BDNF gene expression is reduced in the frontal cortex of dopamine transporter knockout mice

Fumagalli, Fabio; Racagni, Giorgio; Colombo, Elena; Riva, Marco A.

doi:10.1038/sj.mp.4001370

Cited by 76 publications

(60 citation statements)

References 10 publications

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“…Such perturbations might result in "miswiring," as well as alterations in synaptic functioning. Indeed, rodent studies found that prenatal stress reduced expression of brainderived neurotrophic factor (BDNF) in the prefrontal cortex and striatum (Fumagalli, Bedogni, Perez, Racagni, & Riva, 2004 synaptic plasticity and cellular homeostasis, may also play a role in the etiology of psychiatric disorders (Fumagalli, Racagni, Colombo, & Riva, 2003).In addition to the prenatal stress effects, prenatal alcohol exposure in the present study yielded a relatively high withdrawal (aversion) response for the feather stimulus. Prenatal alcohol exposure induced group differences on the initial trial as well as the last trial for the feather.…”

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confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

et al. 2008

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Disrupted sensory processing, characterized by over-or underresponsiveness to environmental stimuli, has been reported in children with a variety of developmental disabilities. This study examined the effects of prenatal stress and moderate-level prenatal alcohol exposure on tactile sensitivity and its relationship to striatal dopamine system function in thirty-eight 5-to 7-year-old rhesus monkeys. The monkeys were from four experimental conditions: (a) prenatal alcohol exposed, (b) prenatal stress, (c) prenatal alcohol exposed + prenatal stress, and (d) sucrose controls. Increased D 2 receptor binding in the striatum, evaluated using positron emission tomography neuroimaging, was related to increased withdrawal (aversion) responses to repetitive tactile stimuli and reduced habituation across trials. Moreover, prenatal stress significantly increased overall withdrawal responses to repetitive tactile stimulation compared to no prenatal stress.Sensory processing disorders, characterized by under-or overresponsiveness to sensory stimulation that most individuals perceive as harmless (Ayres & Robbins, 1979) NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript estimated to occur in 5% of the general population (Ahn, Miller, Milberger, & McIntosh, 2004) and seem to pose a unique challenge for people with developmental disabilities (Baranek, 2002), including autism, attention deficit hyperactivity disorder (ADHD), fragile X syndrome, and other developmental disabilities (Ayres & Tickle, 1980;Baranek, 1999;Baranek & Berkson, 1994;Baranek, Foster, & Berkson, 1997;Cermak & Daunhauer, 1997;Grandin, 1992;Kinnealey, 1973;Larson, 1982;Mangeot et al., 2001;Miller et al., 1999). Understanding the neurobiological processes associated with sensory processing disruptions is important to developing appropriate preventative and intervention approaches.This study examined whether disrupted sensory processing occurs in monkeys as a result of prenatal exposure to alcohol and/or stress, and if so, whether it would be associated with dopamine functioning in the striatum assessed with positron emission tomography (PET) neuroimaging. We employed a primate model for these studies because in human studies causal conclusions are difficult to reach due to confounding variables. Even with the best statistical analyses it is difficult, if not impossible, to separate completely the effects of variables associated with alcohol use, such as psychological stress, tobacco use, or chaotic home life, from the effects of fetal alcohol exposure per se. Nonhuman primates also have the advantage of gestation characteristics and early development similar to the human, and their shorter life span makes longitudinal studies somewhat easier to conduct. Rhesus monkeys were used because of the large amount of available data on their behavior and development in laboratory settings (Harlow & Harlow, 1969;Suomi, 1997) A. Jean Ayres (1964), an occupational therapist and educational psychologist, coined the term "tactile defensiveness" t...

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confidence: 57%

Section: Discussionmentioning

confidence: 99%

Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

et al. 2008

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“…However, it is not clear whether the effects of olanzapine on BDNF levels in PFC are direct, or indirect, such as by its modulation of dopaminergic tone. Lesions and other manipulations of mesocortical dopaminergic function cause significant deficits in cognitive performance (Pioli et al, 2008) and also alter BDNF gene expression in frontal cortical regions (Fumagalli et al, 2003). It is relevant to the current study that BDNF expression and release can change rapidly (minutes to hours) in response to synaptic activity (Poo, 2001).…”

Section: Discussionmentioning

confidence: 99%

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

Elsworth

Morrow

Hajszán

et al. 2011

Neuropsychopharmacol

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Enduring cognitive deficits exist in schizophrenic patients, long-term abusers of phencyclidine (PCP), as well as in animal PCP models of schizophrenia. It has been suggested that cognitive performance and memory processes are coupled with remodeling of pyramidal dendritic spine synapses in prefrontal cortex (PFC), and that reduced spine density and number of spine synapses in the medial PFC of PCP-treated rats may potentially underlie, at least partially, the cognitive dysfunction previously observed in this animal model. The present data show that the decrease in number of asymmetric (excitatory) spine synapses in layer II/III of PFC, previously noted at 1-week post PCP treatment also occurs, to a lesser degree, in layer V. The decrease in the number of spine synapses in layer II/III was sustained and persisted for at least 4 weeks, paralleling the observed cognitive deficits. Both acute and chronic treatment with the atypical antipsychotic drug, olanzapine, starting at 1 week after PCP treatment at doses that restore cognitive function, reversed the asymmetric spine synapse loss in PFC of PCP-treated rats. Olanzapine had no significant effect on spine synapse number in saline-treated controls. These studies demonstrate that the effect of PCP on asymmetric spine synapse number in PFC lasts at least 4 weeks in this model. This spine synapse loss in PFC is reversed by acute treatment with olanzapine, and this reversal is maintained by chronic oral treatment, paralleling the time course of the restoration of the dopamine deficit, and normalization of cognitive function produced by olanzapine.

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“…However, BDNF elevations with AMPH treatment could also be related to drug-induced increases of 5-HT and DA. Monoaminergic activity, which is elevated with AMPH, has been found to enhance the expression of BDNF (Fumagalli et al, 2003;Mattson et al, 2004;Miklic et al, 2004;Juric et al, 2006;Luellen et al, 2007). A third putative mechanism for AMPH to increase BDNF is through the cocaine-and amphetamine-regulated transcript (CART).…”

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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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BDNF gene expression is reduced in the frontal cortex of dopamine transporter knockout mice

Cited by 76 publications

References 10 publications

Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

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

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