Prepuberal subchronic methylphenidate and atomoxetine induce different long-term effects on adult behaviour and forebrain dopamine, norepinephrine and serotonin in Naples High-Excitability rats

Ruocco, L; Carnevale, U.A. Gironi; Treno, C; Sadile, A.G.; Melisi, Daniela; Arra, Claudio; Ibba, M; Schirru, C; Carboni, Ezio

doi:10.1016/j.bbr.2010.02.020

Cited by 12 publications

(11 citation statements)

References 41 publications

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“…Our experimental evidence suggests that only two signaling modulators (DA and 5-HT) are effective in inducing long-term changes within neural networks, which are known to underlie attentive and motivational processes. In fact, prepuberal subchronic treatments with MPH and ATX, which block the reuptake of DA/NE and NE, respectively, did not similarly alter the SSA in adult rats, in spite of significant effects on DA, NA, 5-HT and metabolites at the prefronto-striatal interface in NHE rats [52]. By contrast, we found previously that an INDA-based prepuberal subchronic treatment is effective at a low dose (0.075 mg/kg) [53].…”

Section: Discussionmentioning

confidence: 81%

Prepuberal Stimulation of 5-HT7-R by LP-211 in a Rat Model of Hyper-Activity and Attention-Deficit: Permanent Effects on Attention, Brain Amino Acids and Synaptic Markers in the Fronto-Striatal Interface

et al. 2014

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The cross-talk at the prefronto-striatal interface involves excitatory amino acids, different receptors, transducers and modulators. We investigated long-term effects of a prepuberal, subchronic 5-HT7-R agonist (LP-211) on adult behaviour, amino acids and synaptic markers in a model for Attention-Deficit/Hyperactivity Disorder (ADHD). Naples High Excitability rats (NHE) and their Random Bred controls (NRB) were daily treated with LP-211 in the 5th and 6th postnatal week. One month after treatment, these rats were tested for indices of activity, non selective (NSA), selective spatial attention (SSA) and emotionality. The quantity of L-Glutamate (L-Glu), L-Aspartate (L-Asp) and L-Leucine (L-Leu), dopamine transporter (DAT), NMDAR1 subunit and CAMKIIα, were assessed in prefrontal cortex (PFC), dorsal (DS) and ventral striatum (VS), for their role in synaptic transmission, neural plasticity and information processing. Prepuberal LP-211 (at lower dose) reduced horizontal activity and (at higher dose) increased SSA, only for NHE but not in NRB rats. Prepuberal LP-211 increased, in NHE rats, L-Glu in the PFC and L-Asp in the VS (at 0.250 mg/kg dose), whereas (at 0.125 mg/kg dose) it decreased L-Glu and L-Asp in the DS. The L-Glu was decreased, at 0.125 mg/kg, only in the VS of NRB rats. The DAT levels were decreased with the 0.125 mg/kg dose (in the PFC), and increased with the 0.250 mg/kg dose (in the VS), significantly for NHE rats. The basal NMDAR1 level was higher in the PFC of NHE than NRB rats; LP-211 treatment (at 0.125 mg/kg dose) decreased NMDAR1 in the VS of NRB rats. This study represents a starting point about the impact of developmental 5-HT7-R activation on neuro-physiology of attentive processes, executive functions and their neural substrates.

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Section: Discussionmentioning

confidence: 81%

Prepuberal Stimulation of 5-HT7-R by LP-211 in a Rat Model of Hyper-Activity and Attention-Deficit: Permanent Effects on Attention, Brain Amino Acids and Synaptic Markers in the Fronto-Striatal Interface

et al. 2014

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“…We are also exploring the idea that neurogenesis in the DG of the hippocampus and SVZ is modulated by dopamine terminals from the mesencephalon, which is an attractive hypothesis that provides an explanation for the paradoxical effect of methylphenidate (Ritalin ® ), used for children suffering from attention deficit syndrome (ADS). Dopamine is perhaps needed for inducing neurogenesis in DG and SVZ, promoting neuronal plasticity, as suggested for Ritalin treated children (see Grund et al 2006; Schaeferd et al 2009; Kim et al 2009; also see Banerjee et al 2009; Ruocco et al 2010). The idea is to further investigate the receptors involved in this mechanism, to suggest the use of selective dopamine agonists to treat ADS like syndromes.…”

Section: Apoptosis and Neurogenesis After Perinatal Asphyxiamentioning

confidence: 96%

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

et al. 2010

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Delivery is a stressful and risky event menacing the newborn. The mother-dependent respiration has to be replaced by autonomous pulmonary breathing immediately after delivery. If delayed, it may lead to deficient oxygen supply compromising survival and development of the central nervous system. Lack of oxygen availability gives rise to depletion of NAD+ tissue stores, decrease of ATP formation, weakening of the electron transport pump and anaerobic metabolism and acidosis, leading necessarily to death if oxygenation is not promptly re-established. Re-oxygenation triggers a cascade of compensatory biochemical events to restore function, which may be accompanied by improper homeostasis and oxidative stress. Consequences may be incomplete recovery, or excess reactions that worsen the biological outcome by disturbed metabolism and/or imbalance produced by over-expression of alternative metabolic pathways. Perinatal asphyxia has been associated with severe neurological and psychiatric sequelae with delayed clinical onset. No specific treatments have yet been established. In the clinical setting, after resuscitation of an infant with birth asphyxia, the emphasis is on supportive therapy. Several interventions have been proposed to attenuate secondary neuronal injuries elicited by asphyxia, including hypothermia. Although promising, the clinical efficacy of hypothermia has not been fully demonstrated. It is evident that new approaches are warranted. The purpose of this review is to discuss the concept of sentinel proteins as targets for neuroprotection. Several sentinel proteins have been described to protect the integrity of the genome (e.g. PARP-1; XRCC1; DNA ligase IIIα; DNA polymerase β, ERCC2, DNA-dependent protein kinases). They act by eliciting metabolic cascades leading to (i) activation of cell survival and neurotrophic pathways; (ii) early and delayed programmed cell death, and (iii) promotion of cell proliferation, differentiation, neuritogenesis and synaptogenesis. It is proposed that sentinel proteins can be used as markers for characterising long-term effects of perinatal asphyxia, and as targets for novel therapeutic development and innovative strategies for neonatal care.

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“…However, this is unlikely since they also reported that optogenetic inhibition of the LC, which reduced forebrain NE release to a similar extent, did not produce this arrest. Furthermore, atomoxetine (Ruocco et al 2010) and reboxetine (Grandoso et al 2004) have been shown to suppress LC neuron firing rate or NE metabolism, effects which would block behavioral inhibition according to the present hypothesis. It is more likely, therefore, that the arrest resulted from an enhanced release the noradrenergic cotransmitter, galanin, which occurs at high firing rates and can produce inhibition of neural activity in brain areas supporting motivation and motor behaviors (discussed below).…”

Section: Development Of the Behavioral Inhibition Hypothesismentioning

confidence: 60%

The role of the central noradrenergic system in behavioral inhibition

Stone

Yang

Sarfraz

et al. 2011

Brain Research Reviews

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Although the central noradrenergic system has been shown to be involved in a number of behavioral and neurophysiological processes, the relation of these to its role in depressive illness has been difficult to define. The present review discusses the hypothesis that one of its chief functions that may be related to affective illness is the inhibition of behavioral activation, a prominent symptom of the disorder. This hypothesis is found to be consistent with most previous neuropsychopharmacological and immunohistochemical experiments on active behavior in rodents in a variety of experimental conditions using manipulation of neurotransmission at both locus coeruleus and forebrain adrenergic receptors. The findings support a mechanism in which high rates of noradrenergic neural activity suppress the neural activity of principal neurons in forebrain regions mediating active behavior. The suppression may be mediated through postsynaptic galaninergic and adrenergic receptors, and via the release of corticotrophin-releasing hormone. The hypothesis is consistent with clinical evidence for central noradrenergic system hyperactivity in depressives and with the view that this hyperactivity is a contributing etiological factor in the disorder. A similar mechanism may underlie the ability of the noradrenergic system to suppress seizure activity suggesting that inhibition of the spread of neural activation may be a unifying function.

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Prepuberal subchronic methylphenidate and atomoxetine induce different long-term effects on adult behaviour and forebrain dopamine, norepinephrine and serotonin in Naples High-Excitability rats

Cited by 12 publications

References 41 publications

Prepuberal Stimulation of 5-HT7-R by LP-211 in a Rat Model of Hyper-Activity and Attention-Deficit: Permanent Effects on Attention, Brain Amino Acids and Synaptic Markers in the Fronto-Striatal Interface

Prepuberal Stimulation of 5-HT7-R by LP-211 in a Rat Model of Hyper-Activity and Attention-Deficit: Permanent Effects on Attention, Brain Amino Acids and Synaptic Markers in the Fronto-Striatal Interface

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

The role of the central noradrenergic system in behavioral inhibition

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