The probability of transmitter release at a mammalian central synapse

Hessler, Neal A.; Shirke, Aneil M.; Malinow, Roberto

doi:10.1038/366569a0

Cited by 553 publications

(434 citation statements)

References 18 publications

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“…3b). Put differently, a given amount of random variations in G, simulating random fluctuations of transmitter release 51 , generates more haphazard activation during signal processing if the average value of G of the processing units is reduced. This sequence of effects computationally depicts a potential neurochemical mechanism for aging-related increase in neural noise: as aging attenuates neuromodulation, the impact of transmitter fluctuations on the overall level of haphazard neuronal activity is amplified in the aging brain.…”

Section: From Deficient Neuromodulation To Neural Noisementioning

confidence: 99%

Aging cognition: from neuromodulation to representation

Lindenberger

Sikström

2001

Trends in Cognitive Sciences

824

701

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Section: From Deficient Neuromodulation To Neural Noisementioning

confidence: 99%

Aging cognition: from neuromodulation to representation

Lindenberger

Sikström

2001

Trends in Cognitive Sciences

824

701

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“…1d), and synaptic transmission is typically unreliable [10][11][12][13] . Furthermore, most of these dendritic inputs are not directly related to ongoing sensory stimulation; rather, they reflect spatiotemporally structured internal activity.…”

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confidence: 99%

Regulation of spike timing in visual cortical circuits

2008

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A train of action potentials (a spike train) can carry information in both the average firing rate and the pattern of spikes in the train. But can such a spike-pattern code be supported by cortical circuits? Neurons in vitro produce a spike pattern in response to the injection of a fluctuating current. However, cortical neurons in vivo are modulated by local oscillatory neuronal activity and by top-down inputs. In a cortical circuit, precise spike patterns thus reflect the interaction between internally generated activity and sensory information encoded by input spike trains. We review the evidence for precise and reliable spike timing in the cortex and discuss its computational role.Reliability and precision are two different quantities. When you make an appointment with your friend, she can either keep the appointment or not show up at all. If she does show up, she might or might not be on time. The former uncertainty is related to reliability, whereas the latter is related to precision. When the same stimulus waveform is repeatedly injected at the soma of a neuron in vitro (FIG. 1a), a similar spike train is obtained on each trial 1,2 (FIG. 1b). When approximately the same number of spikes occur on each trial the neuron is said to be reliable, whereas when the spikes occur almost at the same time across trials it is said to be precise (FIG. 1c). For a single neuron, the potential information content of precise and reliable spike times is many times larger than that which is contained in the firing rate, which is averaged across a typical interval of a hundred milliseconds [3][4][5][6] . The information contained in spike timing is available immediately, rather than after an averaging period. Furthermore, the timing of patterns of spikes can potentially transmit even more information than the timing of the individual constituent spikes 3,7 . The potential relevance of spike patterns becomes apparent when we consider neurons at the population level: when a group of similar neurons (a 'pool') produces precise and reliable spike trains, the neurons they project to receive volleys of synchronous spikes 8,9 . This opens up the possibility of communicating between different cortical areas through synchronous spike volleys.In contrast to the in vitro situation described above, in the intact cortex most excitatory synaptic inputs arrive at the dendrites rather than at the soma (FIG. 1d), and synaptic transmission is typically unreliable [10][11][12][13] . Furthermore, most of these dendritic inputs are not directly related to ongoing sensory stimulation; rather, they reflect spatiotemporally structured internal activity. Therefore, when the same stimulus is presented repeatedly, the resulting spike trains are usually neither precise nor reliable when they are aligned to the stimulus onset 6 . Instead, HHMI Author ManuscriptHHMI Author Manuscript HHMI Author Manuscript neural activity in vivo might be dominated by internally generated complex reverberations or rhythmic oscillations, and precise and reliable sp...

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“…11 Other types of synaptic responses were not included because they were not required to account for the behaviour of the cells and because GABAergic and glutamatergic synapses account for the vast majority of synapses in the cerebral cortex. 8,62 Based on whole-cell recordings of hippocampal pyramidal and dentate gyrus cells, 19,47,64 kinetic models of GABA A , NMDA and AMPA receptors were fitted to experimental data using a simplex procedure (see details in Ref. 12).…”

mentioning

confidence: 99%

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Paré¹,

Lang²,

Destexhe³

1998

Neuroscience

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Abstract--The effect of synaptic inputs on somatodendritic interactions during action potentials was investigated, in the cat, using in vivo intracellular recording and computational models of neocortical pyramidal cells. An array of 10 microelectrodes, each ending at a different cortical depth, was used to preferentially evoke synaptic inputs to different somatodendritic regions. Relative to action potentials evoked by current injection, spikes elicited by cortical microstimuli were reduced in amplitude and duration, with stimuli delivered at proximal (somatic) and distal (dendritic) levels evoking the largest and smallest decrements, respectively. When the inhibitory postsynaptic potential reversal was shifted to around 50 mV by recording with KCl pipettes, synaptically-evoked spikes were significantly less reduced than with potassium acetate or cesium acetate pipettes, suggesting that spike decrements are not only due to a shunt, but also to voltage-dependent effects. Computational models of neocortical pyramidal cells were built based on available data on the distribution of active currents and synaptic inputs in the soma and dendrites. The distribution of synapses activated by extracellular stimulation was estimated by matching the model to experimental recordings of postsynaptic potentials evoked at different depths. The model successfully reproduced the progressive spike amplitude reduction as a function of stimulation depth, as well as the effects of chloride and cesium. The model revealed that somatic spikes contain an important contribution from proximal dendritic sodium currents up to ]100 µm and ]300 µm from the soma under control and cesium conditions, respectively. Proximal inhibitory postsynaptic potentials can prevent this dendritic participation thus reducing the spike amplitude at the soma. The model suggests that the somatic spike amplitude and shape can be used as a ''window'' to infer the electrical participation of proximal dendrites.Thus, our results suggest that inhibitory postsynaptic potentials can control the participation of proximal dendrites in somatic sodium spikes.1998 IBRO. Published by Elsevier Science Ltd.Key words: multicompartment models, intrinsic electrophysiological properties, in vivo intracellular recordings, action potentials, dendritic integration.By comparing the shape of antidromic, orthodromic and current-evoked action potentials (APs) in motoneurons, Coombs et al. 7 provided compelling evidence for the idea that APs are initiated at the initial segment (IS) and then invade the somatodendritic compartment. However, the applicability of this model to other cell types was questioned when the first intradendritic recordings revealed that dendrites can sustain active electrogenesis. 33,34,63 In neocortical and hippocampal pyramidal neurons for instance, intracellular recordings revealed that dendritic spikes can be elicited by synaptic inputs 5,9,30,52 and that they can amplify synaptic inputs electrotonically distant from the soma to initiate APs. 5 Moreover, the prox...

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The probability of transmitter release at a mammalian central synapse

Cited by 553 publications

References 18 publications

Aging cognition: from neuromodulation to representation

Aging cognition: from neuromodulation to representation

Regulation of spike timing in visual cortical circuits

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

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