The Role of Mouse Barrel Cortex in Tactile Trace Eye Blink Conditioning

DSpace Repository


Dateien:

URI: http://hdl.handle.net/10900/78259
http://nbn-resolving.de/urn:nbn:de:bsz:21-dspace-782596
http://dx.doi.org/10.15496/publikation-19659
Dokumentart: PhDThesis
Date: 2017-10-20
Language: English
Faculty: 8 Zentrale, interfakultäre und fakultätsübergreifende Einrichtungen
Department: Graduiertenkollegs
Advisor: Schwarz, Cornelius (Prof. Dr.)
Day of Oral Examination: 2017-09-28
DDC Classifikation: 500 - Natural sciences and mathematics
Keywords: Gehirn , Denken , Lernen , Plastizität , Kognition , Assoziation , Großhirn , Maus , Tiermodell
Other Keywords:
barrel cortex
primary sensory cortex
S1
trace eye blink conditioning
associative learning
optogenetics
electrophysiology
License: http://tobias-lib.uni-tuebingen.de/doku/lic_mit_pod.php?la=de http://tobias-lib.uni-tuebingen.de/doku/lic_mit_pod.php?la=en
Order a printed copy: Print-on-Demand
Show full item record

Abstract:

Mouse whisker-related primary somatosensory cortex (also known as barrel cortex, BCx) is required to form an association between a behaviorally relevant tactile stimulus and its consequences, only if the first conditioned stimulus CS (here a single whisker deflection), and the latter unconditioned stimulus US (here a corneal air puff) are separated by a ‘trace’ (brief memory period). I investigated whether tactile trace eye blink conditioning (TTEBC) has a correlate in BCx activity and whether such BCx activity in the two periods, CS and trace are required for learning. I trained three head-fixed mice on TTEBC to assess learning related functional plasticity of BCx by recording LFPs and multi-unit (MU) spiking from 4-shank laminar silicone probes (8 electrodes per shank, inter-shank distance 200μm) spanning the depths of the principal barrel column and its neighbors. Current source density analysis (CSD) showed the known short latency sink (~8ms) in L4 and L5/6 during CS presentation, followed by a weaker current sink during ongoing tactile stimulation, spanning across the column. At the same depth, a novel current source was discovered during the trace period. The latter two currents were consistently attenuated during TTEBC acquisition. Onset MU spike response to the CS (at a latency of <15ms) was stable in most units, while steady state CS-response (50-250ms) typically decreased below the pre-learning level. Spiking during the trace period also depressed during learning. These plastic changes were observed in neighboring shanks at a horizontal distance of up to 400μm. These findings show that BCx is functionally involved in TTEBC acquisition. Matching the lateral spread of the neuronal signal into the neighboring column, I found mice to generalize the CS-US association only to adjacent, but not to near and far whiskers. I next asked whether the involvement of BCx during the trace period has any causal role in TTEBC. I employed the well-established VGAT-ChR2 mouse line that, due to expression of channelrhodopsin-2 in inhibitory neurons (Zhao et al., 2011), blocks virtually all spikes in a column with high temporal precision, using blue light. I found that BCx functionality was required during CS presentation. However, mice learned normally when blocking BCx during the trace period. After learning, BCx activity during CS & trace was entirely dispensable for task performance. In summary, I demonstrate that the barrel column is involved in acquiring the TTEBC association. Nevertheless, the plasticity of the neuronal response in the trace period is a non- causal reflection of learning, and after learning, in the early phase of retention BCx is not needed for task performance. Future research need to establish if BCx assumes a more critical role in late consolidation. Further, the nature and projection of the signals measured during the learning have to be explored on the microscopic network and cellular level.

This item appears in the following Collection(s)