Glucocorticoids modulate the response of ornithine decarboxylase to unilateral removal of the dorsal hippocampus

Kloet, E. Ronald de; Cousin, Marc; Veldhuis, H D; Voorhuis, Th.D.; Lando, D.

doi:10.1016/0006-8993(83)90420-1

Cited by 21 publications

(6 citation statements)

References 34 publications

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“…Unilateral removal of the hippocampus and the overlying cortex produced a sharp increase in ODC activity in the contralateral hippocampus (De Kloet et al, 1983). This effect was maximal at 6 h after surgery and lasted for 2 d. The response of ODC to operation was even more pronounced in animals in which the adrenals had been removed.…”

Section: Lesions Of the Brain Tissuementioning

confidence: 87%

Polyamine metabolism in different pathological states of the brain

Paschen

1992

Molecular and Chemical Neuropathology

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Biosynthesis of the polyamines spermidine and spermine and their precursor putrescine is controlled by the activity of the two key enzymes ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC). In the adult brain, polyamine synthesis is activated by a variety of physiological and pathological stimuli, resulting most prominently in an increase in ODC activity and putrescine levels. The sharp rise in putrescine levels observed following severe cellular stress is most probably the result of an increase in ODC activity and decrease in SAMDC activity or an activation of the interconversion of spermidine into putrescine via the enzymes spermidine N-acetyltransferase and polyamine oxidase. Spermidine and spermine levels are usually less affected by stress and are reduced in severely injured areas. Changes of polyamine synthesis and metabolism are most pronounced in those pathological conditions that induce cell injury, such as severe metabolic stress, exposure to neurotoxins or seizure. Putrescine levels correlate closely with the density of cell necrosis. Because of the close relationship between the extent of post-stress changes in polyamine metabolism and density of cellular injury, it has been suggested that polyamines play a role in the manifestation of structural defects. Four different mechanisms of polyamine-dependent cell injury are plausible: (1) an overactivation of calcium fluxes and neurotransmitter release in areas with an overshoot in putrescine formation; (2) disturbances of the calcium homeostasis resulting from an impairment of the calcium buffering capacity of mitochondria in regions in which spermine levels are reduced; (3) an overactivation of the NMDA receptor complex caused by a release of polyamines into the extracellular space during ischemia or after ischemia and prolonged recirculation in the tissue surrounding severely damaged areas; (4) an overproduction of hydrogen peroxide resulting from an activation of the interconversion of spermidine into putrescine via the enzymes spermidine N-acetyltransferase and polyamine oxidase. Insofar as a sharp activation of polyamine synthesis is a common response to a variety of physiological and pathological stimuli, studying stress-induced changes in polyamine synthesis and metabolism may help to elucidate the molecular mechanisms involved in the development of cell injury induced by severe stress.

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Section: Lesions Of the Brain Tissuementioning

confidence: 87%

Polyamine metabolism in different pathological states of the brain

Paschen

1992

Molecular and Chemical Neuropathology

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“…Furthermore, the contralateral HPC contributes to the synaptic reorganization that occurs following unilateral damage to this structure or to its afferent input (12,23). Other studies in which one HPC was removed (15) or the hilus of one dentate gyrus was electrolytically damaged (5) also found a large and persistent increase in ODC activity on the side contralateral to the damage. These types of neural insult are difficult to quantify and are likely to affect a variety of neural elements in the HPC including granule cells, pyramidal cells, interneurons, and both association and commisural fibers.…”

Section: Discussionmentioning

confidence: 99%

“…54 ious drugs (6,14,16,28), hormones (15,29), environmental toxicants (7), and growth factors (24). ODC activity is also very responsive to neural insult with the degree of increase being related to the extent of damage (16).…”

Section: Introductionmentioning

confidence: 99%

Destruction of specific hippocampal cell fields increases ornithine decarboxylase activity: Modulation of the biochemical but not the histological changes by ganglioside GM1

Walsh

Emerich

Bondy

1989

Experimental Neurology

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Unilateral injection of colchicine into the dentate gyrus, kainic acid into the CA3 pyramidal cell field, or cerebrospinal fluid into either site produced significant increases in ornithine decarboxylase (ODC) activity in both the injected and noninjected hippocampi. The magnitude as well as the time course of these changes varied with the cytotoxin, the site of injection, and whether or not animals had been pretreated with ganglioside GMl. The ganglioside regimen reduced the ODC response in the injected hippocampus but increased it on the side contralateral to the colchicine injection. In contrast, GMl enhanced the ODC response produced by kainic acid in the injected but not the uninjected hippocampus. In a subsequent study morphometric analysis of the hippocampus revealed that pretreatment with GMl did not alter the extent of hippocampal injury induced by either cytotoxin. These data indicate that the changes in ODC activity observed following hippocampal damage represent a complex set of biochemical changes that might serve to protect primary or secondary sites of insult and/or to promote either adaptive or maladaptive neural reorganization. Gan· glioside GMl altered the ODC response without minimizing the histopathological changes induced by the cytotoxins. The role of polyamines in neural, behavioral, and synaptic plasticity is currently under study.

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“…Specificity studies regarding steroid induction of ODC, in addition to a second enzyme of glial cell origin (glycerol phosphate dehydrogenase), demonstrated previously a higher potency of DEX than CORT but inactivity towards aldosterone or sex hormones . It has been considered that the hormonal doses required for ODC induction and the profile of effective hormones are more consistent with involvement of type I1 glucocorticoid receptors (Cousin et al, 1982;De Kloet et al, 1983), probably located in glial cells (McEwen et al, 1986). Therefore, it can be suggested that a population of type I1 sites contained in glial cells of the ventral horn and lateral funiculus was mediating the induction of ODC following DEX therapy.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid Receptors and Enzyme Induction in the Spinal Cord of Rats: Effects of Acute Transection

González

Moses

Nicola

1990

Journal of Neurochemistry

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The spinal cord is a glucocorticoid-responsive tissue, as demonstrated by hormonal effects on enzyme induction and by the presence of type II and type I glucocorticoid receptors in cytoplasmic extracts of this CNS region. Using microdissection techniques, we have found in the present investigation that glucocorticoid type II receptors are the most abundant class detected in gray (ventral and dorsal horns) and white (lateral funiculus) matter and that the distribution of type II sites among these regions was quantitatively similar. Type I sites were also quantified, with a slight prevalence in gray matter as opposed to white matter. Furthermore, stimulation of an inducible enzyme, ornithine decarboxylase (ODC), was found in ventral horn and lateral funiculus but not in dorsal horn after administration of dexamethasone (DEX), a type II receptor ligand. We also found that surgical transection of the spinal cord, while markedly increasing ODC activity per se, did not prevent the stimulatory effect of DEX administration on ODC activity measured in the lumbar enlargement of the spinal cord located below the surgical lesion. Taken together, the results suggest a direct effect of glucocorticoids on ODC activity in the spinal cord of rats, probably mediated by glucocorticoid receptors (type II) found in target cells of the ventral horn and lateral funiculus. The results also indicate that glucocorticoid receptors of the dorsal horn were not involved in ODC induction, and a function for these receptors awaits the results of further experimentation.

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Glucocorticoids modulate the response of ornithine decarboxylase to unilateral removal of the dorsal hippocampus

Cited by 21 publications

References 34 publications

Polyamine metabolism in different pathological states of the brain

Polyamine metabolism in different pathological states of the brain

Destruction of specific hippocampal cell fields increases ornithine decarboxylase activity: Modulation of the biochemical but not the histological changes by ganglioside GM1

Glucocorticoid Receptors and Enzyme Induction in the Spinal Cord of Rats: Effects of Acute Transection

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