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Developmental expression of the basic fibroblast growth factor gene in rat brain
No full textBasic fibroblast growth factor (bFGF) is a trophic factor for a variety of neuronal/glial cell populations. The RNase protection assay, with a cRNA complementary to the coding region of bFGF mRNA, was used to investigate the brain distribution and developmental regulation of bFGF mRNA expression. In adult rats bFGF mRNA is distributed throughout the brain, the highest levels being observed in cerebral cortex, hippocampus and spinal cord. The levels of bFGF mRNA in all the brain structures are low in newborn rats, increase thereafter to reach a peak of expression around postnatal day 21. bFGF mRNA levels are significantly different between various brain structures during the first and second postnatal week. Adult and aged rats (Fisher 344) express the same levels of bFGF mRNA in the various brain regions. The onset of bFGF mRNA expression suggests that this growth factor is important for the maturation as well as for the maintenance of different cell populations of the central nervous system
Basic fibroblast growth factor mRNA increases in specific brain regions following convulsive seizures
No full textBasic fibroblast growth factor (bFGF) is a trophic factor synthesized in the central nervous system (CNS), where it is believed to play a role in neuronal maintenance and repair. Little is known about the regulation of this growth factor in the CNS. To determine whether the expression of the bFGF gene in the brain of adult animals changes in response to alterations of neuronal activity, we examined bFGF mRNA levels in several brain regions of rats experiencing focally-evoked convulsive seizures. Seizures were induced by microinjecting bicuculline unilaterally into an epileptogenic site within the deep prepiriform cortex, area tempestas (AT). By 5 h after initiation of brief limbic motor seizures from AT, there was a four fold increase in the levels of bFGF mRNA in the entorhinal cortex, hippocampus and olfactory bulb, but not in the caudate-putamen. The maximal expression of bFGF mRNA was reached by 10 h after seizure onset. In the same animals, the mRNA encoding nerve growth factor (NGF) was increased in entorhinal cortex and hippocampus, but not in the olfactory bulb. Our results demonstrate that neuronal activity can influence bFGF expression in an anatomically selective fashion and that acute changes in bFGF can occur in the uninjured mature brain. The increase in bFGF expression in response to excessive activation of specific neuronal circuitry may represent an adaptive response to protect against potential injury in those circuits
Stimulation of nerve growth factor biosynthesis in developing rat brain by reserpine: steroids as potential mediators
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Effects of GABA analogues and their interactions with morphine on locomotor activity in two inbred strains of mice
No full textDBA 2J (DBA) and C57BL6J (C57) display significant differences for their sensitivity to the effects of three GABA agonists (muscimol, THIP and SL 76002) on spontaneous locomotor activity. Particularly, these GABA agonists exhibit a biphasic response in locomotion of DBA mice, the lower dose eliciting an increase and the larger doses inducing a decrement of locomotion. Conversely, with the exception of THIP, the above reported GABA agonists cause only a reduction of locomotor activity in the C57 strain. Therefore, DBA mice seem to be more sensitive than C57 ones to the stimulant effect of GABA agonists on locomotoion. Piracetam, a compound structurally related to GABA, does not exhibit the biphasic dose-response curve obtained with muscimol, THIP and SL 76002 in DBA mice. When given in combination with morphine, muscimol, SL 76002 and piracetam do not modify the depressant effect induced by this opiate on locomotor activity of DBA mice; THIP, at the lowest dose used in the present study, antagonizes the decrease of locomotion elicited by morphine in this strain. Furthermore, muscimol, THIP, SL 76002 and piracetam antagonize morphine-induced hypermotility in C57 mice. The results are discussed with reference to the role that the strain of animals, the dosage and the time of testing have in the effects of GABA analogues as well as in their interactions with morphine on locomotor activity
Effects of sciatic nerve transplants after fimbria-fornix lesion: examination of the role of nerve growth factor
No full textTEMPORAL SEQUENCE OF CHANGES IN CENTRAL NORADRENERGIC SYSTEM OF RAT AFTER PROLONGED ANTI-DEPRESSANT TREATMENT - RECEPTOR DESENSITIZATION AND NEUROTRANSMITTER INTERACTIONS
No full textIt has been shown that different receptor components may be involved in the adaptive changes occurring in noradrenergic (NE) neurones after prolonged periods of exposure to antidepressant drugs. In this report the desensitization of NE-coupled adenylate cyclase (NE-AC), β-adrenergic receptors and [3H]imipramine ([3H]-IMI or [3H]desipramine ([3H]DMI) binding sites have been temporally correlated with in vivo changes of NE utilization. Normetanephrine (NMN) was measured as indicator of NE synaptic events involved in antidepressant action. Concentrations of normetanephrine were increased after acute desipramine (DMI), viloxazine and mianserin administration. Following 3 days of treatment, the antidepressant-induced increase of normetanephrine became tolerant and NE neurones were resistant to the antidepressant effect until the 15th day of treatment. After two weeks, DMI elicited a significant decrease in the content of normetanephrine. A different pattern of changes has been found in the temporal modification of [3H]IMI recognition sites, β-adrenoceptors and NE-AC activity after chronic DMI treatment. Binding sites and receptors were down regulated after 10 days of treatment preceding the decrease in normetanephrine content. No down-regulation was observed in [3H]-DMI binding sites. Studies on the effects of antidepressants during brain maturation revealed that the mechanisms which cause desensitization of β-receptors and [3H]-IMI binding sites appear in the early stages of postnatal life. Since [3H]-IMI and [3H]-DMI recognition sites have been shown to be located on serotonergic (5-HT) and noradrenergic neurones respectively, the interactions between NE and 5-HT neurones could represent possible mechanisms implicated in receptor desensitization. The experiments presented involving lesions of 5-HT neurones have clearly demonstrated that NE release in rat cerebral cortex is under a tonic serotonergic influence. Alterations in the chemico-physical properties of the synaptic membranes might be also taken in consideration for the mechanisms underlying receptor modulation. In fact, evidence is provided that in neural tissue phospholipid methylation can be affected. In conclusion, the temporal sequence of changes in cortical noradrenergic neurones, after chronic antidepressant treatment, has demonstrated that integrated mechanisms are operative for the function of the overall system
Serotonergic modulation of cortical rat noradrenergic system in the mechanism of action of antidepressant drugs
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