSP amplitudes and paired-pulse ratios of connections converging onto the same neurons spanned the full range observed across L2/3 and there was no indication that strong synapses nor those with particular short-term plasticity properties were associated with particular cells, which critically constrains theoretical models of cortical filtering. To investigate how different computational primitives of synaptic information processing interact to shape spiking, we developed a computational model of a pyramidal neuron in the rodent L2/3 circuitry: firing rates and pairwise correlations of presynaptic inputs were constrained by in vivo observations, while synaptic strength and short-term plasticity were set based on our experimental data. Importantly, we found that the ability of strong inputs to evoke spiking critically depended on their high temporal synchrony and high firing rates observed in vivo and on synaptic background activity - and not primarily on synaptic strength, which in turn further enhanced information transfer. Depression of strong synapses was critical for maintaining a neuron's responsivity and prevented runaway excitation. Our results provide a holistic framework of how cortical neurons exploit complex synergies between temporal coding, synaptic properties, and noise in order to transform synaptic inputs into output firing.

scholarly journals Short-term plasticity at cerebellar granule cell to molecular layer interneuron synapses expands information processing

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Kevin Dorgans ◽  
Valérie Demais ◽  
Yannick Bailly ◽  
Bernard Poulain ◽  
Philippe Isope ◽  
...  
Keyword(s):  
Information Processing ◽  
Granule Cell ◽  
Motor Behavior ◽  
Molecular Layer ◽  
Short Term ◽  
Short Term Plasticity ◽  
Synapsin Ii ◽  
Heterogeneous Expression ◽  
Molecular Layer Interneuron ◽  
The Brain

Information processing by cerebellar molecular layer interneurons (MLIs) plays a crucial role in motor behavior. MLI recruitment is tightly controlled by the profile of short-term plasticity (STP) at granule cell (GC)-MLI synapses. While GCs are the most numerous neurons in the brain, STP diversity at GC-MLI synapses is poorly documented. Here, we studied how single MLIs are recruited by their distinct GC inputs during burst firing. Using slice recordings at individual GC-MLI synapses of mice, we revealed four classes of connections segregated by their STP profile. Each class differentially drives MLI recruitment. We show that GC synaptic diversity is underlain by heterogeneous expression of synapsin II, a key actor of STP and that GC terminals devoid of synapsin II are associated with slow MLI recruitment. Our study reveals that molecular, structural and functional diversity across GC terminals provides a mechanism to expand the coding range of MLIs.

scholarly journals Memories in a network with excitatory and inhibitory plasticity are encoded in the spiking irregularity

2021 ◽  
Author(s):  
Julia V Gallinaro ◽  
Claudia Clopath
Keyword(s):  
Computational Model ◽  
Firing Rate ◽  
Coefficient Of Variation ◽  
Spiking Neurons ◽  
Theoretical Studies ◽  
Short Term ◽  
Cell Assemblies ◽  
Short Term Plasticity ◽  
Inhibitory Plasticity ◽  
The Brain

Cell assemblies are thought to be the substrate of memory in the brain. Theoretical studies have previously shown that assemblies can be formed in networks with multiple types of plasticity. But how exactly they are formed and how they encode information is yet to be fully understood. One possibility is that memories are stored in silent assemblies. Here we used a computational model to study the formation of silent assemblies in a network of spiking neurons with excitatory and inhibitory plasticity. We found that even though the formed assemblies were silent in terms of mean firing rate, they had an increased coefficient of variation of inter-spike intervals. We also found that this spiking irregularity could be readout with support of short-term plasticity, and that it could contribute to the longevity of memories.

scholarly journals Memories in a network with excitatory and inhibitory plasticity are encoded in the spiking irregularity

2021 ◽  
Vol 17 (11) ◽  
pp. e1009593
Author(s):  
Júlia V. Gallinaro ◽  
Claudia Clopath
Keyword(s):  
Computational Model ◽  
Firing Rate ◽  
Coefficient Of Variation ◽  
Spiking Neurons ◽  
Theoretical Studies ◽  
Short Term ◽  
Cell Assemblies ◽  
Short Term Plasticity ◽  
Inhibitory Plasticity ◽  
The Brain

Cell assemblies are thought to be the substrate of memory in the brain. Theoretical studies have previously shown that assemblies can be formed in networks with multiple types of plasticity. But how exactly they are formed and how they encode information is yet to be fully understood. One possibility is that memories are stored in silent assemblies. Here we used a computational model to study the formation of silent assemblies in a network of spiking neurons with excitatory and inhibitory plasticity. We found that even though the formed assemblies were silent in terms of mean firing rate, they had an increased coefficient of variation of inter-spike intervals. We also found that this spiking irregularity could be read out with support of short-term plasticity, and that it could contribute to the longevity of memories.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

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