SHIRPA, a protocol for behavioral assessment: validation for longitudinal study of neurological dysfunction in mice

Rogers, Derek C.; Peters, Jo; Martin, Joanne E.; Ball, Simon; Nicholson, Sharon J.; Witherden, Abi S.; Hafezparast, Majid; Latcham, Judy; Robinson, Tracy; Quilter, Charlotte A.; Fisher, Elizabeth

doi:10.1016/s0304-3940(01)01885-7

Cited by 172 publications

(140 citation statements)

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“…All experimental procedures were approved by the local ethical committee of the Medical University of Vienna (BMWFW‐66.009/0277‐WF/V/3b/2017) and also met European legislative requirements. A modified SHIRPA protocol (Rogers et al , 2001) was used as comprehensive phenotyping tool. Herein, data on provoked sensory performance were presented as measures of stress responsiveness.…”

Section: Methodsmentioning

confidence: 99%

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

et al. 2018

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Stress‐induced cortical alertness is maintained by a heightened excitability of noradrenergic neurons innervating, notably, the prefrontal cortex. However, neither the signaling axis linking hypothalamic activation to delayed and lasting noradrenergic excitability nor the molecular cascade gating noradrenaline synthesis is defined. Here, we show that hypothalamic corticotropin‐releasing hormone‐releasing neurons innervate ependymal cells of the 3rd ventricle to induce ciliary neurotrophic factor (CNTF) release for transport through the brain's aqueductal system. CNTF binding to its cognate receptors on norepinephrinergic neurons in the locus coeruleus then initiates sequential phosphorylation of extracellular signal‐regulated kinase 1 and tyrosine hydroxylase with the Ca2+‐sensor secretagogin ensuring activity dependence in both rodent and human brains. Both CNTF and secretagogin ablation occlude stress‐induced cortical norepinephrine synthesis, ensuing neuronal excitation and behavioral stereotypes. Cumulatively, we identify a multimodal pathway that is rate‐limited by CNTF volume transmission and poised to directly convert hypothalamic activation into long‐lasting cortical excitability following acute stress.

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Section: Methodsmentioning

confidence: 99%

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

et al. 2018

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“…Health and neurological status were assessed at LAB2 using a 10-min protocol including tests as described in standard check lists such as SHIRPA [40] and the Fox battery [17]. Animals were inspected for physical appearance, and underwent neurological testing including acoustic startle, visual placing, grip strength and reflex functions.…”

Section: General Health Checkmentioning

confidence: 99%

Role of a neuronal small non-messenger RNA: behavioural alterations in BC1 RNA-deleted mice

Lewejohann

Skryabin

Sachser

et al. 2004

Behavioural Brain Research

139

102

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BC1 RNA is a small non-messenger RNA common in dendritic microdomains of neurons in rodents. In order to investigate its possible role in learning and behaviour, we compared controls and knockout mice from three independent founder lines established from separate embryonic stem cells. Mutant mice were healthy with normal brain morphology and appeared to have no neurological deficits. A series of tests for exploration and spatial memory was carried out in three different laboratories. The tests were chosen as to ensure that different aspects of spatial memory and exploration could be separated and that possible effects of confounding variables could be minimised. Exploration was studied in a barrier test, in an open-field test, and in an elevated plus-maze test. Spatial memory was investigated in a Barnes maze and in a Morris water maze (memory for a single location), in a multiple T-maze and in a complex alley maze (route learning), and in a radial maze (working memory). In addition to these laboratory tasks, exploratory behaviour and spatial memory were assessed under semi-naturalistic conditions in a large outdoor pen. The combined results indicate that BC1 RNA-deficient animals show behavioural changes best interpreted in terms of reduced exploration and increased anxiety. In contrast, spatial memory was not affected. In the outdoor pen, the survival rates of BC1-depleted mice were lower than in controls. Thus, we conclude that the neuron-specific non-messenger BC1 RNA contributes to the aptive modulation of behaviour.

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“…To do this, each block included animals of each condition and age. The FOB is a standard method for assessment of general arousal, reflexes, autonomic, motor and neurological deficits, and was performed as described previously [12,24]. This battery was used as a primary screen in order to verify the absence of gross deficits that would prevent or confound the principal behavioral tests.…”

Section: Introductionmentioning

confidence: 99%

“…Controls for visual acuity and exploratory deficits are intrinsic to the design of the task. We also performed a battery of tests, including assessments of motor coordination, such as the balance beam [26] and rotarod assays [3], a functional observation battery (FOB) [12,24] and open field tasks [5]. Furthermore, we tested whether deficits could be detected in relatively young mice prior to manifestation of overt symptoms.…”

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confidence: 99%

“…1B) were not statistically different between hexb−/− and age-matched hexb+/+ mice, demonstrating that the motivation and ability to explore was intact in all mice at 66 and 79 days. Furthermore, all mice (within the age range tested) had normal pupil dilation and visual placing in the FOB (all control mice and all but one of the mutant mice reach for the grid within 2-6 cm) [12,24]. By 97 days, most hexb−/−mice showed little object exploration which resulted in a sample size too small to analyze statistically.…”

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confidence: 99%

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Early deficits in motor coordination and cognitive dysfunction in a mouse model of the neurodegenerative lysosomal storage disorder, Sandhoff disease

Gulinello

Chen

Dobrenis

2008

Behavioural Brain Research

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Mouse models of lysosomal storage diseases, including Sandhoff disease, are frequently employed to test therapies directed at the central nervous system. We backbred such mice and conducted a behavioral test battery which included sensorimotor and cognitive assessments. This is the first report of short-term memory deficits in a murine model of Sandhoff disease. We also document early onset of motor deficits using the balance beam test. KeywordsSandhoff disease; Mouse model; Novel object recognition test; Rotarod; Motor coordination; Balance beam; Open field; Memory Lysosomal storage disorders (LSDs) are a family of inherited diseases with multi-organ involvement frequently including the nervous system. The G M2 gangliosidoses, one class of human LSDs that include Tay-Sachs and Sandhoff diseases, are marked by the lysosomal accumulation of G M2 ganglioside (GM2) in neurons throughout the nervous system. Sandhoff disease arises from defects in the gene encoding the β-subunit (hexb) of β-Nacetyl-d-hexosaminide N-acetylhexosaminohydrolase (EC 3.2.1.52) normally involved in the sequential catabolism of gangliosides and other glycoconjugates [11]. Sandhoff patients have widespread brain pathology which results in clinical symptoms including progressive mental and motor deterioration [10,11,21].Two transgenic murine models of Sandhoff disease exist [23,25] that, like the human equivalent, exhibit premature death and display widespread neuronal storage of ganglioside, in addition to gliotic and inflammatory reactions and neuronal cell death [11,16,23,25,27]. The Sandhoff models have engendered much research directed at overcoming the challenges [1,2,4,11,14,15,18,20]. The knockout model [25] presented here displays ataxia, tremor, muscle wasting, and deficits in motor reflex, coordination and balance [1,4,7,8,13,14,16,18,20,22,25,27,28]. However, systematic studies examining cognitive or affective outcomes are lacking [25]. Clearly, these latter studies would be valuable to evaluate CNS-specific improvements, and would be most meaningful if assays pertinent to human neurologic assessments were employed to facilitate transition to clinical trials. Furthermore, the Sandhoff mice rarely show overt clinical signs before 3 months old and then rapidly decline, typically becoming moribund between 4 and 5 months of age [1,[13][14][15]18,20,22,25,27,28]. Therefore, behavioral assays should ideally be able to identify cognitive deficits in subjects that have multiple behavioral outcomes. In addition, increased assay sensitivity could permit behavioral assessment at earlier ages thereby also providing better evaluation of therapeutic strategies which seek earlier intervention.We Heterozygous breeders of the B6; 129S4-Hexβ tm1R1p strain [25] (Jackson Labs, Maine) were backbred through 10 generations by mating with C57BL/6J mice. Then the backbred heterozygotes were mated together and progeny genotyped using a standardized PCR protocol (provided by Jackson Labs) on tail-tip DNA extracts. Studies were performed using homozy...

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SHIRPA, a protocol for behavioral assessment: validation for longitudinal study of neurological dysfunction in mice

Cited by 172 publications

References 4 publications

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

Role of a neuronal small non-messenger RNA: behavioural alterations in BC1 RNA-deleted mice

Early deficits in motor coordination and cognitive dysfunction in a mouse model of the neurodegenerative lysosomal storage disorder, Sandhoff disease

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