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.

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.

Frequency-Dependent Modulation of Short-Term Plasticity of GABAergic Synaptic Transmission

2018 ◽  
Vol 9 (2) ◽  
pp. 119-126
Author(s):  
Oksana P. Kolesnyk ◽  
Svetlana A. Fedulova ◽  
Mycola S. Veselovsky
Keyword(s):  
Synaptic Transmission ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Gabaergic Synaptic Transmission

scholarly journals Short-Term Plasticity in Cortical GABAergic Synapses on Olfactory Bulb Granule Cells Is Modulated by Endocannabinoids

2021 ◽  
Vol 15 ◽  
Author(s):  
Fu-Wen Zhou ◽  
Adam C. Puche
Keyword(s):  
Olfactory Bulb ◽  
Sensory Processing ◽  
Granule Cell ◽  
Granule Cells ◽  
Cb1 Receptor ◽  
Granule Cell Layer ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Cortical Feedback

Olfactory bulb and higher processing areas are synaptically interconnected, providing rapid regulation of olfactory bulb circuit dynamics and sensory processing. Short-term plasticity changes at any of these synapses could modulate sensory processing and potentially short-term sensory memory. A key olfactory bulb circuit for mediating cortical feedback modulation is granule cells, which are targeted by multiple cortical regions including both glutamatergic excitatory inputs and GABAergic inhibitory inputs. There is robust endocannabinoid modulation of excitatory inputs to granule cells and here we explored whether there was also endocannabinoid modulation of the inhibitory cortical inputs to granule cells. We expressed light-gated cation channel channelrhodopsin-2 (ChR2) in GABAergic neurons in the horizontal limb of the diagonal band of Broca (HDB) and their projections to granule cells in olfactory bulb. Selective optical activation of ChR2 positive axons/terminals generated strong, frequency-dependent short-term depression of GABAA-mediated-IPSC in granule cells. As cannabinoid type 1 (CB1) receptor is heavily expressed in olfactory bulb granule cell layer (GCL) and there is endogenous endocannabinoid release in GCL, we investigated whether activation of CB1 receptor modulated the HDB IPSC and short-term depression at the HDB→granule cell synapse. Activation of the CB1 receptor by the exogenous agonist Win 55,212-2 significantly decreased the peak amplitude of individual IPSC and decreased short-term depression, while blockade of the CB1 receptor by AM 251 slightly increased individual IPSCs and increased short-term depression. Thus, we conclude that there is tonic endocannabinoid activation of the GABAergic projections of the HDB to granule cells, similar to the modulation observed with glutamatergic projections to granule cells. Modulation of inhibitory synaptic currents and frequency-dependent short-term depression could regulate the precise balance of cortical feedback excitation and inhibition of granule cells leading to changes in granule cell mediated inhibition of olfactory bulb output to higher processing areas.

scholarly journals Features of Neuralization Diagnostics Transitor-Ischemic Attacks

2021 ◽  
Vol 8 (7) ◽  
pp. 670
Author(s):  
Tursunova M. O ◽  
Abdullaeva M. B ◽  
Kalanov A. B ◽  
Aktamova M.U
Keyword(s):  
Statistical Data ◽  
Current Knowledge ◽  
Educational Programs ◽  
Transient Ischemic Attacks ◽  
Short Term ◽  
Important Place ◽  
The Past ◽  
The Us ◽  
Long Time ◽  
The Brain

Transient-ischemic attacks (TIA) as precursors of cerebral strokes occupy an important place among all forms of cerebrovascular insufficiency. With regard to the epidemiology of transient ischemic attacks (TIA), most countries do not have accurate data. So, in the US, they carry up to 5 million adult citizens per year, with many TIAs remaining undiagnosed. These episodes of sudden and short-term neurological deficit were considered benign and harmless for a long time. Most general practitioners and patients incorrectly or insufficiently understand the nature and significance of TIA, perhaps this can explain the small interest of doctors and the lack of statistical data on this nosological unit. Transient ischemic attacks (TIA) are defined clinically as rapidly occurring focal and less commonly diffuse (cerebral) dysfunctions of the brain that are caused by local ischemia and disappear within one day (Gafurov: 2006). Over the past two decades, many views on TIA have changed significantly; approaches to the diagnosis and treatment of patients have become much more intense and more aggressive. Current knowledge of TIA is of great importance both for the proper organization of patient care and for educational programs among the population, the importance of which cannot be overestimated.

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 Retinohypothalamic Tract Synapses in the Rat Suprachiasmatic Nucleus Demonstrate Short-Term Synaptic Plasticity

2010 ◽  
Vol 103 (5) ◽  
pp. 2390-2399 ◽  
Author(s):  
Mykhaylo G. Moldavan ◽  
Charles N. Allen
Keyword(s):  
Synaptic Transmission ◽  
Suprachiasmatic Nucleus ◽  
Ganglion Cells ◽  
Brain Slices ◽  
Release Mechanism ◽  
Dependent Manner ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Retinohypothalamic Tract

The master circadian pacemaker located in the suprachiasmatic nucleus (SCN) is entrained by light intensity–dependent signals transmitted via the retinohypothalamic tract (RHT). Short-term plasticity at glutamatergic RHT–SCN synapses was studied using stimulus frequencies that simulated the firing of light sensitive retinal ganglion cells. The evoked excitatory postsynaptic current (eEPSC) was recorded from SCN neurons located in hypothalamic brain slices. The eEPSC amplitude was stable during 0.08 Hz stimulation and exhibited frequency-dependent short-term synaptic depression (SD) during 0.5 to 100 Hz stimulus trains in 95 of 99 (96%) recorded neurons. During SD the steady-state eEPSC amplitude decreased, whereas the cumulative charge transfer increased in a frequency-dependent manner and saturated at 20 Hz. SD was similar during subjective day and night and decreased with increasing temperature. Paired-pulse stimulation (PPS) and voltage-dependent Ca2+ channel (VDCC) blockers were used to characterize a presynaptic release mechanism. Facilitation was present in 30% and depression in 70% of studied neurons during PPS. Synaptic transmission was reduced by blocking both N- and P/Q-type presynaptic VDCCs, but only the N-type channel blocker significantly relieved SD. Aniracetam inhibited AMPA receptor desensitization but did not alter SD. Thus we concluded that SD is the principal form of short-term plasticity at RHT synapses, which presynaptically and frequency-dependently attenuates light-induced glutamatergic RHT synaptic transmission protecting SCN neurons against excessive excitation.

scholarly journals , FREQUENCY-DEPENDENT MODULATION OF SHORT-TERM PLASTICITY OF GABAERGIC SYNAPTIC TRANSMISSION

2017 ◽  
Vol 63 (4) ◽  
pp. 10-16
Author(s):  
О.P. Кolesnyk ◽  
◽  
S. А. Fedulova ◽  
N. S. Veselovsky ◽  
◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Gabaergic Synaptic Transmission
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