Decreases in calmodulin binding proteins and calmodulin dependent protein phosphorylation in the medial preoptic area at the onset of maternal behavior in the rat
✍ Scribed by Danton H. O'Day; Michael Lydan; Jason Watchus; Alison S. Fleming
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 203 KB
- Volume
- 64
- Category
- Article
- ISSN
- 0360-4012
- DOI
- 10.1002/jnr.1112
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The onset of maternal behavior is characterized by the action of certain hormones, neuropeptides and neurotransmitters and a concomitant increase in the expression of c‐Fos in the medial preoptic area (MPOA) but the signaling events that lie between have not been characterized. Because several of these hormones, neuropeptides and neurotransmitters function by activating Ca^2+^/calmodulin (CaM) mediated signaling pathways, many of which can lead to c‐Fos expression, the goal of the current work was to identify calmodulin binding proteins (CaMBPs) or specific CaM‐dependent phosphoproteins that might be involved. Probing of SDS‐PAGE gels of extracts from the hippocampus, parietal cortex, basolateral amygdala and MPOA with recombinant ^35^S‐VU1‐calmodulin (CaM) revealed 30 Ca^2+^‐dependent and 4–6 Ca^2+^‐independent CaMBPs. Statistically significant maternal behavior‐related decreases in four Ca^2+^‐dependent CaMBPs (∼31 kDa, 50% decrease; ∼33 kDa, 32%; ∼50 kDa, 35%; ∼60 kDa, 33%) were observed specifically in the MPOA. Numerous proteins were phosphorylated in a Ca^2+^ CaM‐dependent manner with two (MWs ∼61 Da, ∼58 kDa) showing a lack of phosphophorylation only in the MPOA. The selective decrease in CaMBPs coupled with the absence of CaM‐dependent phosphoproteins implies that changes in Ca^2+^/CaM‐mediated signaling may mediate some of the MPOA‐specific processes during the onset of maternal behavior in the rat. J. Neurosci. Res. 64:599–605, 2001. © 2001 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract The CNS contains high levels of the glycosaminoglycan hyaluronan, and neural cells express a variety of proteins that are members of the hyaladherin family of hyaluronan‐binding proteins. We have previously shown that the hyaladherin RHAMM (receptor for hyaluronan‐mediated motility; CD1
## Abstract Hyperglycemia and acidosis are the key factors in diabetic complications. It has been shown that acute or chronic diabetes alters serotonin levels in brain. However, the mechanism of hyperglycemia‐ or acidosis‐induced changes in serotonin levels remains poorly understood. Because Ca^2+^