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Kamijo, T. C.

Publications and source records attributed to Kamijo, T. C..

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Pathway-specific short-term synaptic dynamics and lateral inhibition shape frequency-dependent input integration and population-level pattern separation in the dentate gyrus

The dentate gyrus (DG) decorrelates overlapping entorhinal inputs into distinct granule-cell representations, a computation central to pattern separation and to reducing interference in episodic memory. The three excitatory pathways to granule cells -- the lateral perforant path (distal dendrites), the medial perforant path (middle dendrites), and proximal inputs -- carry distinct short-term synaptic dynamics, but how these combine with lateral inhibition to set the frequency dependence of DG integration and pattern separation remains unclear. Here we integrate mechanism, function, and robustness into a single computational modeling study spanning three complementary model tiers, using Tsodyks-Markram short-term synaptic parameters grounded in prior slice electrophysiology. In a biophysically detailed 37-compartment granule-cell model (Tier 1), the distal (lateral) pathway facilitates at low frequency, the middle (medial) pathway depresses, and the proximal pathway is mixed, producing frequency- and pathway-dependent integration; three-pathway summation is mildly sublinear, and a direct granule-cell-to-granule-cell lateral inhibition -- a shunting connection emulating disynaptic feedforward inhibition without an explicit interneuron -- further attenuates it. In a reduced leaky-integrate-and-fire network with the same dynamics (Tier 2), pattern separation is frequency-dependent, rising to a gamma-band maximum at 40 Hz that is reproducible across independently wired networks, whereas the basket-cell-inhibition magnitude varies with the random connectivity. In a three-layer population network (Tier 3), pattern separation is robust: although single granule-cell spike counts are highly sensitive to input noise, the population-level separation code is nearly noise-invariant (a roughly 60-fold dissociation), and separation is governed by the magnitude of local lateral inhibition rather than its targeting. Two claims that hold at the single-cell scale -- a microsecond spike-timing-precision requirement and an advantage of finely targeted inhibition -- do not survive at the network scale. Pathway-specific synaptic dynamics and lateral inhibition thus shape frequency-dependent integration and noise-robust population pattern separation in the DG. Author SummaryThe dentate gyrus (DG) performs pattern separation: it takes overlapping cortical inputs and makes their DG representations more distinct, a computation thought to reduce memory interference. How does the DG do this? We approach the question across three scales in a single computational study. First (mechanism), we show in a biophysically detailed granule-cell model that the three anatomical input pathways carry different short-term synaptic dynamics -- the distal (lateral perforant path) input facilitates, the middle (medial perforant path) input depresses, and the proximal input is mixed -- so that the cells response depends on input frequency and pathway. Second (function), in a reduced network model we show that these dynamics, combined with lateral inhibition, tune pattern separation in a frequency-selective way. Third (robustness), we find that although a single granule cells spike count is highly sensitive to input noise, the population-level separation code is nearly noise-invariant -- a "noise paradox" in which population coding rescues what is fragile at the single-cell level. We also show that two claims that appear at the single-cell scale -- a microsecond spike-timing-precision requirement, and an advantage of finely targeted inhibition -- do not survive at the network scale: what matters is the amount of local inhibition, not how it is distributed. The synaptic parameters are grounded in prior slice recordings; the model integrates the mechanism.

neuroscience↗

CA3 sparsity stabilises high-connectivity recurrent autoassociation: complementary binary and spiking computational modes in a DG->CA3 model

The dentate gyrus (DG) decorrelates entorhinal inputs (pattern separation); area CA3 completes partial cues via recurrent autoassociation. The density of CA3 recurrent connectivity is contested, with estimates from ~0.9% (Guzman et al., 2016) to ~9-11% (Sammons et al., 2024). We ask how completion depends on recurrent connectivity (C_RC) and whether the answer is intrinsic to CA3 dynamics or inherited from the DG front-end. Using a trisynaptic model that crosses two DG implementations (a point-LIF network with Santhakumar et al. (2005) topology; an abstract fixed-in-degree spiking network validated size-invariant to N=107) with two CA3 autoassociators (binary k-WTA; spiking excitatory/inhibitory attractor) via burst-gated mossy-fiber detonators, we find: (i) completion in the binary CA3 improves monotonically with C_RC and is robust across DG implementation; (ii) the spiking CA3 exhibits a runaway transition whose boundary is set by the product (active fraction x C_RC), is not rescued by stronger feedback inhibition (8x), is insensitive to input overlap, and is size-invariant (N=104-105); (iii) the two CA3 types have opposite failure modes (binary under-completes at low C_RC; spiking runs away at high active-fraction x C_RC) and a capacity/stability trade-off. Adult neurogenesis flips sign by the same logic: excitability-only young cells densify the code and collapse the spiking attractor, but if they recruit feedback inhibition they instead sparsen it and preserve recall. Consistent with classical sparse-coding attractor theory (Tsodyks & Feigel'man, 1988), we propose that the contested CA3 connectivity is better read as an implementation-mode trade-off, and that the empirically sparse activity of CA3 (a~0.02-0.05) is the condition that lets a highly recurrent network perform stable autoassociation.

neuroscience↗