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Biomedical subjects

T McLardy

Publications and source records attributed to T McLardy.

17 recordsLinked to original sources

Thalamic attention circuitry normal and psychotic.

Cortex is not preprogrammed to recognise transthalamic sensory patterns or to prioritize them for motor reaction. Network subsets for these abilities are taught into neocortex in early life from the hippocampi where species-significant pattern-recognition and reaction-prioritizing ARE genetically preprogrammed. Thereafter whenever an indoctrinated subset of cortex is activated via thalamic sensory relay nuclei it axonally activates a specific subset of neurons within the thalamic pulvinar. Pulvinar analogically integrates this with concurrent specific inputs from the thalamic dorsomedial nucleus which itself is integrating inputs from the prefrontal cortex (goals) and the amygdaloid nuclei (moods). The pulvinar's specific integral is then axonally projected back to cortex UNDER NON-SPECIFIC BOOST from the thalamic centromedian nucleus. This ensures unitary attention focussing influenced by acquired priorities. Given that neocortex is genetically organized as a classifying mechanism, it also permits virtually limitless part-novel learning and best-match reality-testing of percepts (and concepts in humans). In schizophrenia the non-specific booster system is bilaterally blocked at the centromedian nucleus. In mania the non-specific thalamic system is shunted, at midbrain, into the non-specific direct cortical system. In melancholia both of these brainstem systems are subnormal in non-specific output. Figure 1 schematizes the main axonal circuitry. Analogical integration occurs within predominantly dendro-dendritic networks.

Attention

Pulsatory motor of mitosis.

The basic building block of cell nuclei is postulated to be a macromolecule consisting of an exon of DNA linked laterally with a polypeptide whose DNA-distalmost NH2 radical is in an electronic pulsatory state which constitutes a centriole. The pulsating centriole impresses oscillating excitation along the polypeptide to the DNA rendering the DNA partially oxidative of substances in the fluid environment. This oxidation activates a second type of oscillating excitation distad along the polypeptide, keeping the centriole in its pulsatory state. The exon-polypeptide-centriole macromolecule is, in brief, in unique inter-end-dependent steadystate dynamic equilibrium. Replication of the exon and then the polypeptide occurs through oscillatory resonance-attraction, seriatim, of identical sub-entities from the fluid environment. Final duplication of the centriole occurs through pulsatory resonance-induction acting upon the daughter polypeptide's terminal NH2. The resultant daughter centriole is, however, in 180 degrees opposite pulsatory phase. Opposite-phase pulsators repel one-another; like-phase pulsators attract one-another. These postulated pulsator, and oscillator, principles afford explanation of the main phenomena of mitosis. Pathological foreshortening in polypeptide replication offers explanation of malignant mitosis.

Base Sequence

Species-typical IRMs in CAL-3 hippocampi and habituation memory in area dentata.

Sector CA3c hippocampi contains the genetically preprogrammed innate releaser mechanisms (IRMs) for species-typical threats; CS3b/a the genetically preprogrammed innate releaser mechanisms for species-typical nutrients, playmates and surroundings. Activation of these mechanisms, whilst triggering species-appropriate motor responses via the fornix and the mammillo-tegmental tract, teaches the meaningfulness of the recognized patterns, via the mammillo-thalamic tract, into the neocortex which is unprogrammed genetically but passively files all percepts transmitted via the thalamic sensory relay nuclei. Sector CA1 contains the genetically preprogrammed innate releaser mechanisms for mating and parenting, but becomes available only after hormonal activation of its circuitry at puberty. Area dentata, with boosting from the medial septal theta system, automatically filters-out from transmission into CA most once-attended patterns which CA3 has not recognized. The filtered patterns are filed within area dentata, ie. area dentata automatically builds a memory bank of percepts not requiring motor reaction, including a conceptual map of the habitat. Desynchronization of the theta system by reward or punishment signals from the brainstem, in response to some once-attended novel patterns, halts the filter-file habituation mechanism, permitting some early-life learning of non-innate releaser patterns to be added to CA3c and CA3b/a. In adulthood the relatively redundant ammonshorn may continue to be activated in parallel with the immensely more versatile neocortex, and the fornices may be bilaterally transected with relative impunity.

Agonistic Behavior

Anatomical rationale of ablative surgery for temporal lobe seizures and dyscontrol: suggested stereo-chemode chelate-blockade alternative.

Anatomical data now strongly suggest that the common factor in curative ablative operations for the commonest (i.e. ammonshorn-sclerosis) form of temporal-lobe epilepsy is the cutting of the ipsilateral temporoammonic perforant path's "nozzle" where it leaves the entorhinal cortex to "spray" along the length of the ammonshorn. This substantially deafferences ipsilateral dentate granule-cells and hence the unsclerosed pyramidal neurons notably in "resistant sector" CA2, which are probably the source of the seizures. Stereo-chemoding of long-lasting (experimentally tested) chelates along the zone of peculiarly zinc-rich synapses of the mossy fibre system should block the commissural as well as the ipsilateral inputs to these residual neurons, to give higher percentage cures, and could probably be performed bilaterally (where indicated, in adults) without endangering memory function.

Chelating Agents