Olfactory, respiratory, limbic, interoceptive, and entorhinal-hippocampal processes are typically studied separately. This leaves an explanatory gap: how does a chemically sampled environment become a subjectively significant state that acquires a bodily value and a spatiotemporal position, becomes linked to past experience, and to probable action? To close this gap, the present paper introduces the notion of the chemosensory-valence imprint — a distributed, phase-updated configuration that binds chemical content, the side and order of input, respiratory phase, interoceptive state, valence, memory, and available action trajectories.
The architecture of the imprint is derived from the functional organization of the olfactory-respiratory system. The nasal cycle creates recurring windows of active environmental sampling; early olfactory pathways link the chemical object to valence and memory without an obligatory initial thalamic relay; interoceptive circuits calibrate the biological value of the signal; the entorhinal-hippocampal system embeds the state within context, event order, and the geometry of possible transitions. In the human piriform cortex, ipsilateral and contralateral odor representations are temporally segregated within a single sniff, so that the side and sequence of input are preserved at the cortical level. In the proposed architecture, the anterior commissure aligns the two cortical representations of the chemical object; bilateral organization thereby links the shared identity of the odor to its spatiotemporal coordinate.
From this architecture, five transdiagnostic functional modes of disruption are derived: a mismatch between the chemical signal and the autonomic valence response; a failure of contextual salience calibration; selective blunting of positive valence; degradation or lateralization of the chemosensory input; and disruption of spatiotemporal indexing. These modes describe breakdowns of individual operations of the imprint rather than new diagnostic categories.
The model generates distinguishable predictions concerning the dependence of the configuration on interoceptive state, the side and order of chemosensory input, respiratory phase, semantic context, and the spatiotemporal position of the event. Its causal test requires the independent manipulation of these parameters while controlling for chemical identity, intensity, familiarity, sensory load, airflow, trigeminal involvement, attention, and expectation. Predictions separately address the central construct and the functional modes of disruption, and are accompanied by explicit conditions of falsification.
The model occupies a functional and pathophysiological level: it is not a theory of the etiology of the disorders under discussion, and it does not reduce salience, memory, or cognitive mapping to olfaction. Its explanatory territory is limited to the operation by which olfactory-respiratory input links the chemical structure of the environment to bodily state, spatiotemporal context, and probable action. Within these boundaries, the chemosensory-valence imprint forms a testable bridge from sensory physiology to predictive behavior.