We have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5-HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462-471, 1993). This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation. Neonatal 6-OHDA injection causes norepinephrine (NE) depletion in the frontal cortex, which triggers a compensatory increase of dopamine, serotonin (5-HT), and met-enkephalin content correlated by the increased density of tyrosine hydroxylase- and 5-HT-positive axons. In perinatal morphine-treated rats, no compensatory changes are observed after neonatal 6-OHDA depletion of NE in the frontal cortex.

Perinatal morphine.II: changes in cortical plasticity / E. Germani, E. Lesma, S. De Biasi, A.M. Di Giulio, A. Bertelli, A. Gorio. - In: JOURNAL OF NEUROSCIENCE RESEARCH. - ISSN 0360-4012. - 42:6(1995), pp. 829-834.

Perinatal morphine.II: changes in cortical plasticity

E. Lesma
Secondo
;
A.M. Di Giulio;A. Gorio
Ultimo
1995

Abstract

We have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5-HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462-471, 1993). This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation. Neonatal 6-OHDA injection causes norepinephrine (NE) depletion in the frontal cortex, which triggers a compensatory increase of dopamine, serotonin (5-HT), and met-enkephalin content correlated by the increased density of tyrosine hydroxylase- and 5-HT-positive axons. In perinatal morphine-treated rats, no compensatory changes are observed after neonatal 6-OHDA depletion of NE in the frontal cortex.
6-OHDA; morphine; neuronal plasticity; opioid receptors
Settore BIO/14 - Farmacologia
1995
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/200636
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