Differential effects of ziprasidone and haloperidol on immobilization stress-induced mRNA BDNF expression in the hippocampus and neocortex of rats

Park, Sung Woo; Lee, Chan Hong; Lee, Jung Goo; Lee, Sun Jung; Kim, Na Ri; Choi, Soyeon; Kim, Young Hoon

doi:10.1016/j.jpsychires.2008.05.010

Cited by 50 publications

(20 citation statements)

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“…In primates, 6-month treatment with haloperidol also upregulated prefrontal and temporal cortical D2 mRNA expression [20]. In contrast, haloperidol downregulated hippocampal and cortical Bdnf expression in rats [33–35], although one hippocampal study showed no change [36]. …”

Section: Resultsmentioning

confidence: 99%

The Neuroprotective Disease-Modifying Potential of Psychotropics in Parkinson's Disease

Lauterbach

Fontenelle

Teixeira

2012

Parkinson's Disease

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Neuroprotective treatments in Parkinson's disease (PD) have remained elusive. Psychotropics are commonly prescribed in PD without regard to their pathobiological effects. The authors investigated the effects of psychotropics on pathobiological proteins, proteasomal activity, mitochondrial functions, apoptosis, neuroinflammation, trophic factors, stem cells, and neurogenesis. Only findings replicated in at least 2 studies were considered for these actions. Additionally, PD-related gene transcription, animal model, and human neuroprotective clinical trial data were reviewed. Results indicate that, from a PD pathobiology perspective, the safest drugs (i.e., drugs least likely to promote cellular neurodegenerative mechanisms balanced against their likelihood of promoting neuroprotective mechanisms) include pramipexole, valproate, lithium, desipramine, escitalopram, and dextromethorphan. Fluoxetine favorably affects transcription of multiple genes (e.g., MAPT, GBA, CCDC62, HIP1R), although it and desipramine reduced MPTP mouse survival. Haloperidol is best avoided. The most promising neuroprotective investigative priorities will involve disease-modifying trials of the safest agents alone or in combination to capture salutary effects on H3 histone deacetylase, gene transcription, glycogen synthase kinase-3, α-synuclein, reactive oxygen species (ROS), reactive nitrogen species (RNS), apoptosis, inflammation, and trophic factors including GDNF and BDNF.

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Section: Resultsmentioning

confidence: 99%

The Neuroprotective Disease-Modifying Potential of Psychotropics in Parkinson's Disease

Lauterbach

Fontenelle

Teixeira

2012

Parkinson's Disease

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“…Stress triggers increases in markers of apoptosis (Bachis et al 2008, Jalalvand et al 2008, Lucassen et al 2001), decreases in neurogenesis (Alonso et al 2004, Bain et al 2004, Bland et al 2006, Chen H. et al 2006, Cherng et al 2010, Czeh et al 2001, Czeh et al 2002, Czeh et al 2007, Dagyte et al 2009, Ferragud et al 2010, Goshen et al 2008, Gould et al 1997, Heine et al 2004, Hill et al 2006, Koo and Duman 2008, Lagace et al 2010, Lee K.J. et al 2006, Luo et al 2005, Malberg and Duman 2003, Oomen et al 2007, Pham et al 2003, Rosenbrock et al 2005, Thomas et al 2007, Torner et al 2009, Westenbroek et al 2004, Xu H. et al 2006, Zhou et al 2007) but see (Parihar et al 2009), and region-specific changes in brain derived neurotrophic factor (BDNF), both increases (Aguilar-Valles et al 2005, Berton et al 2006, Bland et al 2005, Bland et al 2007, Charrier et al 2006, Dagnino-Subiabre et al 2006, Givalois et al 2001, Givalois et al 2004, Hammack et al 2009, Lee Y. et al 2006, Li et al 2007, Marmigere et al 2003, Molteni et al 2009, Pardon et al 2005, Rage et al 2002, Schulte-Herbruggen et al 2009) and decreases (Adlard and Cotman 2004, Aleisa et al 2006, Bland et al 2007, Cavus and Duman 2003, Charrier et al 2006, Chen JX et al 2008, Duric and McCarson 2005, Duric and McCarson 2006, Dzitoyeva et al 2008, Fuchikami et al 2009, Gronli et al 2006, Kozlovsky et al 2007, Li et al 2009, Luo et al 2004, Murakami et al 2005, Park et al 2009, Scaccianoce et al 2003, Smith et al 1995, Takeda et al 2006, Vaidya et al 1999, van Donk...…”

Section: Stress Can Trigger Remodeling and Microdamage In The Brainmentioning

confidence: 99%

Depression: A repair response to stress-induced neuronal microdamage that can grade into a chronic neuroinflammatory condition?

Wager-Smith

Markou

2011

Neuroscience & Biobehavioral Reviews

134

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Depression is a major contributor to the global burden of disease and disability, yet it is poorly understood. Here we review data supporting a novel theoretical model for the biology of depression. In this model, a stressful life event leads to microdamage in the brain. This damage triggers an injury repair response consisting of a neuroinflammatory phase to clear cellular debris, and a spontaneous tissue regeneration phase involving neurotrophins and neurogenesis. During healing, released inflammatory mediators trigger sickness behavior and psychological pain via mechanisms similar to those that produce physical pain during wound healing. The depression remits if the neuronal injury repair process resolves successfully. Importantly, however, the acute psychological pain and neuroinflammation often transition to chronicity and develop into pathological depressive states. This hypothesis for depression explains substantially more data than alternative models, including why emerging data show that analgesic, anti-inflammatory, pro-neurogenic and pro-neurotrophic treatments have antidepressant effects. Thus, an acute depressive episode can be conceptualized as a normally self-limiting but highly error-prone process of recuperation from stress-triggered neuronal microdamage.

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“…The atypical ziprasidone does not increase BDNF on its own, but prevents stress from decreasing it in the hippocampus. Interestingly, when the older typical antipsychotic (neuroleptic) haloperidol was used as a comparator, it not only did not prevent the stress-induced decreases in BDNF in the hippocampus, but actually exacerbated them (Park et al 2009 neuroprotective effects in patients with bipolar disorder, as revealed by increases in NAA observed via magnetic resonance spectroscopy (MRS) and increases cortical gray matter observable in MRI scans (Moore et al 2000;Bearden et al 2007;Martinowich et al 2007). Sheline et al (2003) found that greater compared with less use of antidepressants protected against the loss of hippocampal volume seen in patients with unipolar depression.…”

Section: Cross-sensitization Among Stressors Affective Episodes Andmentioning

confidence: 99%

Mechanisms of Illness Progression in the Recurrent Affective Disorders

Post

2010

Neurotox Res

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Along with genetic vulnerability, multiple environmental factors convey liability to illness progression, including: (1) distal and proximal stressors; (2) recurrence of episodes; and (3) comorbid cocaine abuse. Recurrence of each of these can increase responsivity (sensitize) to themselves and cross-sensitize to the two other factors and drive illness progression as seen clinically in increases in cycle acceleration, severity or duration of episodes, treatment refractoriness, disability, cognitive dysfunction, and premature death. Some mechanisms appear common to all three types of sensitization, such as decreases of brain-derived neuroprotective factor (BDNF) in hippocampus and blood, as well as increases in BDNF in the nucleus accumbens, suggesting the possibility that single treatments could ameliorate several of these factors at once. A potential example is N-acetylcysteine (NAC), which decreases bipolar affective illness severity (Berk et al. Biol Psychiatry 64:468–475, 2008) and cocaine reinstatement and craving (Baker et al. Ann N Y Acad Sci 1003:349–351, 2003; LaRowe et al. Am J Addict 15:105–110, 2006). Mechanisms of illness progression also involve epigenetic changes and add further rationale to the existing empirical clinical evidence of the importance of early recognition, treatment, and prevention of affective episodes. Adequate treatment could prevent or ameliorate both the increases in pathological factors and erosion of adaptive factors that propel illness exacerbation and treatment resistance. This view of the sensitization and cross-sensitization among stressors, episodes, and abused substances should lead to a fundamental re-conceptualization of the recurrent affective disorders not as benign, isolated episodes of “mental” illness, but as severe, potentially progressive and lethal medical disorders of brain and body that deserve careful life-long monitoring and treatment.

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Differential effects of ziprasidone and haloperidol on immobilization stress-induced mRNA BDNF expression in the hippocampus and neocortex of rats

Cited by 50 publications

References 48 publications

The Neuroprotective Disease-Modifying Potential of Psychotropics in Parkinson's Disease

The Neuroprotective Disease-Modifying Potential of Psychotropics in Parkinson's Disease

Depression: A repair response to stress-induced neuronal microdamage that can grade into a chronic neuroinflammatory condition?

Mechanisms of Illness Progression in the Recurrent Affective Disorders

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