Brain-derived neurotrophic factor expression is increased in the rat amygdala, piriform cortex and hypothalamus following repeated amphetamine administration

Meredith, Gloria E.; Callen, Shannon; Scheuer, Deborah A.

doi:10.1016/s0006-8993(02)03160-8

Cited by 153 publications

(110 citation statements)

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“…Although multiple injections of high-dose AMPH (5 mg/kg) have been reported to increase BDNF expression and production in multiple brain regions (Meredith et al, 2002), to our knowledge this is the first report that low-dose AMPH treatment increases levels of BDNF protein. A 1-week infusion of AMPH (1 mg/kg/day) significantly increased hippocampal BDNF levels in non-exercising sham and CCI groups.…”

Section: Effects Of Amphetaminementioning

confidence: 73%

“…In addition, anti-depressant drugs strengthen BDNF mRNA up-regulation when given in combination with exercise (Russo-Neustadt et al, 1999. Repeated treatments with d-amphetamine (AMPH) have also been reported to increase BDNF levels in multiple brain regions (Meredith et al, 2002). Brain injury induced by experimental stroke or cortical ablation reduces brain levels and/or turnover rates of NE, dopamine (DA) and/or 5-HT for days or weeks after injury .…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

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Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats

et al. 2008

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Prior work has shown that d-amphetamine (AMPH) treatment or voluntary exercise improves cognitive functions after traumatic brain injury (TBI). In addition, voluntary exercise increases levels of brain-derived neurotrophic factor (BDNF). The current study was conducted to determine how AMPH and exercise treatments, either alone or in combination, affect molecular events that may underlie recovery following controlled cortical impact (CCI) injury in rats. We also determined if these treatments reduced injury-induced oxidative stress. Following a CCI or sham injury, rats received AMPH (1 mg/kg/day) or saline treatment via an ALZET ® pump and were housed with or without access to a running wheel for 7 days. CCI rats ran significantly less than sham controls, but exercise level was not altered by drug treatment. On day 7 the hippocampus ipsilateral to injury was harvested and BDNF, synapsin I and phosphorylated (P) -synapsin I proteins were quantified. Exercise or AMPH alone significantly increased BDNF protein in sham and CCI rats, but this effect was lost with the combined treatment. In sham-injured rats synapsin I increased significantly after AMPH or exercise, but did not increase after combined treatment. Synapsin levels, including the Psynapsin/total synapsin ratio, were reduced from sham controls in the saline-treated CCI groups, with or without exercise. AMPH treatment significantly increased the P-synapsin/total synapsin ratio after CCI, an effect that was attenuated by combining AMPH with exercise. Exercise or AMPH treatment alone significantly decreased hippocampal carbonyl groups on oxidized proteins in the CCI rats, compared with saline-treated sedentary counterparts, but this reduction in a marker of oxidative stress was not found with the combination of exercise and AMPH treatment. These results indicate that, whereas exercise or AMPH treatment alone may induce plasticity and reduce oxidative stress after TBI, combining these treatments may cancel each other's therapeutic effects. Keywordscontrolled cortical impact; norepinephrine; oxidized proteins; running wheel; traumatic brain injury *Corresponding author. Tel: +1-310-825-1904; fax: +1-310-794-2147. E-mail address: ggriesbach@mednet.ucla.edu (G. S. Griesbach). 1 G.S.G. and R.L.S. contributed equally to this work. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 June 27. Published in final edited form as:Neuroscience. 2008 June 23; 154(2): 530-540. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptTraumatic brain injury (TBI) continues to be one of the leading causes of mortality and morbidity, with approximately 5.3 million Americans suffering from enduring disabilities resulting from TBI (Binder et al., 2005). Despite many experimental and clinical efforts using numerous therapeutic approaches, there are currently no proven treatments to alleviate the sequelae of TBI or to enhance recovery of function.Our laboratories have been investigating treatment strategies that may faci...

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Section: Effects Of Amphetaminementioning

confidence: 73%

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats

et al. 2008

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“…Role m In satiety; m water reward (Horger et al, 1999;Kernie et al, 2000;Nakagawa et al, 2003); improvement in glucose metabolism (Tonra et al, 1999;Nakagawa et al, 2000;Ono et al, 2000) m Drug reward (Horger et al, 1999) K BDNF in mesolimbic pathways regulates appetitive behavior (Eisch et al, 2003;Itoh et al, 2004); BDNF within hypothalamus regulates energy balance by enhancing catabolic processes (Xu et al, 2003) K BDNF may play a role in behavioral sensitization to drugs (Guillin et al, 2001) and potentially to palatable food via its dopaminergic and opioidergic (Siuciak et al, 1994;Siuciak et al, 1995) effects Repeated exposure kIn the hippocampus (Molteni et al, 2002;Molteni et al, 2004) m In mesocorticolimbic areas including, hypothalamus (Meredith et al, 2002;Butovsky et al, 2005); m and upregulation of BDNF receptors during withdrawal (Toda et al, 2002;Grimm et al, 2003); incubation of drug craving, accompanied by m in BDNF (Grimm et al, 2003) BDNF gene knockout animals m In food intake and obesity (Lyons et al, 1999;Kernie et al, 2000;Rios et al, 2001;Xu et al, 2003) k Drug reward (Hall et al, 2003;Horger et al, 1999) Orexin m Food intake (Edwards et al, 1999;Harris et al, 2005) Relapse to drug seeking behavior (Harris et al, 2005) Activated by SGAs ( Ibanez-Rojo et al, 1993;Bencherif et al, 2005) are available, though, to extend preclinical palatable food opioid findings to humans. Neuroimaging studies in obese people reported in...…”

Section: Bdnfmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

138

142

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Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

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“…(2) Recent evidence from animal studies demonstrated an increase in BDNF expression in rat amygdala, piriform cortex and hypothalamus following repeated amphetamine administration, 10 suggesting that BDNF may have a role in psychostimulant response. (3) Reduced central serotonergic activity has been implicated in poor impulse regulation (a key feature of ADHD) in young children, adults and animals; 11,12 heterozygous bdnf7mice demonstrate physiologic disturbances in central serotonergic neurons linked with behavioural abnormalities (including increased aggressiveness) suggesting that endogenous BDNF may be critical for the normal development and function of central serotonergic neurons 13 and, hence, impulse regulation.…”

mentioning

confidence: 99%

Association of the paternally transmitted copy of common Valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene with susceptibility to ADHD

et al. 2005

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Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable, neurodevelopmental disorder with onset in early childhood. Genes involved in neuronal development and growth are, thus, important etiological candidates and brain-derived neurotrophic factor (BDNF), has been hypothesized to play a role in the pathogenesis of ADHD. BDNF is a member of the neurotrophin family and is involved in the survival and differentiation of dopaminergic neurons in the developing brain (of relevance because drugs that block the dopamine transporter can be effective therapeutically). The common Val66Met functional polymorphism in the human BDNF gene (rs 6265) was genotyped in a collaborative family-based sample of 341 white UK or Irish ADHD probands and their parents. We found evidence for preferential transmission of the valine (G) allele of BDNF (odds ratio, OR ¼ 1.6, P ¼ 0.02) with a strong paternal effect (paternal transmissions: OR ¼ 3.2, P ¼ 0.0005; maternal transmissions: OR ¼ 1.00; P ¼ 1.00). Our findings support the hypothesis that BDNF is involved in the pathogenesis of ADHD. The transmission difference between parents raises the possibility that an epigenetic process may be involved. Keywords: attention deficit hyperactivity disorder; association study; neurotrophic factor; polymorphism Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder that affects 2-5% of school-aged children with more boys diagnosed than girls. 1 It is characterized by marked and pervasive inattention, overactivity and impulsiveness and causes significant social, educational and psychological problems. Quantitative genetic research over the last decade, from family, twin and adoption studies has firmly established that ADHD has a significant genetic contribution. 2 The medications most often used for ADHD are psychostimulants including methylphenidate and dexamphetamine. Precise therapeutic mechanisms of these drugs in ADHD remain unclear, although methylphenidate is known to inhibit the dopamine transporter. As a result, most candidate gene studies to date have focused on the dopamine system. 3 Positive findings have been successfully replicated for variants in the D4 dopamine receptor (DRD4), 4 D5 dopamine receptor (DRD5) 5 and the dopamine transporter (DAT1). 6 These family-based meta-analyses each report small effect sizes with odds ratios of less than 1.5, indicating that if they are true susceptibility variants for ADHD their contribution to the overall phenotype is small. Given that ADHD is a neurodevelopmental disorder, genes involved in neuronal development and growth represent an important set of candidates for involvement in the pathogenesis. One such candidate that has been postulated to play a role in ADHD is BDNF (MIM 113505). 7 The gene encoding BDNF is located at 11p13 and codes for a precursor peptide (proBDNF), which is proteolytically cleaved to form the mature protein. Only one nonsynonymous polymorphism in the human BDNF gene (rs 6265) has been identified, a single nucleotide polymorph...

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Brain-derived neurotrophic factor expression is increased in the rat amygdala, piriform cortex and hypothalamus following repeated amphetamine administration

Cited by 153 publications

References 63 publications

Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats

Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Association of the paternally transmitted copy of common Valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene with susceptibility to ADHD

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