Cell state · L2
NEU.EXC_CT.Ca2_sensor
245 cells in the full atlas (not the displayed sample).
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Marker genes
ALCAM, APOD, ATP1B2, BHLHE40, CAMK2A, CTNNB1, DCBLD1, GABRA5, GABRD, GLRA3, HPCA, HPCAL1, ITM2C, KCNG3, LGMN, MRAP2, NR4A2, NRGN, NTM, OLFML2B, PCDH11X, RAB8B, SCN3B, SEZ6L, ZBTB7C
Annotation genes
BHLHE40, CAMK2A, GABRA5, GABRD, GLRA3, HPCA, HPCAL1, NR4A2, NRGN
Annotation rationales
The Ca²⁺-sensor triad NRGN, HPCA, HPCAL1 confers subthreshold Ca²⁺ decoding in distal dendrites, while CAMK2A converts Ca²⁺ pulses into long-term synaptic changes typical of corticothalamic (CT) neurons. Activity-dependent TFs NR4A2 and BHLHE40 indicate ongoing spiking/plasticity. Extrasynaptic inhibitory subunits GABRA5/GABRD and glycine receptor GLRA3 provide tonic shunt inhibition that tempers dendritic noise and stabilizes firing thresholds.
Functional implications
CT neurons integrate thalamic feedback while maintaining stability: Ca²⁺-driven plasticity (NRGN/HPCA/HPCAL1 → CAMK2A) strengthens relevant synapses, and tonic GABA/glycine currents (GABRA5/GABRD/GLRA3) prevent over-excitation. This combination supports learning-dependent tuning of sensory gain, contributes to spindle/ripple coordination, and reduces seizure propensity by enforcing homeostatic E/I control during corticothalamic loops.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.