Ontology deals with questions concerning what things exist, and how such things may be associated according to similarities and differences and related within a hierarchy. Ontology provides a rigorous way to develop a general definition of a mineral species. Properties may be divided into two principal groups: an intrinsic property is characteristic of the object and is independent of anything else; an extrinsic property depends on the relation between the object and other things. A universal is an entity that is common to all objects in a set. Here the objects are mineral samples, each entity is a specific property of these minerals, and the set of objects is all mineral samples of that mineral species. The key intrinsic properties of a mineral species are its name, its end-member formula and Z (the number of formula units in the unit cell), its space group and the bond topology of the end-member structure. These are also universals as they are common to all mineral samples belonging to that mineral species. An archetype is a pure form which embodies the fundamental characteristics of an object. Thus the archetype of a mineral species embodies the above set of universals. Real mineral samples of this mineral species are imperfect copies of that archetype, with a range of chemical composition defined by the boundaries between end-member formulae of this and other end members of the same bond topology. The result is a formal definition of a mineral species: A specific mineral species is the set of imperfect copies of the corresponding archetype and is defined by the following set of universals: name, end-member formula and Z, space group, and bond topology of the end-member structure, with the range of chemical composition limited by the compositional boundaries between end members with the same bond topology.

Matter’s real essence is a ground for certain features of phenomena. Things in themselves are likewise a ground for certain features of phenomena. How do these claims relate? The former is a causal essentialism about physics, Stang argues; and the features so grounded are phenomenally nomically necessary. The latter involves a distinctive ontology of things in themselves, I argue; but the features so grounded are not noumenally nomically necessary. Stang’s version of Kant’s modal metaphysics is admirable, but does not go far enough. Kant’s causal essentialism involves the essences of fundamental properties, as well as of matter. And things in themselves are grounds, because they are substances, the ‘substrate’ of phenomena.

n-3 PUFA are receiving growing attention for their therapeutic potential in central nervous system (CNS) disorders. We have recently shown that long-term treatment with DHA alters the physiology of entorhinal cortex (EC) neurons. In the present study, we investigated by patch-clamp the effect of another major dietary n-3 PUFA, α-linolenic acid (LNA), on the intrinsic properties of EC neurons. Mice were chronically exposed to isoenergetic diets deficient in n-3 PUFA or enriched in either DHA or LNA on an equimolar basis. GC analyses revealed an increase in DHA (34 %) and a decrease in arachidonic acid (AA, − 23 %) in brain fatty acid concentrations after consumption of the DHA-enriched diet. Dietary intake of LNA similarly affected brain fatty acid profiles, but at a lower magnitude (DHA: 23 %, AA: − 13 %). Compared to the n-3 PUFA-deficient diet, consumption of DHA, but not LNA, induced membrane hyperpolarisation ( − 60 to − 70 mV), increased cellular capacitance (32 %) and spontaneous excitatory postsynaptic current frequency (50 %). We propose that the inefficiency of LNA to modulate cellular capacitance was related to its inability to increase the brain DHA:AA ratio over the threshold necessary to up-regulate syntaxin-3 (46 %) and translocate drebrin (40 % membrane:cytosol ratio). In summary, our present study shows that the increase in brain DHA content following chronic administration of LNA was not sufficient to alter the passive and synaptic properties of EC neurons, compared to direct dietary intake of DHA. These diverging results have important implications for the therapeutic use of n-3 PUFA in CNS disease, favouring the use of preformed DHA.

Thalamic and cortical neurons are richly and reciprocally interconnected and support recurrent functional loops in the intact brain, but the role of this circuitry is still poorly understood. Here, we present evidence—from cellular and from functional neuroimaging in control and clinical domains—that thalamocortical resonance is not only a prerequisite for normal cognition, but that its perturbation, in a dynamic sense (e.g. a dysrhythmia) can underlie a variety of neurological and psychiatric disorders.

The interaction between cortical input frequency and intrinsic thalamic neuron (TN) properties were investigated using intracellular recordings from mice TNs in thalamocortical (TC) slices. Excitatory postsynaptic potentials (EPSPs) of corticothalamic (CT) origin were recorded at TN membrane potentials (Vm) held, by current clamp means, between −59 and −55 mV to avoid low-threshold calcium currents (IT) activation. EPSPs elicited in ventrobasal neurons (n = 25) by stimulation in the internal capsule showed constant latency, relatively fast rise time (2.9 ± 0.56 ms) and short duration (26.6 ± 9.11 ms). EPSPs evoked by threshold stimulation (n = 10) showed similar characteristics (mean rise time, 2.74 ± 0.42 ms; mean duration, 30 ± 8.00 ms). The time course of CT synaptic facilitation was determined using pairs of stimuli. Paired-pulse facilitation (PPF) of CT EPSPs peaked at 25–30 ms stimulus intervals and decayed exponentially with an average time constant of 130 ms (n = 50). Application of the NMDA receptor blocker APV (25 μM, n = 4) did not modify PPF for any interstimulus interval studied but suppressed frequency facilitation evoked by trains of CT stimuli. We compared the number of spikes per stimulus (Fs) evoked in TNs by repetitive CT stimulation over a range of frequencies at different Vm. At hyperpolarized Vm (below −65 mV) and frequencies of stimulation ≥ 10 Hz, Fs decreased along the train while at depolarized Vm (above −59 mV) Fs increased along the train. Decremental patterns resulted from the activation of IT while facilitatory patterns emerged from superposition of synaptic and intrinsic mechanisms. At hyperpolarized Vm, steady-state Fs was maximal for frequencies ≤ 2 Hz, intermediate for frequencies between 2 and 10 Hz and zero at ≥ 10 Hz. At depolarized Vm, steady-state Fs increased with increasing frequencies (from 1 to 40 Hz).

We conclude that the CT–TN junctions are tuned to establish stable thalamocortical resonant dynamics.