4.7 Article

Frequency-Dependent Plasticity in the Temporal Association Cortex Originates from the Primary Auditory Cortex, and Is Modified by the Secondary Auditory Cortex and the Medial Geniculate Body

Journal

JOURNAL OF NEUROSCIENCE
Volume 42, Issue 26, Pages 5254-5267

Publisher

SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1481-21.2022

Keywords

auditory cortex; auditory fear conditioning; medial geniculate body; plasticity; temporal association cortex

Categories

Funding

  1. National Natural Science Foundation of China [32070994, 31872769]
  2. Key-Area Research and Development Program of Guangdong Province [2018B030340001]
  3. Science and Technology Program of Guangzhou [202007030013]

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The brain regions responsible for the formation of auditory threat memory and perceptual decisions remain uncertain. This study used chemogenetic and optogenetic manipulations to investigate the roles of different brain regions in threat memory learning. The results suggest that the temporal association cortex plays a crucial role in auditory threat memory formation, with inputs from A1, A2, and MGm.
The brain areas that mediate the formation of auditory threat memory and perceptual decisions remain uncertain to date. Candidates include the primary (A1) and secondary (A2) auditory cortex, the medial division of the medial geniculate body (MGm), amygdala, and the temporal association cortex. We used chemogenetic and optogenetic manipulations with in vivo and in vitro patch-clamp recordings to assess the roles of these brain regions in threat memory learning in female mice. We found that conditioned sound (CS) frequency-dependent plasticity resulted in the formation of auditory threat memory in the temporal association cortex. This neural correlated auditory threat memory depended on CS frequency information from A1 glutamatergic subthreshold monosynaptic inputs, CS lateral inhibition from A2 glutamatergic disynaptic inputs, and non-frequency-specific facilitation from MGm glutamatergic monosynaptic inputs. These results indicate that the A2 and MGm work together in an inhibitory-facilitative role.

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