Thalamic afferent activation of supragranular layers in auditory cortex in vitro: a voltage sensitive dye study

Abstract

We studied auditory thalamocortical interactions in vitro, using an auditory thalamocortical brain slice preparation. Cortical activity evoked by electrical stimulation of the medial geniculate nucleus (MGN) was investigated through field potential recordings and voltage sensitive dyes. Experiments were performed in slices obtained from adult mice (9–14 weeks). Stimulus evoked activity was detected in the granular and supragranular layers after a short latency (5–6 ms). In 9–14 weeks old mice infragranular activity was detected in 10 of 24 preparations and was found to be increased in younger mice (p 31–64). In 14 of 24 slices a prominent horizontal spread was observed, which extended into cortical areas lateral to A1. In these experiments, the shortest onset latencies and largest signal amplitudes were located in the supragranular layers of A1. In areas lateral to A1, shortest onset latencies were located in the granular layer, while largest signal amplitudes were found in the supragranular layers. Evoked cortical activity was sensitive to removal of extracellular Ca 2+ or application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM). Short repetitive stimulation, resembling thalamic burst activity (three pulses at 100 Hz), resulted in an increase of signal amplitude and excited area by ∼25%, without changing the overall spatiotemporal activity profile. Blockade of N-methyl- d-aspartate receptors by 2-amino-5-phosphonopentanoate (AP5, 50 μM) reduced amplitudes and excited area by ∼15–30%, irrespective of stimulation frequency. Application of bicuculline (10 μM) greatly increased cortical responses to thalamic stimulation. Under these conditions, evoked activity displayed a pronounced horizontal spread in combination with a 2–3-fold increase in amplitude. In conclusion, afferent thalamic inputs primarily activate supragranular and granular layers in the auditory cortex of adult mice. This activation is predominantly mediated by non-NMDA receptors, while GABA A receptor-mediated inhibition limits the horizontal and vertical spread of activity.