The Golgi–Cox Method

Das, Gitanjali; Reuhl, Kenneth R.; Zhou, Ran

doi:10.1007/978-1-62703-444-9_29

Cited by 53 publications

(41 citation statements)

References 5 publications

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“…Since dynorphin is found in mossy fiber axons and boutons, an increase in dynorphin immunostaining was consistent with the hypothesis that that there was sprouting of the mossy fibers into the pyramidal cell layer and stratum oriens of orchidectomized animals (Skucas et al 2013). The present results, albeit probably representing only a few of the mossy fibers in each animal because the Golgi method only impregnates a fraction of the neurons present (Das et al 2013), are consistent with the data from this previous study. In addition, the results show increased dendritic branching in stratum radiatum of orchidectomized rats, providing an anatomical substrate for the potentiation of recurrent collateral transmission.…”

Section: Discussionsupporting

confidence: 93%

Expansion of mossy fibers and CA3 apical dendritic length accompanies the fall in dendritic spine density after gonadectomy in male, but not female, rats

et al. 2016

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Androgen loss is an important clinical concern because of its cognitive and behavioral effects. Changes in androgen levels are also suspected to contribute to neurological disease. However, the available data on the effects of androgen deprivation in areas of the brain that are central to cognition, like the hippocampus, are mixed. In this study, morphological analysis of pyramidal cells was used to investigate if structural changes could potentially contribute to the mixed cognitive effects that have been observed after androgen loss in males. Male Sprague–Dawley rats were orchidectomized or sham-operated. Two months later, their brains were Golgi-impregnated for morphological analysis. Morphological endpoints were studied in areas CA3 and CA1, with comparisons to females either intact or 2 months after ovariectomy. CA3 pyramidal neurons of orchidectomized rats exhibited marked increases in apical dendritic arborization. There were increases in mossy fiber afferent density in area CA3, as well as robust enhancements to dendritic structure in area CA3 of orchidectomized males, but not in CA1. Remarkably, apical dendritic length of CA3 pyramidal cells increased, while spine density declined. By contrast, in females overall dendritic structure was minimally affected by ovariectomy, while dendritic spine density was greatly reduced. Sex differences and subfield-specific effects of gonadal hormone deprivation on the hippocampal circuitry may help explain the different behavioral effects reported in males and females after gonadectomy, or other conditions associated with declining gonadal hormone secretion.

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Section: Discussionsupporting

confidence: 93%

Expansion of mossy fibers and CA3 apical dendritic length accompanies the fall in dendritic spine density after gonadectomy in male, but not female, rats

et al. 2016

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“…Golgi-Cox Staining Golgi-Cox staining was performed as described previously [24]. In short, the fresh brain was removed quickly and immersed in the Golgi-Cox solution without perfusion and fixation at room temperature for 2 weeks.…”

Section: Methodsmentioning

confidence: 99%

Nafamostat Mesilate Improves Neurological Outcome and Axonal Regeneration after Stroke in Rats

Liu

Wang

et al. 2016

Mol Neurobiol

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Disability including deficiency in sensorimotor and cognition functions is a dominant consequence after stroke. Evidence suggests that serine proteases play an important role in the physiology and pathology of the brain. Previous studies reported that nafamostat mesilate (NM), a synthetic serine protease inhibitor, attenuates neuronal damage in the acute phase after stroke. However, its efficacy in the chronic phase and the mechanism underlying its beneficial effect are not fully known. Here, we have studied whether NM improves long-term functional recovery after ischemic stroke. Experimental ischemic stroke was induced by transient middle cerebral artery occlusion (tMCAO). NM treatment attenuated the brain infarct volume and the loss of body weight and improved the recovery of sensorimotor and cognitive functions. One month after tMCAO, neuronal axons and dendrites were preserved in the NM group, accompanied by increasedsynaptic proteins and structures in the ipsilateral hippocampus. The expression of brain-derived neurotrophic factor, nerve growth factor and neurotrophin-3 was increased in the contralateral sensorimotor cortex and ipsilateral hippocampus by the administration of NM. Furthermore, NM activated tyrosine receptor kinase B (TrkB), extracellular signal-regulated kinas1/2(ERK1/2) and cAMP-response element binding protein (CREB) and inhibited the activity of Cyclin-dependent Kinase 5 (Cdk5) in the contralateral sensorimotor cortex and ipsilateral hippocampus. These results demonstrated that NM treatment could improve neurological outcome and axonal regeneration, which might be correlated with down-regulating Cdk5 activity and up-regulating TrkB-ERK1/2-CREB pathway.

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“…The left hemisphere was retained for the current study, while the right hemisphere was frozen and retained for future studies. Left hemisphere frontal lobe blocks were wrapped in gauze and placed in Golgi-Cox solution (working concentrations: 1% potassium dichromate, 1% mercuric chloride and 0.83% potassium chromate) for 12 weeks (Das et al, 2013; Rosoklija et al, 2003). Tissue blocks were then dehydrated in alcohols, embedded in parlodion, and cut on a sliding microtome in to 150μm thick sections (Microm HM440E).…”

Section: Methodsmentioning

confidence: 99%

Preliminary evidence of neuropathology in nonhuman primates prenatally exposed to maternal immune activation

Weir

Forghany

Smith

et al. 2015

Brain, Behavior, and Immunity

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Maternal infection during pregnancy increases the risk for neurodevelopmental disorders in offspring. Rodent models have played a critical role in establishing maternal immune activation (MIA) as a causal factor for altered brain and behavioral development in offspring. We recently extended these findings to a species more closely related to humans by demonstrating that rhesus monkeys (Macaca mulatta) prenatally exposed to MIA also develop abnormal behaviors. Here, for the first time, we present initial evidence of underlying brain pathology in this novel nonhuman primate MIA model. Pregnant rhesus monkeys were injected with a modified form of the viral mimic polyI:C (poly ICLC) or saline at the end of the first trimester. Brain tissue was collected from the offspring at 3.5 years and blocks of dorsolateral prefrontal cortex (BA46) were used to analyze neuronal dendritic morphology and spine density using the Golgi-Cox impregnation method. For each case, 10 layer III pyramidal cells were traced in their entirety, including all apical, oblique and basal dendrites, and their spines. We further analyzed somal size and apical dendrite trunk morphology in 30 cells per case over a 30μm section located 100±10μm from the soma. Compared to controls, apical dendrites of MIA-treated offspring were smaller in diameter and exhibited a greater number of oblique dendrites. These data provide the first evidence that prenatal exposure to MIA alters dendritic morphology in a nonhuman primate MIA model, which may have profound implications for revealing the underlying neuropathology of neurodevelopmental disorders related to maternal infection.

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The Golgi–Cox Method

Cited by 53 publications

References 5 publications

Expansion of mossy fibers and CA3 apical dendritic length accompanies the fall in dendritic spine density after gonadectomy in male, but not female, rats

Expansion of mossy fibers and CA3 apical dendritic length accompanies the fall in dendritic spine density after gonadectomy in male, but not female, rats

Nafamostat Mesilate Improves Neurological Outcome and Axonal Regeneration after Stroke in Rats

Preliminary evidence of neuropathology in nonhuman primates prenatally exposed to maternal immune activation

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