Occipital cortex ablation in adult rat causes retrograde neuronal death in the lateral geniculate nucleus that resembles apoptosis

Al-Abdulla, Nael A.; Portera‐Cailliau, Carlos; Martin, Lee J.

doi:10.1016/s0306-4522(98)00014-1

Cited by 63 publications

(71 citation statements)

References 47 publications

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“…In CoCl 2 -injected hemispheres, we demonstrated an increase in DNA fragmentation in the penumbra area via TUNEL and Hoescht 33342 staining, although TUNEL per se does not distinguish between the modes of cell death (apoptosis or necrosis) (Al-Abdulla et al 1998).…”

Section: Discussionmentioning

confidence: 72%

Neuronal and Glial Alterations Due to Focal Cortical Hypoxia Induced by Direct Cobalt Chloride (CoCl2) Brain Injection

et al. 2009

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Ischemic brain injury is a dynamic process that involves oxidative stress, inflammation, and cell death, as well as activation of endogenous adaptive and regenerative mechanisms depending on activation of transcription factors such as hypoxia inducible factor 1-alpha (HIF-1alpha). Because CoCl2 activates HIF-1alpha, we described a new focal-hypoxia model by direct intracerebral CoCl2 injection. Adult male Wistar rats were intracerebrally injected with CoCl2 (2 microl-50 mM), in frontoparietal cortex of right hemisphere, and saline (2 microl) in the contralateral hemisphere. In slides of fixed brains at 1, 6, 9, 24 h or 5 day after treatment, TTC, histochemistry (toluidine blue, Hoescht-33342, TUNEL), immunostaining (HIF-1alpha, GFAP), Lycopersicon esculentum lectin staining, and electron microscopy (EM) were performed. Immediately after 1 h post CoCl2 injection, HIF-1alpha stabilization and neuronal nuclear shrinkage and cromathin condensation were observed by immunostaining and EM, respectively. Neuronal apoptotic nuclear morphology and GFAP immunoreactivity and lectin maximal reactivity were detected during 6-9 h. Ultrastructural alterations of morphology included edematous perinuclear cytoplasm, organelles and endoplasmic reticulum (RE) enlargement, mitochondrial swelling with increased matrix density, and deposits of electron-dense material. Neurons showed particular nuclear indentations. Astrocytes and oligodendrocytes presented alterations in both nuclei and RE with dilated lumen and altered mitochondrias, and all these ultrastructural changes became detectable at day 5. CoCl2 cortical injection mimics focal brain ischemia, inducing neuronal death and glial activation. This model brings the opportunity to develop focal ischemia in selected brain areas to study their functional consequences and potential pharmacological therapies for in vivo models of stroke.

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Section: Discussionmentioning

confidence: 72%

Neuronal and Glial Alterations Due to Focal Cortical Hypoxia Induced by Direct Cobalt Chloride (CoCl2) Brain Injection

et al. 2009

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“…Neurons also die via apoptosis following growth factor withdrawal (Cardone et al, 1998), glutamate excitotoxicity (Portera-Cailliau et al, 1997), cell exposure to reactive oxygen species (Volbracht et al, 2001;Leist et al, 1997), ischemia (Namura et al, 1998;Velier et al, 1999), and normal development (O'Connor et al, 1974). Other previous reports indicate that caspases are activated following axotomy of CNS retinal ganglion cells (Kermer et al, 1998;Chaudary et al, 1999) or axotomy of the dorsal lateral geniculate nucleus (Al-Abdulla et al, 1998). In addition, broad caspase inhibition increased the percentage of cells that survived in vivo following traumatic (percussive) brain injury in rat (Yakovlev et al, 1997;Franz et al, 2000) and spinal-cord contusions in rat (Chan et al, 2001).…”

Section: Cell Death Following Neurite Transection Near a B104 Soma Ocmentioning

confidence: 84%

Critical interval of somal calcium transient after neurite transection determines B104 cell survival

Nguyen

Bittner

Fishman

2005

J of Neuroscience Research

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Nerve cells may survive or die after axonal or dendritic transection. After neurite transection near (<50μm) the cell body of Fura-2 loaded B104 neuroblastoma (rat brain derived) cells, the somal calcium concentration (SCC) undergoes a three-phase transient change: a rapid (0 to 0.15 min posttransection (PT)) rise phase followed by an early (0.15 to 1.5 min PT) rapid decay phase, succeeded by a late (1.5 to 60 min PT) slower decay phase that restores SCC to preinjury levels. The SCC in a critical interval (1.5 to 12.5 min PT) of the third transient phase correlates with cell fate, i.e., most transected cells that exclude dye (restore a barrier) and die have a significantly higher (p<0.005) SCC in this Critical Interval than transected cells that exclude dye and survive at 24h PT. Loading BAPTA (chelation of somal Ca 2+ ) before, but not after, the Critical Interval increases the percentage of cells that survive compared to cells transected without BAPTA loading. Furthermore, most transected cells that die, despite successful barrier restoration, exhibit characteristics consistent with apoptosis initiated during the Critical Interval of the SCC, including caspase activation and plasmalemmal phosphatidylserine translocation. These data suggest that decreased cell survival for injuries near the soma is due to Ca 2+ -initiated apoptosis during the Critical Interval of the third phase of the SCC transient.

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“…These sections were used for volumetric analysis of the striatum using point counting and the Cavalieri principle as described (Calhoun et al, 1996; Mouton et al, 1998) and for microscopic examination of the striatal mosaic cytology and developmental cell death by profile counting of apoptotic figures. Cresyl violet staining is very useful for identifying apoptotic cells in nervous tissue (Al-Abdulla et al, 1998; Martin et al, 1999; Northington et al, 2001; Lok and Martin, 2002; Mueller et al, 2005). The other selected sections were processed immunohistochemically using a standard peroxidase anti-peroxidase procedure with diaminobenzidine as chromogen and primary antibodies to tyrosine hydroxylase (TH), substance P (SP), leucine-enkephalin (LENK), and calcium binding protein calbindin-D28 as described (Martin et al, 1991a,b,c).…”

Section: Methodsmentioning

confidence: 99%

The non-human primate striatum undergoes marked prolonged remodeling during postnatal development

Martin

Cork

2014

Front. Cell. Neurosci.

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We examined the postnatal ontogeny of the striatum in rhesus monkeys (Macaca mulatta) to identify temporal and spatial patterns of histological and chemical maturation. Our goal was to determine whether this forebrain structure is developmentally static or dynamic in postnatal life. Brains from monkeys at 1 day, 1, 4, 6, 9, and 12 months of age (N = 12) and adult monkeys (N = 4) were analyzed. Nissl staining was used to assess striatal volume, cytoarchitecture, and apoptosis. Immunohistochemistry was used to localize and measure substance P (SP), leucine-enkephalin (LENK), tyrosine hydroxylase (TH), and calbindin D28 (CAL) immunoreactivities. Mature brain to body weight ratio was achieved at 4 months of age, and striatal volume increased from ∼1.2 to ∼1.4 cm3 during the first postnatal year. Nissl staining identified, prominently in the caudate nucleus, developmentally persistent discrete cell islands with neuronal densities greater than the surrounding striatal parenchyma (matrix). Losses in neuronal density were observed in island and matrix regions during maturation, and differential developmental programmed cell death was observed in islands and matrix regions. Immunohistochemistry revealed striking changes occurring postnatally in striatal chemical neuroanatomy. At birth, the immature dopaminergic nigrostriatal innervation was characterized by islands enriched in TH-immunoreactive puncta (putative terminals) in the neuropil; TH-enriched islands aligned completely with areas enriched in SP immunoreactivity but low in LENK immunoreactivity. These areas enriched in SP immunoreactivity but low in LENK immunoreactivity were identified as striosome and matrix areas, respectively, because CAL immunoreactivity clearly delineated these territories. SP, LENK, and CAL immunoreactivities appeared as positive neuronal cell bodies, processes, and puncta. The matrix compartment at birth contained relatively low TH-immunoreactive processes and few SP-positive neurons but was densely populated with LENK-immunoreactive neurons. The nucleus accumbens part of the ventral striatum also showed prominent differences in SP, LENK, and CAL immunoreactivities in shell and core territories. During 12 months of postnatal maturation salient changes occurred in neurotransmitter marker localization: TH-positive afferents densely innervated the matrix to exceed levels of immunoreactivity in the striosomes; SP immunoreactivity levels increased in the matrix; and LENK-immunoreactivity levels decreased in the matrix and increased in the striosomes. At 12 months of age, striatal chemoarchitecture was similar qualitatively to adult patterns, but quantitatively different in LENK and SP in caudate, putamen, and nucleus accumbens. This study shows for the first time that the rhesus monkey striatum requires more than 12 months after birth to develop an adult-like pattern of chemical neuroanatomy and that principal neurons within striosomes and matrix have different developmental programs for neuropeptide expression. We conclude that postnatal matura...

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Occipital cortex ablation in adult rat causes retrograde neuronal death in the lateral geniculate nucleus that resembles apoptosis

Cited by 63 publications

References 47 publications

Neuronal and Glial Alterations Due to Focal Cortical Hypoxia Induced by Direct Cobalt Chloride (CoCl2) Brain Injection

Neuronal and Glial Alterations Due to Focal Cortical Hypoxia Induced by Direct Cobalt Chloride (CoCl2) Brain Injection

Critical interval of somal calcium transient after neurite transection determines B104 cell survival

The non-human primate striatum undergoes marked prolonged remodeling during postnatal development

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