C-fos protein expression in the anterior amygdaloid area and nc. accumbens in the hypoxic rat brain

Babovic, Sinisa; Zigic, Sonja; Šakić, Branislav

doi:10.2298/mpns1412379b

Cited by 2 publications

(2 citation statements)

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“…The number of corticotropin-releasing factor- (CRF-) and neuropeptide-Y- (NPY-) positive neurons were found to be decreased distinctly in the amygdala after postnatal day 3 hypoxia-ischemia [ 99 ], and c-fos protein expression increased in the nc. accumbens and the anterior amygdaloid area in the rat brain exposed to hypoxic injury [ 101 ]. These long-term changes in the amygdala may be functionally associated with the specific behavioral disorders including bipolar disorder [ 102 ].…”

Section: Hypoxic Injury and Neuronal Plasticitymentioning

confidence: 99%

Effect of Hypoxic Injury in Mood Disorder

2017

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Hypoxemia is a common complication of the diseases associated with the central nervous system, and neurons are highly sensitive to the availability of oxygen. Neuroplasticity is an important property of the neural system controlling breathing, memory, and cognitive ability. However, the underlying mechanism has not yet been clearly elucidated. In recent years, several pieces of evidence have highlighted the effect of hypoxic injury on neuronal plasticity in the pathogenesis and treatment of mood disorder. Therefore, the present study reviewed the relevant articles regarding hypoxic injury and neuronal plasticity and discussed the pathological changes and physiological functions of neurons in hypoxemia in order to provide a translational perspective to the relevance of hypoxic injury and mood disorder.

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Section: Hypoxic Injury and Neuronal Plasticitymentioning

confidence: 99%

Effect of Hypoxic Injury in Mood Disorder

2017

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“…The activation of these pathways is crucial for the survival of the organism, as they trigger a series of responses that increase oxygen delivery to the tissues and maintain cellular homeostasis under hypoxic conditions. From there, the signals are transmitted to other regions of the brain, such as the hypothalamus, hippocampus, and amygdala, where they modulate a wide range of physiological processes, including stress responses, emotional regulation, and memory formation [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

K252a Prevents Microglial Activation Induced by Anoxic Stimulation of Carotid Bodies in Rats

Cuéllar-Pérez,

Jauregui-Huerta,

Ruvalcaba-Delgadillo

et al. 2023

Toxics

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Inducing carotid body anoxia through the administration of cyanide can result in oxygen deprivation. The lack of oxygen activates cellular responses in specific regions of the central nervous system, including the Nucleus Tractus Solitarius, hypothalamus, hippocampus, and amygdala, which are regulated by afferent pathways from chemosensitive receptors. These receptors are modulated by the brain-derived neurotrophic factor receptor TrkB. Oxygen deprivation can cause neuroinflammation in the brain regions that are activated by the afferent pathways from the chemosensitive carotid body. To investigate how microglia, a type of immune cell in the brain, respond to an anoxic environment resulting from the administration of NaCN, we studied the effects of blocking the TrkB receptor on this cell-type response. Male Wistar rats were anesthetized, and a dose of NaCN was injected into their carotid sinus to induce anoxia. Prior to the anoxic stimulus, the rats were given an intracerebroventricular (icv) infusion of either K252a, a TrkB receptor inhibitor, BDNF, or an artificial cerebrospinal fluid (aCSF). After the anoxic stimulus, the rats were perfused with paraformaldehyde, and their brains were processed for microglia immunohistochemistry. The results indicated that the anoxic stimulation caused an increase in the number of reactive microglial cells in the hypothalamic arcuate, basolateral amygdala, and dentate gyrus of the hippocampus. However, the infusion of the K252a TrkB receptor inhibitor prevented microglial activation in these regions.

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C-fos protein expression in the anterior amygdaloid area and nc. accumbens in the hypoxic rat brain

Abstract: We have concluded that parts of the brain with an important role for the survival have a strong expression of c-fos gene.

Cited by 2 publications

References 18 publications

Effect of Hypoxic Injury in Mood Disorder

Effect of Hypoxic Injury in Mood Disorder

K252a Prevents Microglial Activation Induced by Anoxic Stimulation of Carotid Bodies in Rats

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