Methods for behavioral testing of spinal cord injured rats

Bancroft

2017

Journal of Neurotrauma

Opioids are frequently used for the treatment of pain following spinal cord injury (SCI). Unfortunately, we have shown that morphine administered in the acute phase of SCI results in significant, adverse secondary consequences including compromised locomotor and sensory recovery. Similarly, we showed that selective activation of the j-opioid receptor (KOR), even at a dose 32-fold lower than morphine, is sufficient to attenuate recovery of locomotor function. In the current study, we tested whether activation of the KOR is necessary to produce morphine's adverse effects using norBinaltorphimine (norBNI), a selective KOR antagonist. Rats received a moderate spinal contusion (T12) and 24 h later, baseline locomotor function and nociceptive reactivity were assessed. Rats were then administered norBNI (0, 0.02, 0.08, or 0.32 lmol) followed by morphine (0 or 0.32 lmol). Nociception was reassessed 30 min after drug treatment, and recovery was evaluated for 21 days. The effects of norBNI on morphine-induced attenuation of recovery were dose dependent. At higher doses, norBNI blocked the adverse effects of morphine on locomotor recovery, but analgesia was also significantly decreased. Conversely, at low doses, analgesia was maintained, but the adverse effects on recovery persisted. A moderate dose of norBNI, however, adequately protected against morphine's adverse effects without eliminating its analgesic efficacy. This suggests that activation of the KOR system plays a significant role in the morphineinduced attenuation of recovery. Our research suggests that morphine, and other opioid analgesics, may be contraindicated for the SCI population. Blocking KOR activity may be a viable strategy for improving the safety of clinical opioid use.

Section: Assessments Of Sensory Reactivitymentioning

confidence: 99%

Section: Assessments Of Sensory Reactivitymentioning

confidence: 99%

Section: Locomotor Recoverymentioning

confidence: 99%

Section: Locomotor Recoverymentioning

confidence: 99%

Section: Locomotor Recoverymentioning

confidence: 99%

See 3 more Smart Citations

Nor-Binaltorphimine Blocks the Adverse Effects of Morphine after Spinal Cord Injury

Bancroft

2017

Journal of Neurotrauma

J of Comparative Neurology

Inter‐Strain Differences in the Lumbar Spinal Cord Anatomy and Neuromorphology: Wistar Versus Dark Agouti Rats

Veshchitskii,

Shkorbatova,

Efimova

et al. 2024

Rat strains differ in physiology, behavior, and recovery after central nervous system injury. To assess these differences, we compared the gross and local anatomy and neuromorphology of the lumbar spinal cord of the Wistar and Dark Agouti (DA) strains. The key findings include (i) distinct spatial relationships between vertebrae and spinal segments in the two strains; (ii) Wistar rats have larger volumes of spinal cord gray and white matter; (iii) DA rats have smaller total neuronal populations, thus indicating an expectation of smaller local neuronal populations; (iv) this expectation was confirmed for interneurons expressing calbindin 28 kDa. But contrary to expectations, (v) DA rats had more numerous populations of the interneurons expressing parvalbumin and a population of α‐motoneurons. Consequently, these strains displayed divergent ratios in specific spinal neuronal populations. Researchers should consider these inter‐strain differences when comparing data across different strains.

Behavioral Assays for Comprehensive Evaluation of Cognitive and Neuropsychiatric Comorbidities of Traumatic Brain Injury and Chronic Neurological Disorders

Reddy,

Li,

Qamari

et al. 2024

Current Protocols

Neurological deficits, psychiatric disorders, and cognitive impairments often accompany stroke, brain injury, epilepsy, and many neurological disorders, which present intricate comorbidities that challenge recognition and management. There are many tools and paradigms for evaluating learning, memory, anxiety, and depression‐like behaviors in lab animal models of brain disorders. However, there is a significant gap between clinical observations and experimental models, which limit understanding of the complex interplay between chronic brain conditions and their impact on cognitive dysfunction and psychiatric impairments. This article describes an overview of experimental rationale, methods, protocols, and strategies for evaluating sensorimotor, affective and cognitive‐associated comorbid behaviors in epilepsy, traumatic brain injury (TBI), stroke, spinal cord injury (SCI), and many other neurological disorders. First, we delve into clinical evidence elucidating the profound impact of comorbidities, e.g., psychiatric disorders and cognitive deficits, in individuals with epilepsy. Then, we discuss diverse approaches to assess these comorbidities in experimental models of brain diseases. Finally, we explore the methodologies for assessing motor function, sensorimotor, behavior, and psychiatric health. We cover strategies and protocols enabling these assays, including implementing behavioral paradigms to assess learning and memory, anxiety, and depression‐like behaviors in rodents in health and disease conditions. It is essential to consider a comprehensive battery of tests to investigate various behavioral deficits, considering environment, age, and sex differences relevant to the disease, such as TBI, SCI, epilepsy, stroke, and other complex neurological conditions. © 2024 The Author(s). Current Protocols published by Wiley Periodicals LLC.