Transient occlusion of uterine arteries and intra-amniotic injection of lipopolysaccharide in rats as a model of cerebral palsy

Hamimi, Sarah; Robinson, Shenandoah; Jantzie, Lauren L.

doi:10.1016/b978-0-323-89833-1.00003-3

Cited by 1 publication

(2 citation statements)

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“…Indeed, all the known risk factors besides birth prematurity (with ~75% of cerebral palsy patients having been born premature), display rates of cerebral palsy in <15% of all cases (in utero ischemia/infection/inflammation 12%, stroke < 1%, hypoxia-ischemia encephalopathy 15% and asphyxia 2–10%) [ 38 ]. Nonetheless, hypoxia, ischemia, in utero infections and combinations of these have been modelled in rabbits, rats and many other species [ 38 , 315 , 317 ]. Unsurprisingly, due to the low risk-association with cerebral palsy, most of these models do not recapitulate motor dysfunctions [ 38 , 318 ], spasticity or hypertona [ 38 , 318 , 319 ], have an excessive mortality rate or deaths shortly following experiments (unlike the clinical scenario, where mortality in associated with symptom severity) [ 292 , 319 , 320 , 321 ] and lack spasticity [ 38 , 292 , 318 ].…”

Section: Inhibitory Influences On Spastic Cerebral Palsymentioning

confidence: 99%

“…Unsurprisingly, due to the low risk-association with cerebral palsy, most of these models do not recapitulate motor dysfunctions [ 38 , 318 ], spasticity or hypertona [ 38 , 318 , 319 ], have an excessive mortality rate or deaths shortly following experiments (unlike the clinical scenario, where mortality in associated with symptom severity) [ 292 , 319 , 320 , 321 ] and lack spasticity [ 38 , 292 , 318 ]. One exception to this general lack of suitability is the rat model of transient occlusion of uterine arteries and intra-amniotic injection of lipopolysaccharide [ 317 , 322 ], which despite high experimental mortality [ 317 ], the surviving offspring exhibit locomotor and postural deficits and some indications of spasticity [ 317 ], although there seems to be ventriculomegaly, other white and grey matter lesions and cognitive declines that do not match some aspects of clinical sCP [ 317 ]. Overall, the risk factor models succeed in providing information about the impact of various lesions on brain development but do little to move the needle of sCP translation.…”

Section: Inhibitory Influences On Spastic Cerebral Palsymentioning

confidence: 99%

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Inhibitory Synaptic Influences on Developmental Motor Disorders

Fogarty

2023

IJMS

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During development, GABA and glycine play major trophic and synaptic roles in the establishment of the neuromotor system. In this review, we summarise the formation, function and maturation of GABAergic and glycinergic synapses within neuromotor circuits during development. We take special care to discuss the differences in limb and respiratory neuromotor control. We then investigate the influences that GABAergic and glycinergic neurotransmission has on two major developmental neuromotor disorders: Rett syndrome and spastic cerebral palsy. We present these two syndromes in order to contrast the approaches to disease mechanism and therapy. While both conditions have motor dysfunctions at their core, one condition Rett syndrome, despite having myriad symptoms, has scientists focused on the breathing abnormalities and their alleviation—to great clinical advances. By contrast, cerebral palsy remains a scientific quagmire or poor definitions, no widely adopted model and a lack of therapeutic focus. We conclude that the sheer abundance of diversity of inhibitory neurotransmitter targets should provide hope for intractable conditions, particularly those that exhibit broad spectra of dysfunction—such as spastic cerebral palsy and Rett syndrome.

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