Morphological and physiological properties of chronically isolated immature neocortex

Purpura, Dominick P.; Housepian, Edgar M.

doi:10.1016/0014-4886(61)90025-5

Cited by 99 publications

(20 citation statements)

References 21 publications

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“…The latter is likely to be associated with changes in gene expression and in reorganization of the local circuit. This view is supported by anatomical data showing axonal sprouting and synaptic changes in both animal (Purpura and Houdepian, 1961) and human (Castejon et al, 2002) epileptic cortex. Furthermore, clinical data demonstrate that early and delayed post-insult epilepsies differ in characteristics and responses to antiepileptic medications (Herman, 2002).…”

Section: Discussionsupporting

confidence: 52%

Lasting Blood-Brain Barrier Disruption Induces Epileptic Focus in the Rat Somatosensory Cortex

Seiffert¹,

Dreier²,

Ivens³

et al. 2004

J. Neurosci.

457

395

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Perturbations in the integrity of the blood-brain barrier have been reported in both humans and animals under numerous pathological conditions. Although the blood-brain barrier prevents the penetration of many blood constituents into the brain extracellular space, the effect of such perturbations on the brain function and their roles in the pathogenesis of cortical diseases are unknown.In this study we established a model for focal disruption of the blood-brain barrier in the rat cortex by direct application of bile salts. Exposure of the cerebral cortex in vivo to bile salts resulted in long-lasting extravasation of serum albumin to the brain extracellular space and was associated with a prominent activation of astrocytes with no inflammatory response or marked cell loss. Using electrophysiological recordings in brain slices we found that a focus of epileptiform discharges developed within 4 -7 d after treatment and could be recorded up to 49 d postoperatively in Ͼ60% of slices from treated animals but only rarely (10%) in sham-operated controls. Epileptiform activity involved both glutamatergic and GABAergic neurotransmission. Epileptiform activity was also induced by direct cortical application of native serum, denatured serum, or albumin-containing solution. In contrast, perfusion with serum-adapted electrolyte solution did not induce abnormal activity, thereby suggesting that the exposure of the serum-devoid brain environment to serum proteins underlies epileptogenesis in the blood-brain barrier-disrupted cortex. Although many neuropathologies entail a compromised bloodbrain barrier, this is the first direct evidence that it may have a role in the pathogenesis of focal cortical epilepsy, a common neurological disease.

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Section: Discussionsupporting

confidence: 52%

Lasting Blood-Brain Barrier Disruption Induces Epileptic Focus in the Rat Somatosensory Cortex

Seiffert¹,

Dreier²,

Ivens³

et al. 2004

J. Neurosci.

457

395

View full text Add to dashboard Cite

show abstract

“…One source, however, may be collaterals from the 'pruned' callosal projection neurons which are present in the vicinity. It has been demonstrated in the immature neocortex of kitten that when projecting axons are severed by undercutting the cortex, a proliferation of axon collaterals is induced along the proximal stumps of the severed axons (Purpura & Housepian, 1961). More recently, however, Laurenberg & Zimmer (1980) have demonstrated in the hippocampus of the rat that the magnitude of such a compensatory response is age-dependent.…”

Section: Discussionmentioning

confidence: 95%

Synaptic proliferation in the auditory cortex of the young adult rat following callosal lesions

Vaughan

Foundas

1982

J Neurocytol

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The long-term effects of partial deafferentation in the neocortex of adult rats were studied in four-month old rats in which the corpus callosum had been completely sectioned when they were one-month old. Quantitative light microscopy was used to identify morphological changes in the auditory cortex resulting from the loss of established callosal connections. Particular attention was directed at those cortical layers known to receive the heaviest callosal projection (layers II and III) and at neurons known to be postsynaptic to callosal afferents (layer V pyramidal neurons). The comparative analysis of both semithin plastic sections and Golgi-impregnated material from long-term, callosally-lesioned rats and age-matched control animals reveals no differences in the overall cortical thickness, the thickness of cortical layers, the numbers of neurons or the density of spines along apical dendrites of layer V pyramidal neurons. However, as a result of the callosal lesion, large diameter apical dendrites are significantly thinner in the callosally deafferented cortex and there is a small increase in the number of neuroglial cells in the deeper cortical layers. To determine whether another system of afferents to the auditory cortex spreads into the deafferented callosal domain, geniculate lesions were made in long-term, callosally-lesioned animals and age-matched controls. The terminal projection patterns of thalamic afferents were compared using the Fink-Heimer technique and quantitative electron microscopy. Normally in the auditory cortex there is only a small region of overlap between the terminal projection fields of callosal afferents and thalamic afferents, the latter projecting chiefly to layer IV and low layer III. However, three months after callosal lesions, thalamic axons had proliferated superficially into part of the callosal domain. Furthermore, in the normal auditory cortex after geniculate lesions, there were three rostrocaudally oriented bands of relatively dense thalamocortical terminal degeneration separated by regions of less dense degeneration. In the doubly lesioned animals these bands of degeneration were less distinct due to a proliferation of thalamic axons into the regions characterized by sparse projections.

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“…The brain restores its activity after injury by extensive reorganization of cortical connectivity, such as axonal sprouting with formation of new synapses (Purpura and Housepian, 1961;Sutula et al, 1989;Salin et al, 1995;Dancause et al, 2005); by selective loss of inhibitory synapses (Ribak and Reiffenstein, 1982); or by increased synaptic and intrinsic neuronal responsiveness (Bush et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Synaptic Strength Modulation after Cortical Trauma: A Role in Epileptogenesis

Avramescu¹,

Timofeev²

2008

Journal of Neuroscience

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Traumatic brain injuries are often followed by abnormal hyperexcitability, leading to acute seizures and epilepsy. Previous studies documented the rewiring capacity of neocortical neurons in response to various cortical and subcortical lesions. However, little information is available on the functional consequences of these anatomical changes after cortical trauma and the adaptation of synaptic connectivity to a decreased input produced by chronic deafferentation. In this study, we recorded intracellular (IC) activities of cortical neurons simultaneously with extracellular (EC) unit activities and field potentials of neighboring cells in cat cortex, after a large transection of the white matter underneath the suprasylvian gyrus, in acute and chronic conditions (at 2, 4, and 6 weeks) in ketamine-xylazineanesthetized cats. Using EC spikes to compute the spike-triggered averages of IC membrane potential, we found an increased connection probability and efficacy between cortical neurons weeks after cortical trauma. Inhibitory interactions showed no significant changes in the traumatized cortex compared with control. The increased synaptic efficacy was accompanied by enhanced input resistance and intrinsic excitability of cortical neurons, as well as by increased duration of silent network periods. Our electrophysiological data revealed functional consequences of previously reported anatomical changes in the injured cortex. We suggest that homeostatic synaptic plasticity compensating the decreased activity in the undercut cortex leads to an uncontrollable cortical hyperexcitability and seizure generation.

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Morphological and physiological properties of chronically isolated immature neocortex

Cited by 99 publications

References 21 publications

Lasting Blood-Brain Barrier Disruption Induces Epileptic Focus in the Rat Somatosensory Cortex

Lasting Blood-Brain Barrier Disruption Induces Epileptic Focus in the Rat Somatosensory Cortex

Synaptic proliferation in the auditory cortex of the young adult rat following callosal lesions

Synaptic Strength Modulation after Cortical Trauma: A Role in Epileptogenesis

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