scholarly journals Lateralized role of prefrontal cortex in guiding orienting behavior

2020 ◽  
Author(s):  
Ali Mohebi ◽  
Karim G. Oweiss

Orienting movements are essential to sensory-guided reward-seeking behaviors. Prefrontal cortex (PFC) is believed to exert top-down control over a range of goal-directed behaviors and is hypothesized to bias sensory-guided movements. However, the nature of PFC involvement in controlling sensory-guided orienting behaviors has remained largely unknown. Here, we trained rats on a delayed two-alternative forced-choice task requiring them to hold an orienting decision in working memory before execution is cued. Medial PFC (mPFC) Inactivation using either Muscimol or optogenetics impaired choice behavior. However, optogenetic impairment depended on the specific trial epoch during which inactivation took place. In particular, we found a lateralized role for mPFC during the presentation of instruction cues but this role became bilateral when inactivation occurred later in the delay period. Electrophysiological recording of multiple single-unit activity further provided evidence that this lateralized selectivity is cell-type specific. Our results suggest a previously unknown role of mPFC in mediating sensory-guided representation of orienting behavior and a potentially distinct cell-type specific role in shaping such representation across time.

1999 ◽  
Vol 274 (40) ◽  
pp. 28697-28707 ◽  
Author(s):  
Robert M. Tjin Tham Sjin ◽  
Kenneth A. Lord ◽  
Abbas Abdollahi ◽  
Barbara Hoffman ◽  
Dan A. Liebermann

2007 ◽  
Vol 353 (4) ◽  
pp. 1017-1022 ◽  
Author(s):  
Johji Nomura ◽  
Akinori Hisatsune ◽  
Takeshi Miyata ◽  
Yoichiro Isohama

2016 ◽  
Vol 116 (3) ◽  
pp. 1261-1274 ◽  
Author(s):  
Amanda K. Kinnischtzke ◽  
Erika E. Fanselow ◽  
Daniel J. Simons

The functional role of input from the primary motor cortex (M1) to primary somatosensory cortex (S1) is unclear; one key to understanding this pathway may lie in elucidating the cell-type specific microcircuits that connect S1 and M1. Recently, we discovered that a subset of pyramidal neurons in the infragranular layers of S1 receive especially strong input from M1 (Kinnischtzke AK, Simons DJ, Fanselow EE. Cereb Cortex 24: 2237–2248, 2014), suggesting that M1 may affect specific classes of pyramidal neurons differently. Here, using combined optogenetic and retrograde labeling approaches in the mouse, we examined the strengths of M1 inputs to five classes of infragranular S1 neurons categorized by their projections to particular cortical and subcortical targets. We found that the magnitude of M1 synaptic input to S1 pyramidal neurons varies greatly depending on the projection target of the postsynaptic neuron. Of the populations examined, M1-projecting corticocortical neurons in L6 received the strongest M1 inputs, whereas ventral posterior medial nucleus-projecting corticothalamic neurons, also located in L6, received the weakest. Each population also possessed distinct intrinsic properties. The results suggest that M1 differentially engages specific classes of S1 projection neurons, thereby regulating the motor-related influence S1 exerts over subcortical structures.


2018 ◽  
Vol 27 (9) ◽  
pp. 1533-1544 ◽  
Author(s):  
Daniel J Flores ◽  
ThuyVy Duong ◽  
Luke O Brandenberger ◽  
Apratim Mitra ◽  
Aditya Shirali ◽  
...  

2018 ◽  
Vol 115 (20) ◽  
pp. 5253-5258 ◽  
Author(s):  
Hideyuki Yanai ◽  
Shiho Chiba ◽  
Sho Hangai ◽  
Kohei Kometani ◽  
Asuka Inoue ◽  
...  

IFN regulatory factor 3 (IRF3) is a transcription regulator of cellular responses in many cell types that is known to be essential for innate immunity. To confirm IRF3’s broad role in immunity and to more fully discern its role in various cellular subsets, we engineered Irf3-floxed mice to allow for the cell type-specific ablation of Irf3. Analysis of these mice confirmed the general requirement of IRF3 for the evocation of type I IFN responses in vitro and in vivo. Furthermore, immune cell ontogeny and frequencies of immune cell types were unaffected when Irf3 was selectively inactivated in either T cells or B cells in the mice. Interestingly, in a model of lipopolysaccharide-induced septic shock, selective Irf3 deficiency in myeloid cells led to reduced levels of type I IFN in the sera and increased survival of these mice, indicating the myeloid-specific, pathogenic role of the Toll-like receptor 4–IRF3 type I IFN axis in this model of sepsis. Thus, Irf3-floxed mice can serve as useful tool for further exploring the cell type-specific functions of this transcription factor.


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