Repeated amphetamine administration induces Fos in prefrontal cortical neurons that project to the lateral hypothalamus but not the nucleus accumbens or basolateral amygdala

Morshedi, Maud M.; Meredith, Gloria E.

doi:10.1007/s00213-007-1021-7

Cited by 27 publications

(26 citation statements)

References 73 publications

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“…Previous studies have reported that repeated doses of d-AMPH increase the activation of LH neurons in response to a challenge dose of d-AMPH [30]. Our finding that d-AMPH sensitization increases both spinophilin and VGLUT1 in LH is consistent with these earlier suggestions of d-AMPH-induced remodeling of inputs to LH [1].…”

Section: Discussionsupporting

confidence: 92%

A sensitizing d-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon

Boikess

O’Dell

Marshall

2010

Neuroscience Letters

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Numerous studies in this lab and others have reported psychostimulant-induced alterations in both synaptic protein expression and synaptic density in striatum and prefrontal cortex. Recently we have shown that chronic d-amphetamine (d-AMPH) administration in rats increased synaptic protein expression in striatum and limbic brain regions including hippocampus, amygdala, septum, and paraventricular nucleus of the thalamus (PVT). Potential synaptic changes in thalamic nuclei are interesting since the thalamus serves as a gateway to cerebral cortex and a nodal point for basal ganglia influences. Therefore we sought to examine drug-induced differences in synaptic protein expression throughout the diencephalon. Rats received an escalating (1-8 mg/kg) dosing regimen of d-AMPH for 5 weeks and were euthanized 28 days later. Radioimmunocytochemistry (RICC) revealed significant upregulation of both spinophilin and the vesicular glutamate transporter, VGLUT1, in PVT, mediodorsal (MD), and ventromedial (VM) thalamic nuclei as well as in lateral hypothalamus (LH) and habenula. Strong positive correlations were observed between VGLUT1 and spinophilin expression in PVT, medial habenula, MD, VM and LH of d-AMPH-treated rats. No significant d-AMPH effect was seen in sensorimotor cortices for either protein. Additionally, no significant differences in the general vesicular protein synaptophysin were observed for any brain region. These findings add to evidence suggesting that long-lasting stimulant-induced synaptic alterations are widespread but not ubiquitous. Moreover, they suggest that d-AMPH-induced synaptic changes may occur preferentially in excitatory synapses.

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Section: Discussionsupporting

confidence: 92%

A sensitizing d-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon

Boikess

O’Dell

Marshall

2010

Neuroscience Letters

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“…Interestingly, these authors were able to reverse this elevation in orexin cell activity with 6 weeks of fluoxetine treatment. Similarly, exposure to unpredictable chronic mild stress produced depressive-like behaviors in the tail suspension test, elevated plus maze and resident-intruder task; and 7 weeks exposure to the DORA almorexant produced an antidepressant-like behavioral effect in these tasks (Nollet et al, 2012). And, in a recent study, OxR1 mRNA expression in the amygdala was reported to be positively correlated with increased depressive-like behavior in the forced swim test (Arendt et al, 2013) - however it is possible that this effect might be caused by downregulated orexin system function.…”

Section: Effect Of Chronic Stress On the Orexin System And Implicatiomentioning

confidence: 99%

“…For example, Steiner et al (2013c) showed that 12 days of chronic almorexant treatment had no effect on the maintenance of CPP or locomotor sensitization in animals exposed to cocaine, morphine or amphetamine. However, as mentioned above, Nollet et al (2012) exposed mice to chronic almorexant treatment (7 weeks), which produced an antidepressant-like effect in the tail suspension test, elevated plus maze and resident-intruder task following exposure to unpredictable chronic mild stress. Interestingly, chronic treatment with the OxR1 antagonist ACT-335827 (4 weeks) did not alter total energy intake in cafeteria diet fed rats compared to controls (Steiner et al, 2013b).…”

Section: Potential Pitfalls For Approaches To Treat Neuropsychiatric mentioning

confidence: 99%

Orexin antagonists for neuropsychiatric disease: progress and potential pitfalls

Yeoh¹,

Campbell²,

James³

et al. 2014

Front. Neurosci.

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The tight regulation of sleep/wake states is critical for mental and physiological wellbeing. For example, dysregulation of sleep/wake systems predisposes individuals to metabolic disorders such as obesity and psychiatric problems, including depression. Contributing to this understanding, the last decade has seen significant advances in our appreciation of the complex interactions between brain systems that control the transition between sleep and wake states. Pivotal to our increased understanding of this pathway was the description of a group of neurons in the lateral hypothalamus (LH) that express the neuropeptides orexin A and B (hypocretin, Hcrt-1 and Hcrt-2). Orexin neurons were quickly placed at center stage with the demonstration that loss of normal orexin function is associated with the development of narcolepsy—a condition in which sufferers fail to maintain normal levels of daytime wakefulness. Since these initial seminal findings, much progress has been made in our understanding of the physiology and function of the orexin system. For example, the orexin system has been identified as a key modulator of autonomic and neuroendocrine function, arousal, reward and attention. Notably, studies in animals suggest that dysregulation of orexin function is associated with neuropsychiatric states such as addiction and mood disorders including depression and anxiety. This review discusses the progress associated with therapeutic attempts to restore orexin system function and treat neuropsychiatric conditions such as addiction, depression and anxiety. We also highlight potential pitfalls and challenges associated with targeting this system to treat these neuropsychiatric states.

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“…Importantly, the ORX system is involved in processing of food and drug rewards via circuitry that engages the LHA, nucleus accumbens, ventral tegmental area, and the prefrontal cortex (e.g., [120–124]). Notably, ORX neurons have been shown to respond to contextual cues for food and drugs in the conditioned place preference task [122, 125].…”

Section: Learning and The Motivation To Eat I: Cue-induced Feedingmentioning

confidence: 99%

Learning and the motivation to eat: Forebrain circuitry

Petrovich

2011

Physiology & Behavior

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Appetite and eating are not only controlled by energy needs, but also by extrinsic factors that are not directly related to energy balance. Environmental signals that acquire motivational properties through associative learning—learned cues—can override homeostatic signals and stimulate eating in sated states, or inhibit eating in states of hunger. Such influences are important, as environmental factors are believed to contribute to the increased susceptibility to overeating and the rise in obesity in the developed world. Similarly, environmental and social factors contribute to the onset and maintenance of anorexia nervosa and other eating disorders through interactions with the individual genetic background. Nevertheless, how learning enables environmental signals to control feeding, and the underlying brain mechanisms are poorly understood. We developed two rodent models to study how learned cues are integrated with homeostatic signals within functional forebrain networks, and how these networks are modulated by experience. In one model, a cue previously paired with food when an animal was hungry induces eating in sated rats. In the other model, food-deprived rats inhibit feeding when presented with a cue that signals danger, a tone previously paired with footshocks. Here evidence will be reviewed that the forebrain network formed by the amygdala, lateral hypothalamus and medial prefrontal cortex mediates cue-driven feeding, while a parallel amygdalar circuitry mediates suppression of eating by the fear cue. Findings from the animal models may be relevant for understanding aspects of human appetite and eating, and maladaptive mechanisms that could lead to overeating and anorexia.

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Repeated amphetamine administration induces Fos in prefrontal cortical neurons that project to the lateral hypothalamus but not the nucleus accumbens or basolateral amygdala

Cited by 27 publications

References 73 publications

A sensitizing d-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon

A sensitizing d-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon

Orexin antagonists for neuropsychiatric disease: progress and potential pitfalls

Learning and the motivation to eat: Forebrain circuitry

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