Region-specific effects on BDNF expression after contingent or non-contingent cocaine i.v. self-administration in rats

Fumagalli, Fabio; Moro, Federico; Caffino, Lucia; Orrù, Alessandro; Cassina, Chiara; Giannotti, Giuseppe; Clemente, Angelo Di; Racagni, Giorgio; Riva, Marco A.; Cervo, Luigi

doi:10.1017/s146114571200096x

Cited by 45 publications

(42 citation statements)

References 26 publications

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“…It is known [60] that after an appropriate stimulus, a homogenous increase of BDNF mRNAs is carried out in the cell body, and it can be selectively targeted to the active synapse or non-selectively translocated to dendrites, but trapped by an active spine, where it would be quickly translated to BDNF protein. Therefore BDNF mRNA and BDNF protein may be non-simultaneously stored in different locations inside the neurons [61], which would explain the discrepancy between mRNA and protein levels found in the present study. We cannot dismiss the idea that in our model, the absence of injury in the hippocampus is due to the generation of BDNF in this area [62].…”

Section: Discussioncontrasting

confidence: 73%

Adaptive Plasticity in the Hippocampus of Young Mice Intermittently Exposed to MDMA Could Be the Origin of Memory Deficits

et al. 2015

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Concise title: Adaptive plasticity in the hippocampus of young mice exposed to MDMA 2 ABSTRACT (±)3,4-methylenedioxymethamphetamine (MDMA) is a relatively selective dopaminergic neurotoxin in mice. This study was designed to evaluate whether MDMA exposure affects their recognition memory and hippocampal expression of plasticity markers. Mice were administered with increasing doses of MDMA once per week for 8 weeks (three times in one day, every 3h) and sacrificed two weeks (2 w) or three months (3 m) later. The treatment did not modify hippocampal tryptophan hydroxylase 2, a serotonergic indicator, but induced an initial reduction in dopaminergic markers in substantia nigra, which remained stable for at least 3 months. In parallel, MDMA produced a decrease in dopamine (DA) levels in the striatum at 2 w, which were restored 3 months later, suggesting dopaminergic terminal regeneration (sprouting phenomenon). Moreover, recognition memory was assessed using the object recognition test. Young (2 w) and mature (3 m) adult mice exhibited impaired memory after 24 h but not after just 1 h retention interval. Two weeks after the treatment, animals showed constant levels of CREB but an increase in its phosphorylated form and in cFos expression. BDNF and especially Arc overexpression was sustained and long lasting.We cannot rule out the absence of MDMA injury in the hippocampus being due to the generation of BDNF. The levels of NMDAR2B, PSD-95 and synaptophysin were unaffected.In conclusion, the young mice exposed to MDMA showed increased expression of early key markers of plasticity, which sometimes remained for three months, and suggests hippocampal maladaptive plasticity that could explain memory deficits evidenced here.

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Section: Discussioncontrasting

confidence: 73%

Adaptive Plasticity in the Hippocampus of Young Mice Intermittently Exposed to MDMA Could Be the Origin of Memory Deficits

et al. 2015

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“…As previously described, cocaine enhances BDNF signaling in Nac (Fumagalli et al, 2013;Grimm et al, 2003;Huang et al, 2011;Li et al, 2013). When animals received BDNF infusions in Nac shell during cocaine self-administration and were tested after 10 days of withdrawal in extinction conditions, an increase in cocaine infusion was observed, suggesting an enhancement of cocaine-seeking behavior by BDNF infusions.…”

Section: … or When Bdnf Enhances Drug Seekingsupporting

confidence: 56%

“…However, an increase of the mature protein was only observed in the crude synaptosomal fraction obtained from brains of yoked animals. On the contrary, after 24 h of withdrawal, no change was evident in Nac, whereas an increase of BDNF was reported in mPFC in the crude synaptosomal fraction for all cocaine-treated animals (Fumagalli et al, 2013). Thus, the early abstinence appears as a dynamic phenomenon and depends on several parameters such as the presence of the drug, the brain location, and how the drug is administered.…”

Section: Dynamic Alterations Of Bdnf Levels During Withdrawalmentioning

confidence: 92%

BDNF During Withdrawal

Geoffroy¹,

Noble²

2017

Vitamins and Hormones

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“…In animal models of addiction, it has been extensively demonstrated that after cocaine withdrawal BDNF levels rise significantly and progressively in different brain regions such as the nucleus accumbens, amygdala and prefrontal cortex [50,51,52]. In human addicts, higher serum BDNF levels have been reported after 3 weeks of abstinence relative to healthy controls [53].…”

Section: Discussionmentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor Levels and Cocaine-Induced Transient Psychotic Symptoms

Corominas-Roso

Roncero²,

Eiroá-Orosa

et al. 2013

Neuropsychobiology

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Background: Cocaine-induced psychosis (CIP) is among the most serious adverse effects of cocaine. Reduced serum brain-derived neurotrophic factor (BDNF) levels have been reported in schizophrenia and psychosis; however, studies assessing the involvement of BDNF in CIP are lacking. Methods: A total of 22 cocaine-dependent patients (aged 33.65 ± 6.85) who had never experienced psychotic symptoms under the influence of cocaine (non-CIP) and 18 patients (aged 34.18 ± 8.54) with a history of CIP completed a 2-week detoxification program in an inpatient facility. Two serum samples were collected from each patient at baseline and at the end of the protocol. Demographic, consumption and clinical data were recorded for all patients. A paired group of healthy controls was also included. Results: At the beginning of the detoxification treatment, serum BDNF levels were similar in both the non-CIP and the CIP groups. During early abstinence, the non-CIP group exhibited a significant increase in serum BDNF levels (p = 0.030), whereas the CIP group exhibited a decrease. Improvements in depression (Beck Depression Inventory, BDI, p = 0.003) and withdrawal symptoms (Cocaine Selective Severity Assessment, CSSA, p = 0.013) show a significant positive correlation with serum BDNF levels in the non-CIP group, whereas no correlation between the same variables was found in the CIP group. Conclusions: This study suggests that BDNF plays a role in the transient psychotic symptoms associated with cocaine consumption. In the non-CIP group, the increase in serum BDNF appears to be driven by the effects of chronic cocaine consumption and withdrawal. In contrast, patients with CIP share some of the neurotrophic deficiencies that characterize schizophrenia and psychosis.

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Region-specific effects on BDNF expression after contingent or non-contingent cocaine i.v. self-administration in rats

Cited by 45 publications

References 26 publications

Adaptive Plasticity in the Hippocampus of Young Mice Intermittently Exposed to MDMA Could Be the Origin of Memory Deficits

Adaptive Plasticity in the Hippocampus of Young Mice Intermittently Exposed to MDMA Could Be the Origin of Memory Deficits

BDNF During Withdrawal

Serum Brain-Derived Neurotrophic Factor Levels and Cocaine-Induced Transient Psychotic Symptoms

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