ArticleBrain research2007
Regulation of neuronal PLCgamma by chronic morphine.
Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- PLCγ1 in dopamine neurons critically regulates striatal dopamine release via VMAT2 and synapsin III.Experimental & molecular medicine · 2023Article
- Effects of Compound 511 on BDNF-TrkB Signaling in the Mice Ventral Tegmental Area in Morphine-Induced Conditioned Place Preference.Cellular and molecular neurobiology · 2021Article
- Morphine and cocaine increase serum- and glucocorticoid-inducible kinase 1 activity in the ventral tegmental area.Journal of neurochemistry · 2015Article
- Opiate-induced molecular and cellular plasticity of ventral tegmental area and locus coeruleus catecholamine neurons.Cold Spring Harbor perspectives in medicine · 2012Review
- Removal of polysialylated neural cell adhesion molecule increases morphine analgesia and interferes with tolerance in mice.Brain research · 2011Article
- Neurotrophic factors and structural plasticity in addiction.Neuropharmacology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alterations in neurotrophic signaling pathways may contribute to the changes in the mesolimbic dopamine system induced by chronic morphine exposure. In a rat model of morphine dependence, we previously identified increased levels of phospholipase C gamma-1 (PLCgamma1) immunoreactivity specifically within the ventral tegmental area (VTA) following chronic morphine treatment. Using an antibody specific for the tyrosine-phosphorylated, activated form of PLCgamma1, we now show that chronic morphine also significantly upregulates PLCgamma1 activity in the VTA, as well as in the nucleus accumbens and hippocampus, regions which are also implicated in the reinforcing properties of morphine. In contrast, no increase in PLCgamma1 activity was found in the substantia nigra or dorsal striatum. HSV-mediated overexpression of PLCgamma1 in PC12 cells induced ERK activation via a mechanism dependent, in part, on both MAP-ERK kinase (MEK) and protein kinase C. PLCgamma1 overexpression in the VTA similarly induced ERK activation in the VTA in vivo. As chronic morphine treatment has been shown to increase ERK activity within the VTA, the current results suggest that increased PLCgamma1 activity may be an upstream mediator of this effect.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.