Comparison of behavioral changes in cats treated with intracerebroventricular 6-hydroxydopamine and reserpine

Beleslin, D.B.; Samardic, Ranka; Krstić, S.K.; Micić, D; Terzić, Branka

doi:10.1016/s0361-9230(81)80060-3

Cited by 13 publications

(4 citation statements)

References 8 publications

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“…For example, dysregulation of norepinephrine due to early NFT accumulation in the locus coeruleus may contribute to the increased odds for agitation in Braak I–IV [62–64]. Several experimental studies have demonstrated increased agitation in response to dysfunction of norepinephrine-producing neurons, including those of the locus coeruleus [65–67]. In a review of neuroanatomical correlates of NPS in AD, Rosenberg and colleagues highlight studies correlating agitation with volumetric loss in the frontal cortex, anterior and posterior cingulate cortices, insula, amygdala, and hippocampus, rather than subcortical pathology [63].…”

Section: Discussionmentioning

confidence: 99%

Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer’s Disease

Ehrenberg

Suemoto

Resende

et al. 2018

JAD

159

127

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Clarifying the relationships between neuropsychiatric symptoms and Alzheimer's disease (AD)-related pathology may open avenues for effective treatments. Here, we investigate the odds of developing neuropsychiatric symptoms across increasing burdens of neurofibrillary tangle and amyloid-β pathology. Participants who passed away between 2004 and 2014 underwent comprehensive neuropathologic evaluation at the Biobank for Aging Studies from the Faculty of Medicine at the University of São Paulo. Postmortem interviews with reliable informants were used to collect information regarding neuropsychiatric and cognitive status. Of 1,092 cases collected, those with any non-Alzheimer pathology were excluded, bringing the cohort to 455 cases. Braak staging was used to evaluate neurofibrillary tangle burden, and the CERAD neuropathology score was used to evaluate amyloid-β burden. The 12-item neuropsychiatric inventory was used to evaluate neuropsychiatric symptoms and CDR-SOB score was used to evaluate dementia status. In Braak I/II, significantly increased odds were detected for agitation, anxiety, appetite changes, depression, and sleep disturbances, compared to controls. Increased odds of agitation continue into Braak III/IV. Braak V/VI is associated with higher odds for delusions. No increased odds for neuropsychiatric symptoms were found to correlate with amyloid-β pathology. Increased odds of neuropsychiatric symptoms are associated with early neurofibrillary tangle pathology, suggesting that subcortical neurofibrillary tangle accumulation with minimal cortical pathology is sufficient to impact quality of life and that neuropsychiatric symptoms are a manifestation of AD biological processes.

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Section: Discussionmentioning

confidence: 99%

Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer’s Disease

Ehrenberg

Suemoto

Resende

et al. 2018

JAD

159

127

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“…Further experiments have continued to show a link between pharmacological VMAT2 inhibition and fear behavior . These results have been complicated by the sedative effects of VMAT2 inhibitors and by the lack of a positive modulator for VMAT2. Furthermore, pharmacological manipulation does not best reflect the genetic nature of VMAT2 and PTSD risk.…”

Section: Introductionmentioning

confidence: 99%

Vesicular monoamine transporter 2 mediates fear behavior in mice

Branco

Burkett

Black

et al. 2020

Genes Brain and Behavior

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A subset of people exposed to a traumatic event develops post-traumatic stress disorder (PTSD), which is associated with dysregulated fear behavior. Genetic variation in SLC18A2, the gene that encodes vesicular monoamine transporter 2 (VMAT2), has been reported to affect risk for the development of PTSD in humans. Here, we use transgenic mice that express either 5% (VMAT2-LO mice) or 200% (VMAT2-HI mice) of wild-type levels of VMAT2 protein. We report that VMAT2-LO mice have reduced VMAT2 protein in the hippocampus and amygdala, impaired monoaminergic vesicular storage capacity in both the striatum and frontal cortex, decreased monoamine metabolite abundance and a greatly reduced capacity to release dopamine upon stimulation. Furthermore, VMAT2-LO mice showed exaggerated cued and contextual fear expression, altered fear habituation, inability to discriminate threat from safety cues, altered startle response compared with wild-type mice and an anxiogenic-like phenotype, but displayed no deficits in social function. By contrast, VMAT2-HI mice exhibited increased VMAT2 protein throughout the brain, higher vesicular storage capacity and greater dopamine release upon stimulation compared with wild-type controls. Behaviorally, VMAT2-HI mice were similar to wild-type mice in most assays, with some evidence of a reduced anxiety-like responses. Together, these data show that presynaptic monoamine function mediates PTSD-like outcomes in our mouse model, and suggest a causal link between reduced VMAT2 expression and fear behavior, consistent with the correlational relationship between VMAT2 genotype and PTSD risk in humans. Targeting this system is a potential strategy for the development of pharmacotherapies for disorders like PTSD. K E Y W O R D Sbehavior, fast-scan cyclic voltammetry,

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“…This phenomenon, which is known as ‘passive aggressiveness’, exhibits the following pattern: Without external stimuli, the animals are quiet and lack spontaneity. However, when the animals are stimulated by certain slightly stressful stimuli, such as a rod touch, an air puff, crowded housing or the removal of their pups, they suddenly become extremely agitated and aggressive. Pharmacological studies have revealed that the enhancement of shock‐induced aggression after intraventricular 6‐OHDA treatment derives from the denervation supersensitivity of the central NA system …”

Section: What Mental Symptoms Does Noradrenergic Dysfunction Cause?mentioning

confidence: 99%

Psychiatric symptoms of noradrenergic dysfunction: A pathophysiological view

Yamamoto

Shinba

Yoshii

2013

Psychiatry Clin Neurosci

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What psychiatric symptoms are caused by central noradrenergic dysfunction? The hypothesis considered in this review is that noradrenergic dysfunction causes the abnormalities in arousal level observed in functional psychoses. In this review, the psychiatric symptoms of noradrenergic dysfunction were inferred pathophysiologically from the neuroscience literature. This inference was examined based on the literature on the biology of psychiatric disorders and psychotropics. Additionally, hypotheses were generated as to the cause of the noradrenergic dysfunction. The central noradrenaline system, like the peripheral system, mediates the alarm reaction during stress. Overactivity of the system increases the arousal level and amplifies the emotional reaction to stress, which could manifest as a cluster of symptoms, such as insomnia, anxiety, irritability, emotional instability and exaggerated fear or aggressiveness (hyperarousal symptoms). Underactivity of the system lowers the arousal level and attenuates the alarm reaction, which could result in hypersomnia and insensitivity to stress (hypoarousal symptoms). Clinical data support the hypothesis that, in functional psychoses, the noradrenergic dysfunction is in fact associated with the arousal symptoms described above. The antinoradrenergic action of anxiolytics and antipsychotics can explain their sedative effects on the hyperarousal symptoms of these disorders. The results of animal experiments suggest that excessive stress can be a cause of long-term noradrenergic dysfunction.

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Comparison of behavioral changes in cats treated with intracerebroventricular 6-hydroxydopamine and reserpine

Cited by 13 publications

References 8 publications

Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer’s Disease

Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer’s Disease

Vesicular monoamine transporter 2 mediates fear behavior in mice

Psychiatric symptoms of noradrenergic dysfunction: A pathophysiological view

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