Abstract
Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry.
| Original language | English |
|---|---|
| Article number | e0179377 |
| Journal | PloS one |
| Volume | 12 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Jun 1 2017 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Agricultural and Biological Sciences(all)
Cite this
PirB regulates asymmetries in hippocampal circuitry. / Ukai, Hikari; Kawahara, Aiko; Hirayama, Keiko; Case, Matthew Julian; Aino, Shotaro; Miyabe, Masahiro; Wakita, Ken; Oogi, Ryohei; Kasayuki, Michiyo; Kawashima, Shihomi; Sugimoto, Shunichi; Chikamatsu, Kanako; Nitta, Noritaka; Koga, Tsuneyuki; Shigemoto, Ryuichi; Takai, Toshiyuki; Ito, Isao.
In: PloS one, Vol. 12, No. 6, e0179377, 01.06.2017.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - PirB regulates asymmetries in hippocampal circuitry
AU - Ukai, Hikari
AU - Kawahara, Aiko
AU - Hirayama, Keiko
AU - Case, Matthew Julian
AU - Aino, Shotaro
AU - Miyabe, Masahiro
AU - Wakita, Ken
AU - Oogi, Ryohei
AU - Kasayuki, Michiyo
AU - Kawashima, Shihomi
AU - Sugimoto, Shunichi
AU - Chikamatsu, Kanako
AU - Nitta, Noritaka
AU - Koga, Tsuneyuki
AU - Shigemoto, Ryuichi
AU - Takai, Toshiyuki
AU - Ito, Isao
PY - 2017/6/1
Y1 - 2017/6/1
N2 - Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry.
AB - Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry.
UR - http://www.scopus.com/inward/record.url?scp=85020437977&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85020437977&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0179377
DO - 10.1371/journal.pone.0179377
M3 - Article
VL - 12
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 6
M1 - e0179377
ER -