Britain, Ireland and the Crusades, c.1000–1300

Hurlock, Kathryn

doi:10.1007/978-1-137-29273-5

Cited by 6 publications

(7 citation statements)

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“…Kv3.3 channels are expressed in both the somata and the dendrites of cerebellar Purkinje cells. Consistent with a role for Kv3.3 in shaping the firing patterns of these neurons, Purkinje cell action potentials are broader in Kv3.3 −/− mice than in wild type animals (Hurlock et al 2008). In addition the Purkinje cells have fewer complex spikes and a reduced frequency of spikelets (Fig.…”

Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 66%

“…Their gait is altered in that they make increased lateral deviations while walking (Joho et al 2006). They are more likely to slip while walking on a narrow beam (Joho et al 2006;Hurlock et al 2008). They are also prone to spontaneous muscle twitches.…”

Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 99%

“…1A). These electrophysiological changes can be rescued by re-introducing wild type Kv3.3 channels selectively into Purkinje cells of Kv3.3 −/− animals, but this does not rescue the motor behaviours (Hurlock et al 2008). The excitability of the distal dendrites, and the amplitude of cytoplasmic Ca 2+ signals evoked by stimulation of the dendrites, is also increased in Purkinje cells of Kv3.3 −/− knockout mice (Zagha et al 2010).…”

Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 99%

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Kv3.3 potassium channels and spinocerebellar ataxia

Zhang

Kaczmarek

2015

The Journal of Physiology

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The voltage-dependent potassium channel subunit Kv3.3 is expressed at high levels in cerebellar Purkinje cells, in auditory brainstem nuclei and in many other neurons capable of firing at high rates. In the cerebellum, it helps to shape the very characteristic complex spike of Purkinje cells. Kv3.3 differs from other closely related channels in that human mutations in the gene Abstract figure legend Mutations in the Kv3.3 potassium channels produce spinocerebellar ataxia type 13, a disease that results in progressive degeneration of the cerebellum.

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Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 66%

Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 99%

Section: Lessons From Kv33 Knockout Animalsmentioning

confidence: 99%

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Kv3.3 potassium channels and spinocerebellar ataxia

Zhang

Kaczmarek

2015

The Journal of Physiology

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“…3Cb and D), the cerebellum of Kv3.3 knockout mice shows neither dendritic shrinkage of PCs nor cerebellar atrophy (Zagha et al 2010). Furthermore, the knockout mice display only moderate motor dysfunction and no ataxic phenotype, although SCA13 patients show severe ataxia (Joho et al 2006;Hurlock et al 2008;Waters & Pulst, 2008;Figueroa et al 2010). This difference may be attributable to the following factors.…”

Section: Purkinje Cell Death By R424h Mutant Expression and The Inhibmentioning

confidence: 99%

“…In the rodent brain, Kv3.3 mRNA and protein are abundantly expressed in the cerebellum, in which the mRNA is most intensely expressed in PCs (Weiser et al 1994;Chang et al 2007). Interestingly, Kv3.3-deficient mice show normal PC morphology and no ataxic phenotype (Joho et al 2006;Hurlock et al 2008;Zagha et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Kv3.3 channels harbouring a mutation of spinocerebellar ataxia type 13 alter excitability and induce cell death in cultured cerebellar Purkinje cells

Irie

Matsuzaki

Sekino

et al. 2013

The Journal of Physiology

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Key points• The cerebellum plays crucial roles in controlling sensorimotor functions, and patients with spinocerebellar ataxia type 13 exhibit cerebellar atrophy and cerebellar symptoms.• The disease is an autosomal dominant disorder caused by missense mutations in the voltage-gated K + channel Kv3.3, which is expressed intensely in the cerebellar Purkinje cells, the sole output neurons from the cerebellar cortex.• Here, we examined how these mutations cause the cerebellar disease by lentiviral expression of the mutant Kv3.3 in mouse cultured Purkinje cells.• Expression of the mutant Kv3.3 suppressed outward currents, broadened action potentials and elevated basal intracellular calcium concentration in Purkinje cells. Moreover, the mutant-expressing Purkinje cells showed impaired dendrites and extensive cell death, both of which were significantly rescued by blockade of P/Q-type Ca 2+ channels.• These results suggest that Purkinje cells in the patients also exhibit similar abnormalities, which may account for the pathology of the disease. AbstractThe cerebellum plays crucial roles in controlling sensorimotor functions. The neural output from the cerebellar cortex is transmitted solely by Purkinje cells (PCs), whose impairment causes cerebellar ataxia. Spinocerebellar ataxia type 13 (SCA13) is an autosomal dominant disease, and SCA13 patients exhibit cerebellar atrophy and cerebellar symptoms. Recent studies have shown that missense mutations in the voltage-gated K + channel Kv3.3 are responsible for SCA13. In the rodent brain, Kv3.3 mRNAs are expressed most strongly in PCs, suggesting that the mutations severely affect PCs in SCA13 patients. Nevertheless, how these mutations affect the function of Kv3.3 in PCs and, consequently, the morphology and neuronal excitability of PCs remains unclear. To address these questions, we used lentiviral vectors to express mutant mouse Kv3.3 (mKv3.3) channels harbouring an R424H missense mutation, which corresponds to the R423H mutation in the Kv3.3 channels of SCA13 patients, in mouse cerebellar cultures. The R424H mutant-expressing PCs showed decreased outward current density, broadened action potentials and elevated basal [Ca 2+ ] i compared with PCs expressing wild-type mKv3.3 subunits or those expressing green fluorescent protein alone. Moreover, expression of R424H mutant subunits induced impaired dendrite development and cell death selectively in PCs, both of which were rescued by blocking P/Q-type Ca 2+ channels in the culture conditions. We therefore concluded that expression of R424H mutant subunits in PCs markedly affects the function of endogenous Kv3 channels, neuronal excitability and, eventually, basal [Ca 2+ ] i , leading to cell death. These

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Battling the Lion: Visual Commemorations of Crusade in Twelfth- And Thirteenth-Century Seals From the British Isles

Reynolds

2023

Antiq. J.

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This article examines a group of five surviving twelfth- and thirteenth-century wax seal impressions from the British Isles that depict a scene of an armed knight in combat with a lion. This seal motif has tenuously been linked with crusading in the past, and so this paper seeks to address the connections between the sigillants and crusade, as well as the significance of commemoration of crusade culture on medieval seals. It highlights numerous links between this specific design and crusading experiences, literature and allegory. This paper focuses on an aspect of the medieval memory of crusade and the means of displaying chivalric, crusading identities within literate culture (on charters and letters) and in personal adornment.

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Britain, Ireland and the Crusades, c.1000–1300

Cited by 6 publications

References 0 publications

Kv3.3 potassium channels and spinocerebellar ataxia

Kv3.3 potassium channels and spinocerebellar ataxia

Kv3.3 channels harbouring a mutation of spinocerebellar ataxia type 13 alter excitability and induce cell death in cultured cerebellar Purkinje cells

Battling the Lion: Visual Commemorations of Crusade in Twelfth- And Thirteenth-Century Seals From the British Isles

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