| First Author | Glickstein SB | Year | 2007 |
| Journal | Development | Volume | 134 |
| Issue | 22 | Pages | 4083-93 |
| PubMed ID | 17965053 | Mgi Jnum | J:127074 |
| Mgi Id | MGI:3762736 | Doi | 10.1242/dev.008524 |
| Citation | Glickstein SB, et al. (2007) Selective cortical interneuron and GABA deficits in cyclin D2-null mice. Development 134(22):4083-93 |
| abstractText | In contrast to cyclin D1 nulls (cD1(-/-)), mice without cyclin D2 (cD2(-/-)) lack cerebellar stellate interneurons; the reason for this is unknown. In the present study in cortex, we found a disproportionate loss of parvalbumin (PV) interneurons in cD2(-/-) mice. This selective reduction in PV subtypes was associated with reduced frequency of GABA-mediated inhibitory postsynaptic currents in pyramidal neurons, as measured by voltage-clamp recordings, and increased cortical sharp activity in the EEGs of awake-behaving cD2(-/-) mice. Cell cycle regulation was examined in the medial ganglionic eminence (MGE), the major source of PV interneurons in mouse brain, and differences between cD2(-/-) and cD1(-/-) suggested that cD2 promotes subventricular zone (SVZ) divisions, exerting a stronger inhibitory influence on the p27 Cdk-inhibitor (Cdkn1b) to delay cell cycle exit of progenitors. We propose that cD2 promotes transit-amplifying divisions in the SVZ and that these ensure proper output of at least a subset of PV interneurons. |
