scholarly journals Recent Advancements in Behavioral Testing in Rodents

MethodsX ◽  
2021 ◽  
pp. 101536
Author(s):  
Zeynep Sena
Keyword(s):  
2015 ◽  
Vol 223 (3) ◽  
pp. 151-156 ◽  
Author(s):  
Nina Schweinfurth ◽  
Undine E. Lang

Abstract. In the development of new psychiatric drugs and the exploration of their efficacy, behavioral testing in mice has always shown to be an inevitable procedure. By studying the behavior of mice, diverse pathophysiological processes leading to depression, anxiety, and sickness behavior have been revealed. Moreover, laboratory research in animals increased at least the knowledge about the involvement of a multitude of genes in anxiety and depression. However, multiple new possibilities to study human behavior have been developed recently and improved and enable a direct acquisition of human epigenetic, imaging, and neurotransmission data on psychiatric pathologies. In human beings, the high influence of environmental and resilience factors gained scientific importance during the last years as the search for key genes in the development of affective and anxiety disorders has not been successful. However, environmental influences in human beings themselves might be better understood and controllable than in mice, where environmental influences might be as complex and subtle. The increasing possibilities in clinical research and the knowledge about the complexity of environmental influences and interferences in animal trials, which had been underestimated yet, question more and more to what extent findings from laboratory animal research translate to human conditions. However, new developments in behavioral testing of mice involve the animals’ welfare and show that housing conditions of laboratory mice can be markedly improved without affecting the standardization of results.


1993 ◽  
Vol 4 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Donald G. Stein ◽  
Marylou M. Glasier ◽  
Stuart W. Hoffman

It is only within the last ten years that research on treatment for central nervous system (CNS) recovery after injury has become more focused on the complexities involved in promoting recovery from brain injury when the CNS is viewed as an integrated and dynamic system. There have been major advances in research in recovery over the last decade, including new information on the mechanics and genetics of metabolism and chemical activity, the definition of excitotoxic effects and the discovery that the brain itself secretes complex proteins, peptides and hormones which are capable of directly stimulating the repair of damaged neurons or blocking some of the degenerative processes caused by the injury cascade. Many of these agents, plus other nontoxic naturally occurring substances, are being tested as treatment for brain injury. Further work is needed to determine appropriate combinations of treatments and optimum times of administration with respect to the time course of the CNS disorder. In order to understand the mechanisms that mediate traumatic brain injury and repair, there must be a merging of findings from neurochemical studies with data from intensive behavioral testing.


PLoS ONE ◽  
2017 ◽  
Vol 12 (12) ◽  
pp. e0188880 ◽  
Author(s):  
Kajal Kumari ◽  
Hennariikka Koivisto ◽  
Matti Viluksela ◽  
Kaisa M. A. Paldanius ◽  
Mikael Marttinen ◽  
...  

2011 ◽  
Vol 14 (5) ◽  
pp. 583-597 ◽  
Author(s):  
Friederike Knerlich-Lukoschus ◽  
Beata von der Ropp-Brenner ◽  
Ralph Lucius ◽  
Hubertus Maximilian Mehdorn ◽  
Janka Held-Feindt

Object Central neuropathic pain is a frequent challenging complication after spinal cord injury (SCI), and specific therapeutic approaches remain elusive. The purpose of the present investigations was to identify potential key mediators of these pain syndromes by analyzing detailed expression profiles of important chemokines in an experimental SCI paradigm of posttraumatic neuropathic pain in rats. Methods Expression of CCR1, CCL3(MIP-1α), CXCR4, and CXCL12(SDF-1α) was investigated in parallel with behavioral testing for mechanical and thermal nociceptive thresholds after standardized SCI; 100-kdyn (moderate injury) and 200-kdyn (severe injury) force-defined thoracic spinal cord contusion lesions were applied via an Infinite Horizon Impactor at the T-9 level. Sham controls received laminectomies. Hindlimb locomotor function as well as mechanical and thermal sensitivities were monitored weekly by standardized behavioral testing after SCI. Chemokine expression was analyzed by real-time reverse transcriptase polymerase chain reaction in the early (7 days postoperatively) and late (42 days postoperatively) time courses after SCI, and immunohistochemical analysis (anatomical and quantitative) was performed 2, 7, 14, and 42 days after lesioning. Double staining with cellular markers and pain-related peptides (substance P and CGRP) or receptors (TRPV-1, TRPV-2, VRL-1, and TLR-4) was performed. Based on data obtained from behavioral testing, quantified immunohistochemical chemokine expressions in individual animals were correlated with the respective mechanical and thermal sensitivity thresholds 6 weeks after SCI. Results After 200-kdyn lesions, the animals exhibited prolonged reduction in their nociceptive thresholds, while 100-kdyn groups showed pain-related behaviors only in the early time course after SCI. Investigated chemokines were widely induced after SCI, involving cervical, thoracic, and lumbar spinal cord levels far beyond the lesion core. CCR1 and CCL3 were induced significantly in the dorsal horns 2 days after lesioning and remained at high levels after SCI with significantly higher intensities after 200-kdyn than 100-kdyn contusions. CXCR4 and CXCL12 levels continuously increased from 2 to 42 days after moderate and severe lesions. Additionally, chemokines were induced significantly in dorsal columns, with highest density levels 42 days after 200-kdyn lesions. In dorsal horns, CCR1 was coexpressed with TRPV-1 while CXCR4 and CXCL12 were partially coexpressed with substance P and CGRP. In dorsal columns, CCL3/CCR1 colabeled with GFAP, TRPV-2, TRPV-1, TLR-4; CXCR4/CXCL12 coexpressed with GFAP, CD68/ED1, and TLR4. Chemokine immunoreactivity density levels, especially CCL3 and its receptor, correlated in part significantly with nociceptive thresholds. Conclusions The authors report lesion grade–dependent upregulation of different chemokines/chemokine receptors after spinal cord contusion lesions in pain-processing spinal cord regions in a clinically relevant model of traumatic SCI in rats. Prolonged chemokine induction further correlated with below-level pain development in the delayed time course after severe SCI and was coexpressed with pain-associated peptides and receptors, suggesting that chemokines play a crucial role in chronic central pain mechanisms after SCI.


Author(s):  
René Bernard ◽  
Mustafa Balkaya ◽  
André Rex

Aspartame ◽  
2020 ◽  
pp. 379-404
Author(s):  
Richard E. Butcher ◽  
Charles V. Vorhees

2004 ◽  
Author(s):  
Doug Constance ◽  
Alexander N. Makris ◽  
Michael B. Wisbiski ◽  
Michael A. Kropinski ◽  
Michael A. Turley ◽  
...  

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