A free-energy principle has been proposed recently that accounts for action, perception and learning. This Review looks at some key brain theories in the biological (for example, neural Darwinism) and physical (for example, information theory and optimal control theory) sciences from the free-energy perspective. Crucially, one key theme runs through each of these theories — optimization. Furthermore, if we look closely at what is optimized, the same quantity keeps emerging, namely value (expected reward, expected utility) or its complement, surprise (prediction error, expected cost). This is the quantity that is optimized under the free-energy principle, which suggests that several global brain theories might be unified within a free-energy framework.

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The free-energy principle: a unified brain theory?

Prelude. Cycle 1. Introduction. Cycle 2. Structure defines function. Cycle 3. Diversity of cortical functions is provided by inhibition. Cycle 4. Windows on the brain. Cycle 5. A system of rhythms: from simple to complex dynamics. Cycle 6. Synchronization by oscillation. Cycle 7. The brain's default state: self-organized oscillations in rest and sleep. Cycle 8. Perturbation of the default patterns by experience. Cycle 9. The gamma buzz: gluing by oscillations in the waking brain. Cycle 10. Perceptions and actions are brain state-dependent. Cycle 11. Oscillations in the "other cortex:" navigation in real and memory space. Cycle 12. Coupling of systems by oscillations. Cycle 13. The tough problem. References.

Rhythms of the brain

The ionotropic glutamate receptors are ligand-gated ion channels that mediate the vast majority of excitatory neurotransmission in the brain. The cloning of cDNAs encoding glutamate receptor subunits, which occurred mainly between 1989 and 1992 ([Hollmann and Heinemann, 1994][1]), stimulated this

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The glutamate receptor ion channels

1980 Preface * 1999 Preface * 1999 Acknowledgements * Introduction * 1 Circular Logic * 2 Phase Singularities (Screwy Results of Circular Logic) * 3 The Rules of the Ring * 4 Ring Populations * 5 Getting Off the Ring * 6 Attracting Cycles and Isochrons * 7 Measuring the Trajectories of a Circadian Clock * 8 Populations of Attractor Cycle Oscillators * 9 Excitable Kinetics and Excitable Media * 10 The Varieties of Phaseless Experience: In Which the Geometrical Orderliness of Rhythmic Organization Breaks Down in Diverse Ways * 11 The Firefly Machine 12 Energy Metabolism in Cells * 13 The Malonic Acid Reagent ('Sodium Geometrate') * 14 Electrical Rhythmicity and Excitability in Cell Membranes * 15 The Aggregation of Slime Mold Amoebae * 16 Numerical Organizing Centers * 17 Electrical Singular Filaments in the Heart Wall * 18 Pattern Formation in the Fungi * 19 Circadian Rhythms in General * 20 The Circadian Clocks of Insect Eclosion * 21 The Flower of Kalanchoe * 22 The Cell Mitotic Cycle * 23 The Female Cycle * References * Index of Names * Index of Subjects

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/596B270197FE27DE5FABB598B6210622/S0025557200150892a.pdf/div-class-title-span-class-italic-the-geometry-of-biological-time-span-by-a-t-winfree-pp-544-dm68-corrected-second-printing-1990-isbn-3-540-52528-9-springer-div.pdf

The geometry of biological time , by A. T. Winfree. Pp 544. DM68. Corrected Second Printing 1990. ISBN 3-540-52528-9 (Springer)

Neuronal activity in the brain gives rise to transmembrane currents that can be measured in the extracellular medium. Although the major contributor of the extracellular signal is the synaptic transmembrane current, other sources — including Na+ and Ca2+ spikes, ionic fluxes through voltage- and ligand-gated channels, and intrinsic membrane oscillations — can substantially shape the extracellular field. High-density recordings of field activity in animals and subdural grid recordings in humans, combined with recently developed data processing tools and computational modelling, can provide insight into the cooperative behaviour of neurons, their average synaptic input and their spiking output, and can increase our understanding of how these processes contribute to the extracellular signal.

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The origin of extracellular fields and currents — EEG, ECoG, LFP and spikes

1. Dual intracellular recordings were made from synaptically coupled pyramidal cell-to-interneurone pairs (n = 5) of the cat visual cortex in vitro. Pre- and postsynaptic neurones were labelled with biocytin, followed by correlated light and electron microscopic analysis to determine all sites of synaptic interaction. 2. Pyramidal neurones in layers II-III elicited monosynaptic EPSPs in three distinct classes of smooth dendritic local-circuit neurones, namely basket cells (n = 3), a dendrite-targeting cell (n = 1) and a double bouquet cell (n = 1). Unitary EPSPs in basket cells were mediated by one, two, and two synaptic junctions, whereas the pyramid-to-dendrite-targeting cell and pyramid-to-double bouquet cell interaction were mediated by five and seven synaptic junctions, respectively. Recurrent synaptic junctions were found on all somato-dendritic compartments, with a tendency to be clustered close to the soma on the double bouquet and dendrite-targeting cells. The latter interneurones were reciprocally connected with pyramidal cells. 3. Unitary EPSPs had an average peak amplitude of 1005 +/- 518 microV, fast rise times (10-90%; 0.67 +/- 0.25 ms) and were of short duration (at half-amplitude, 4.7 +/- 1.0 ms). Their decay was monoexponential (tau = 7.8 +/- 4.3 ms) at hyperpolarized membrane potentials and appeared to be shaped by passive membrane properties (tau = 9.2 +/- 8.5 ms). All parameters of concomitantly recorded spontaneous EPSPs were remarkably similar (mean amplitude, 981 +/- 433 microV; mean rise time, 0.68 +/- 0.18 ms; mean duration, 4.7 +/- 1.7 ms). 4. In all three pyramidal-to-basket cell pairs, closely timed (10-50 ms) pairs of presynaptic action potentials resulted in statistically significant paired-pulse depression, the mean of the averaged second EPSPs being 80 +/- 11% of the averaged conditioning event. The overall degree of paired-pulse modulation was relatively little affected by either the amplitude of the preceding event or the inter-event interval. 5. The probability density function of the peak amplitudes of the unitary EPSPs could be adequately fitted with a quantal model. Without quantal variance, however, the minimum number of components in the model, excluding the failures, exceeded the number of electron microscopically determined synaptic junctions for all five connections. In contrast, incorporating quantal variance gave a minimum number of components which was compatible with the number of synaptic junctions, and which fitted the data equally well as models incorporating additional components but no quantal variance. For this model with quantal variance with the minimum number of components the estimate of the quantal coefficient of variation ranged between 0.33 and 0.46, and the corresponding quantal sizes ranged between 260 and 657 microV. The peak EPSP amplitudes in two of the four connections with more than one synaptic junction could be adequately described by a uniform binomial model for transmitter release. 6. In conclusion, at least three distinct interneurone classes receive local excitatory pyramidal cell input which they relay to different compartments on their postsynaptic target neurones. The reliability of transmission is high, but the fast time course of the EPSPs constrains their temporal summation. Due to the relatively small amplitude of unitary EPSPs several convergent inputs will therefore be required to elicit suprathreshold responses.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1997.sp022053

Effect, number and location of synapses made by single pyramidal cells onto aspiny interneurones of cat visual cortex

In synaptically connected layer 4 and 2/3 cells, NMDA receptors are required postsynaptically for the expression of LTP and presynaptically for the expression of LTD. NMDA receptors are necessary for both synaptic potentiation and depression, but the precise location of these receptors has not been established. By loading MK-801 into pre- or postsynaptic neurons during paired recordings of synaptically connected layer 4 and layer 2/3 neurons in mouse barrel cortex, we found that synaptic potentiation requires postsynaptic, but not presynaptic, NMDA receptors, whereas synaptic depression requires presynaptic, but not postsynaptic, NMDA receptors.

Spike timing–dependent long-term depression requires presynaptic NMDA receptors

2009 Special Issue: Network mechanisms of gamma oscillations in the CA3 region of the hippocampus

Hippocampal area CA3 is widely considered to function as an autoassociative memory. However, it is insufficiently understood how it does so. In particular, the extensive experimental evidence for the importance of carefully regulated spiking times poses the question as to how spike timing-based dynamics may support memory functions. Here, we develop a normative theory of autoassociative memory encompassing such network dynamics. Our theory specifies the way that the synaptic plasticity rule of a memory constrains the form of neuronal interactions that will retrieve memories optimally. If memories are stored by spike timing-dependent plasticity, neuronal interactions should be formalized in terms of a phase response curve, indicating the effect of presynaptic spikes on the timing of postsynaptic spikes. We show through simulation that such memories are competent analog autoassociators and demonstrate directly that the attributes of phase response curves of CA3 pyramidal cells recorded in vitro qualitatively conform with the theory.

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Matching storage and recall: hippocampal spike timing-dependent plasticity and phase response curves.

GABAergic interneurones are necessary for the emergence of hippocampal gamma-frequency network oscillations, during which they play a key role in the synchronization of pyramidal cell firing. However, it remains to be resolved how distinct interneurone subtypes contribute to gamma-frequency oscillations, in what way the spatiotemporal pattern of interneuronal input affects principal cell activity, and by which mechanisms the interneurones themselves are synchronized. Here we summarize recent evidence from cholinergically induced gamma-frequency network oscillations in vitro, showing that perisomatic-targeting GABAergic interneurones provide prominent rhythmic inhibition in pyramidal cells, and that these interneurones are synchronized by recurrent excitation. We conclude by presenting a minimal integrate-and-fire network model which demonstrates that this excitatory-inhibitory feedback loop is sufficient to explain the generation of intrahippocampal gamma-frequency oscillations.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2004.078758

Ole Paulsen

Papers

Effect, number and location of synapses made by single pyramidal cells onto aspiny interneurones of cat visual cortex

Spike timing–dependent long-term depression requires presynaptic NMDA receptors

2009 Special Issue: Network mechanisms of gamma oscillations in the CA3 region of the hippocampus

Matching storage and recall: hippocampal spike timing-dependent plasticity and phase response curves.

Hippocampal gamma-frequency oscillations: from interneurones to pyramidal cells, and back.