Ibotenic acid lesions of the substantia nigra pars reticulata ipsilateral to a visual cortical lesion fail to restore visual orienting responses in the cat

Ciaramitaro, Vivian; Wallace, Steven F.; Rosenquist, Alan C.

doi:10.1002/(sici)1096-9861(19970127)377:4<596::aid-cne9>3.0.co;2-y

Cited by 16 publications

(6 citation statements)

References 103 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies at the Karolinska Institute revealed that another exogenous excitotoxin, ibotenic acid, was devoid of these unbecoming properties (Figure 3). Originally isolated from the mushroom Amanita muscaria (Eugster, 1968), ibotenate caused well-circumscribed neuronal loss upon focal injection into various brain regions and was therefore soon recognized as a superior tool for producing excitotoxic lesions in rats (Schwarcz et al, 1979b) and other experimental animals (Ciaramitaro et al, 1997; Wenk, 1993). Ibotenate-induced striatal lesions also created an improved animal model of HD, which became widely used – maybe most famously by Björklund and his collaborators in their first attempts to develop cell transplantation therapies for HD (Isacson et al, 1984).…”

Section: The Swedish Connection: Rotational Behavior and Ibotenic mentioning

confidence: 99%

Of mice, rats and men: Revisiting the quinolinic acid hypothesis of Huntington's disease

Schwarcz

Guidetti

Sathyasaikumar

et al. 2010

Progress in Neurobiology

154

View full text Add to dashboard Cite

The neurodegenerative disease Huntington's Disease (HD) is caused by an expanded polyglutamine (polyQ) tract in the protein huntingtin (htt). Although the gene encoding htt was identified and cloned more than 15 years ago, and in spite of impressive efforts to unravel the mechanism(s) by which mutant htt induces nerve cell death, these studies have so far not led to a good understanding of pathophysiology or an effective therapy. Set against a historical background, we review data supporting the idea that metabolites of the kynurenine pathway (KP) of tryptophan degradation provide a critical link between mutant htt and the pathophysiology of HD. New studies in HD brain and genetic model organisms suggest that the disease may in fact be causally related to early abnormalities in KP metabolism, favoring the formation of two neurotoxic metabolites, 3-hydroxykynurenine and quinolinic acid, over the related neuroprotective agent kynurenic acid. These findings not only link the excitotoxic hypothesis of HD pathology to an impairment of the KP but also define new drug targets and therefore have direct therapeutic implications. Thus, pharmacological normalization of the imbalance in brain KP metabolism may provide clinical benefits, which could be especially effective in the early stages of the disease. KeywordsExcitotoxicity; 3-Hydroxykynurenine; Kynurenines; Microglia; Neuroprotection Excitotoxins and Huntington's disease: the beginningHuntington's disease (HD), originally termed Huntington's chorea because of the characteristic involuntary movements shown by affected individuals, is a chronic neurodegenerative disorder, which is inherited in an autosomal dominant fashion. Overt motor symptoms usually develop in mid-life, and patients succumb to the disease after another 15-20 years on average. Long believed to be an exclusive basal ganglia disease because of the substantial and progressive neostriatal shrinkage and the massive dilation of the adjacent lateral ventricles, the neuropathology of HD is now known to involve a large number of brain regions and neuronal populations (Jackson et al., 1995;Rosas et al., 2008;Vonsattel et al., 1985).* We dedicate this article to the memory of our friend Paolo Guidetti, who passed away, prematurely on December 28, 2007.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptFor a century following the first description of the disease by George Huntington in 1872 (Huntington, 1872), speculations about the cause of neuronal loss in HD were sporadic a...

show abstract

Section: The Swedish Connection: Rotational Behavior and Ibotenic mentioning

confidence: 99%

Of mice, rats and men: Revisiting the quinolinic acid hypothesis of Huntington's disease

Schwarcz

Guidetti

Sathyasaikumar

et al. 2010

Progress in Neurobiology

154

View full text Add to dashboard Cite

show abstract

“…The release of eye movements that occurs in the Sprague effect when the tectal commissure is cut was initially ascribed to a general mutual inhibition between the two tecti (Sprague, 1966). However, it has more recently been suggested that it is due to cutting non-collicular fibers that cross in the commissure (Wallace et al, 1989(Wallace et al, , 1990Ciaramitaro et al, 1997). As noted above, the limited distribution and topographic character of the tectotectal projection in the cat argue against it acting as a general inhibitory agent.…”

Section: Tectotectal Cells and Mutual Collicular Inhibitionmentioning

confidence: 99%

“…Edwards (1977) demonstrated that a population of neurons in the cat superior colliculus does indeed project through the commissure to the contralateral side (see also Martin, 1969). However, more recent studies of the Sprague effect have suggested that it is the destruction of non-tectal axons crossing the midline in the collicular commissure that produces the recovery of visual orientation behaviour in the field contralateral to a visual cortical lesion (Wallace et al, 1989(Wallace et al, , 1990Ciaramitaro et al, 1997; but see Withington & McCrossan, 1996;Lomber and Payne, 1996).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the distribution and somatodendritic morphology of tectotectal neurons in the cat and monkey

1998

View full text Add to dashboard Cite

The presence of a commissure connecting the two superior colliculi suggests they do not act independently, but the function of the tectotectal connection has never been firmly identified. To develop a better understanding of this commissural system, the present study determined the distribution and morphology of tectotectal neurons in the cat and macaque monkey, two animals with well-studied, but different orienting strategies. First, we compared the distribution of tectotectal cells retrogradely labeled following WGA-HRP injections into the contralateral superior colliculus. In monkeys, labeled tectotectal cells were found in all layers, but were concentrated in the intermediate gray layer (75%), particularly dorsally, and the adjacent optic layer (12%). Tectotectal cells were distributed throughout nearly the entire rostrocaudal extent of the colliculus. In cats, tectotectal cells were found in all the layers beneath the superficial gray, but the intermediate gray layer contained the greatest concentration (56%). Labeled cells were almost exclusively located in the rostral half of the cat superior colliculus, in contrast to the monkey distribution. In the context of the representation of visuomotor space in the colliculus, the distribution of monkey and cat tectotectal cells suggests a correspondence with oculomotor range. So these neurons may be involved in directing orienting movements performed within the oculomotor range. The somatodendritic morphology of tectotectal cells in these two species was revealed by homogeneous retrograde labeling from injections of biocytin or biotinylated dextran amine into the contralateral colliculus. The cell classes contributing to this pathway are fairly consistent across the two species. A variety of neuronal morphologies were observed, so there is no single tectotectal cell type. Instead, cell types similar to those found in each layer, excepting the largest neurons, were present among tectotectal cells. This suggests that a sample of each layer's output is sent to the contralateral colliculus.

show abstract

“…The restoration of visual orienting after large visual cortical ablations is a phenomenon that has become known as the "Sprague Effect." This restoration was repeatedly demonstrated in numerous studies of the cat (Ciaramitaro et al 1997;Lomber et al 2002;Rosenquist et al 1996;Sherman 1977;Wallace et al 1989Wallace et al , 1990) and a recent human case also suggests that the effect can be identified in human subjects (Weddell 2004).…”

Section: Introductionmentioning

confidence: 68%

Restoration of Acoustic Orienting Into a Cortically Deaf Hemifield by Reversible Deactivation of the Contralesional Superior Colliculus: The Acoustic “Sprague Effect”

Lomber¹,

Malhotra²,

Sprague³

2007

Journal of Neurophysiology

View full text Add to dashboard Cite

Removal of all contiguous visual cortical areas of one hemisphere results in a contralateral hemianopia. Subsequent deactivation of the contralesional superior colliculus (SC) nullifies the effects of the visual cortex ablation and restores visual orienting responses into the cortically blind hemifield. This deficit nullification has become known as the "Sprague Effect." Similarly, in the auditory system, unilateral ablation of auditory cortex results in severe sound localization deficits, as assessed by acoustic orienting, to stimuli in the contralateral hemifield. The purpose of this study was to examine whether auditory orienting responses can be restored into the impaired hemifield during deactivation of the contralesional SC. Three mature cats were trained to orient toward and approach an acoustic stimulus (broadband, white noise burst) that was presented centrally, or at one of 12 peripheral loci, spaced at 15 degrees intervals. After training, a cryoloop was chronically implanted over the dorsal surface of the right SC. During cooling of the cooling loop to temperatures sufficient to deactivate the superficial and intermediate layers (SZ, SGS, SO, SGI), auditory orienting responses were eliminated into the left (contracooled) hemifield while leaving acoustic orienting into the right (ipsicooled) hemifield unimpaired. This deficit was temperature-dependently graded from periphery to center. After the effectiveness of the SC cooling loop was verified, auditory cortex of the middle and posterior ectosylvian and anterior and posterior sylvian gyri was removed from the left hemisphere. As expected, the auditory cortex ablation resulted in a profound deficit in orienting to acoustic stimuli presented at any position in the right (contralesional) hemifield, while leaving acoustic orienting into the left (ipsilesional) hemifield unimpaired. The ablations of auditory cortex did not have any impact on a visual detection and orienting task. The additional deactivation of the contralesional SC to temperatures sufficient to cool the superficial and intermediate layers nullified the deficit caused by the auditory cortex ablation and acoustic orienting responses were restored into the right hemifield. This restoration was temperature-dependently graded from center to periphery. The deactivations were localized and confirmed with reduced uptake of radiolabeled 2-deoxyglucose. Therefore deactivation of the right superior colliculus after the ablation of the left auditory cortex yields a fundamentally different result from that identified during deactivation of the right superior colliculus before the removal of left auditory cortex in the same animal. Thus the "Sprague Effect" is not unique to a particular sensory system and deactivation of the contralesional SC can restore either visual or acoustic orienting responses into an impaired hemifield after cortical damage.

show abstract

Ibotenic acid lesions of the substantia nigra pars reticulata ipsilateral to a visual cortical lesion fail to restore visual orienting responses in the cat

Cited by 16 publications

References 103 publications

Of mice, rats and men: Revisiting the quinolinic acid hypothesis of Huntington's disease

Of mice, rats and men: Revisiting the quinolinic acid hypothesis of Huntington's disease

Comparison of the distribution and somatodendritic morphology of tectotectal neurons in the cat and monkey

Restoration of Acoustic Orienting Into a Cortically Deaf Hemifield by Reversible Deactivation of the Contralesional Superior Colliculus: The Acoustic “Sprague Effect”

Contact Info

Product

Resources

About