Cell Proliferation is Influenced by Bulbectomy and Normalized by Imipramine Treatment in a Region-Specific Manner

Keilhoff, Gerburg; Becker, Axel; Grecksch, Gisela; Bernstein, Hans‐Gert; Wolf, Gerald

doi:10.1038/sj.npp.1300924

Cited by 98 publications

(64 citation statements)

References 58 publications

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“…Increased neuronal activation in the CeAMY and BLA of the OB rat following open-field exposure confirms that the amygdaloid nuclei are integral in mounting a stress response in these animals. Altered gene expression (Wrynn et al, 2000b) and cell proliferation (Keilhoff et al, 2006) has been previously reported in the BLA of OB rats and this region has been proposed as a potential site of antidepressant activity. The decrease in cFOS expression in the BNST of OB rat would suggest that this area is not activated in response to openfield exposure in the model.…”

Section: Discussionmentioning

confidence: 80%

Chronic Fluoxetine Treatment Attenuates Stressor-Induced Changes in Temperature, Heart Rate, and Neuronal Activation in the Olfactory Bulbectomized Rat

Roche

Harkin

Kelly

2006

Neuropsychopharmacol

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The olfactory bulbectomized (OB) rat is a well-characterized animal model that exhibits a number of behavioral and neurochemical changes that have relevance to clinical depression. Hyperactivity in the open field is the most widely used parameter assessed in this model and is reversed following chronic, but not acute, antidepressant treatment. This study investigated OB-induced alterations in heart rate, body temperature, and neuronal activation following open-field exposure and the impact of chronic treatment with fluoxetine on these parameters. Upon placement in the open field, OB rats exhibited a characteristic hyperactivity response. Heart rate and body temperature were increased in sham-operated rats following open-field exposure, a predictable response to stress, which was significantly reduced in OB rats. Moreover bulbectomy reduced open field-induced cFOS expression in the basal nucleus of the stria terminalis while concurrently increasing expression in the hippocampus, amygdala, paraventricular nucleus of the thalamus, and dorsal raphe nucleus. Chronic fluoxetine treatment (10 mg/kg subcutaneous once daily for 5 weeks) attenuated all of these OB-associated changes. In conclusion, OB rats exhibit alterations in behavior, body temperature, heart rate, and neuronal activation in response to open-field exposure, which are reversed following chronic fluoxetine administration. These results identify stress-sensitive regions within the brain which are altered following bulbectomy and which may underlie the abnormal behavioral and physiological changes observed in this rodent model of depression.

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Section: Discussionmentioning

confidence: 80%

Chronic Fluoxetine Treatment Attenuates Stressor-Induced Changes in Temperature, Heart Rate, and Neuronal Activation in the Olfactory Bulbectomized Rat

Roche

Harkin

Kelly

2006

Neuropsychopharmacol

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“…Adult neurogenesis has been reported in the amygdala of rodents and monkeys (Bernier et al, 2002;Jiang et al, 2014;Takemura, 2005), although the evidence for double labeling of the proliferation marker BrdU and mature neuronal markers is not especially strong. Effects of olfactory bulbectomy, fear conditioning, and fluoxetine have been observed on the numbers of adult-born cells in the amygdala Keilhoff et al, 2006;Okuda et al, 2009), but it is unclear how many of the affected cells are neurons.…”

Section: Neurogenesis In Other Regionsmentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

162

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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“…5,16,17 The mechanisms controlling progenitor cell and neuroblast proliferation have not been clarified but circulating factors, including hormones, may play a role. As an example, IGF-I is needed to induce hippocampal proliferation by physical exercise, 18 and stress-elevated circulating levels of adrenal steroids inhibit the production of new granular neurons.…”

Section: Introductionmentioning

confidence: 99%

Modulation of adult hippocampal neurogenesis by thyroid hormones: implications in depressive-like behavior

et al. 2006

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Hormonal imbalances are involved in many of the age-related pathologies, as neurodegenerative and psychiatric diseases. Specifically, thyroid state alterations in the adult are related to psychological changes and mood disorders as depression. The dentate gyrus of the hippocampal formation undergoes neurogenesis in adult mammals including humans. Recent evidence suggests that depressive disorders and their treatment are tightly related to the number of newly born neurons in the dentate gyrus. We have studied the effect of thyroid hormones (TH) on hippocampal neurogenesis in adult rats in vivo. A short period of adultonset hypothyroidism impaired normal neurogenesis in the subgranular zone of the dentate gyrus with a 30% reduction in the number of proliferating cells. Hypothyroidism also reduced the number of newborn neuroblasts and immature neurons (doublecortin (DCX) immunopositive cells) which had a severely hypoplastic dendritic arborization. To correlate these changes with hippocampal function, we subjected the rats to the forced swimming and novel object recognition tests. Hypothyroid rats showed normal memory in object recognition, but displayed abnormal behavior in the forced swimming test, indicating a depressive-like disorder. Chronic treatment of hypothyroid rats with TH not only normalized the abnormal behavior but also restored the number of proliferative and DCX-positive cells, and induced growth of their dendritic trees. Therefore, hypothyroidism induced a reversible depressive-like disorder, which correlated to changes in neurogenesis. Our results indicate that TH are essential for adult hippocampal neurogenesis and suggest that mood disorders related to adult-onset hypothyroidism in humans could be due, in part, to impaired neurogenesis.

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Cell Proliferation is Influenced by Bulbectomy and Normalized by Imipramine Treatment in a Region-Specific Manner

Cited by 98 publications

References 58 publications

Chronic Fluoxetine Treatment Attenuates Stressor-Induced Changes in Temperature, Heart Rate, and Neuronal Activation in the Olfactory Bulbectomized Rat

Chronic Fluoxetine Treatment Attenuates Stressor-Induced Changes in Temperature, Heart Rate, and Neuronal Activation in the Olfactory Bulbectomized Rat

Adult Neurogenesis and Mental Illness

Modulation of adult hippocampal neurogenesis by thyroid hormones: implications in depressive-like behavior

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