MATSAP: An automated analysis of stretch-attend posture in rodent behavioral experiments

Holly, Kevin S.; Orndorff, Casey O.; Murray, Teresa A.

doi:10.1038/srep31286

Cited by 58 publications

(44 citation statements)

References 40 publications

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“…Rodents naturally elicit this risk assessment behaviour when in a new environment by performing a forward elongation of the head followed by retraction to the initial position. However, a high frequency of this behaviour shows a high level of anxiety (Holly et al, 2016). In line with findings from this study, aluminium has been reported to induce anxiety and memory decline (Crépeaux et al, 2017;Morris et al, 2017;Olajide et al, 2018).…”

Section: Discussionsupporting

confidence: 91%

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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Alzheimer's disease is the most common cause of dementia and is hallmarked by β-amyloid plaque and neurofibrillary tangles deposition in the CNS. The complex mechanism that underlies AD pathogenesis has made the development of a definitive cure futile. Exploring the possible therapeutic advantages of combining two neuromodulatory molecules with different mechanisms of neuroprotection is an interesting way of drug discovery. Ascorbic acid (AA), a potent antioxidant molecule, and nicotine (NIC), an allosteric modulator of nAChRs, have both been documented to independently proffer neuroprotection in experimental and clinical neurodegenerative cases. This study elucidated the putative therapeutic advantages of combining ascorbic acid and nicotine as a treatment regimen against the aluminium induced anxiety, corticohippocampal histopathology and perturbed neuroenergetics in rats induced with Alzheimer-like neuropathology Rats treated with 100 mg/kg aluminium chloride for 28 days presented with significantly increased stretch attend posture frequency and centre square entry. Aluminium significantly depleted the activities of G6PDH while increasing lactate levels. Corticohippocampal histomorphology of these animals showed poor histoarchitecture, increased congophilic and argentophilic densities that were coupled with increased anti-NSE immunopositivity. Animals post-treated with NIC (10mg/kg) and AA (100mg/kg) for 28 days presented with reduced anxiety level and improved corticohippocampal histomorphology. AA normalized G6PDH and lactate levels while the congophilic density was reduced by NIC. Corticohippocampal argentophilic density anti-NSE immunopositivity were also normalized by AA+NIC. The findings from this study have shown that a combination of ascorbic acid and nicotine effectively mitigated aluminium-induced corticohippocampal neuropathology and perturbed neuroenergetics.

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Section: Discussionsupporting

confidence: 91%

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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“…Moreover, stretch attend postures occur a risk-assessment behavior indicating that the rodent is hesitant to move from its present location to a new position 52 , 53 ; thus, a high frequency of these postures indicates a higher level of anxiety. We observed that NMS rats showed decreased stretching numbers in adolescence.…”

Section: Discussionmentioning

confidence: 99%

Early-life stress induces EAAC1 expression reduction and attention-deficit and depressive behaviors in adolescent rats

Kim

Yoo

et al. 2020

Cell Death Discov.

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Neonatal maternal separation (NMS), as an early-life stress (ELS), is a risk factor to develop emotional disorders. However, the exact mechanisms remain to be defined. In the present study, we investigated the mechanisms involved in developing emotional disorders caused by NMS. First, we confirmed that NMS provoked impulsive behavior, orienting and nonselective attention-deficit, abnormal grooming, and depressive-like behaviors in adolescence. Excitatory amino acid carrier 1 (EAAC1) is an excitatory amino acid transporter expressed specifically by neurons and is the route for the neuronal uptake of glutamate/aspartate/cysteine. Compared with that in the normal control group, EAAC1 expression was remarkably reduced in the ventral hippocampus and cerebral cortex in the NMS group. Additionally, EAAC1 expression was reduced in parvalbumin-positive hippocampal GABAergic neurons in the NMS group. We also found that EAAC1-knockout (EAAC1−/−) mice exhibited impulsive-like, nonselective attention-deficit, and depressive-like behaviors compared with WT mice in adolescence, characteristics similar to those of the NMS behavior phenotype. Taken together, our results revealed that ELS induced a reduction in EAAC1 expression, suggesting that reduced EAAC1 expression is involved in the pathophysiology of attention-deficit and depressive behaviors in adolescence caused by NMS.

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“…In agreement with their robust avoidance of the center of the OF, the number of transitions of Nlgn2 KO mice was too low to perform a powerful statistical analysis (4.4 ± 2.6 transitions). However, we noticed that Nlgn2 KO mice displayed frequent stretch-attend postures (SAPs), a risk-assessment behavior that reflects an internal conflict between anxiety and the exploratory drive 30,31 (Fig. 3j).…”

Section: Resultsmentioning

confidence: 99%

IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses

et al. 2018

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Abnormalities in synaptic inhibition play a critical role in psychiatric disorders, and accordingly, it is essential to understand the molecular mechanisms linking components of the inhibitory postsynapse to psychiatrically relevant neural circuits and behaviors. Here we study the role of IgSF9b, an adhesion protein that has been associated with affective disorders, in the amygdala anxiety circuitry. We show that deletion of IgSF9b normalizes anxiety-related behaviors and neural processing in mice lacking the synapse organizer Neuroligin-2 (Nlgn2), which was proposed to complex with IgSF9b. This normalization occurs through differential effects of Nlgn2 and IgSF9b at inhibitory synapses in the basal and centromedial amygdala (CeM), respectively. Moreover, deletion of IgSF9b in the CeM of adult Nlgn2 knockout mice has a prominent anxiolytic effect. Our data place IgSF9b as a key regulator of inhibition in the amygdala and indicate that IgSF9b-expressing synapses in the CeM may represent a target for anxiolytic therapies.

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MATSAP: An automated analysis of stretch-attend posture in rodent behavioral experiments

Cited by 58 publications

References 40 publications

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Early-life stress induces EAAC1 expression reduction and attention-deficit and depressive behaviors in adolescent rats

IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses

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