Long-term effects of early pain and injury

2021 ◽  
pp. 21-37
Author(s):  
Orla Moriarty ◽  
Suellen M. Walker
Keyword(s):  
Nervous System ◽  
Early Life ◽  
Tissue Injury ◽  
Afferent Input ◽  
Laboratory Studies ◽  
Long Term Effects ◽  
Nociceptive Pathways ◽  
Noxious Stimuli ◽  
Underlying Mechanisms

Nociceptive pathways are functional following birth, and acute responses to noxious stimuli have been documented from early in development in clinical and laboratory studies. The ability of noxious afferent input to alter the level of sensitivity of nociceptive pathways in the adult nervous system, with, for example, the development of central sensitization, is well established. However, the developing nervous system has additional susceptibilities to alterations in neural activity, and pain in early life may produce effects not seen following the same input at older ages. As a result, early tissue injury may lead to persistent changes in somatosensory processing and altered sensitivity to future noxious stimuli. Furthermore, there is increasing evidence that neonatal pain can result in long-term changes in cognitive and affective behavior. Effects of pain in early life are superimposed on a highly plastic developing system, and long-term outcomes vary depending on the type and severity of the injury, and on the evaluation methods used. Laboratory studies allow evaluation of different injuries, potential confounding factors, underlying mechanisms, and potential analgesic modulation.

Long-term effects of early pain and injury: animal models

2013 ◽  
pp. 20-29 ◽  
Author(s):  
Suellen M. Walker
Keyword(s):  
Nervous System ◽  
Tissue Injury ◽  
Afferent Input ◽  
Somatosensory Processing ◽  
Laboratory Studies ◽  
Long Term Effects ◽  
Nociceptive Pathways ◽  
Acute Responses ◽  
Noxious Stimuli ◽  
Underlying Mechanisms

Nociceptive pathways are functional following birth and acute responses to noxious stimuli have been documented from early development in both clinical and laboratory studies. The ability of noxious afferent input to alter the level of sensitivity of nociceptive pathways in the adult nervous system, with, for example the development of central sensitization, is well established (Woolf, 2011). However, the developing nervous system has additional susceptibilities to alterations in neural activity, and increases due to pain and injury in early life may produce effects not seen following the same input at older ages. As a result, early tissue injury may lead to persistent changes in somatosensory processing and altered sensitivity to future noxious stimuli. The impact of early pain and injury cannot be simply viewed as increasing or decreasing sensitivity as results vary depending on the type and severity of injury and the outcomes used for assessment. Laboratory studies allow evaluation of different forms of injury, potential confounding factors, underlying mechanisms, and potential for modulation by analgesia.

Off to the right start: how pregnancy and early life can determine future animal health and production

2018 ◽  
Vol 58 (3) ◽  
pp. 459 ◽  
Author(s):  
K. L. Gatford ◽  
C. T. Roberts ◽  
K. L. Kind ◽  
P. I. Hynd
Keyword(s):  
Early Life ◽  
Low Birthweight ◽  
Animal Health ◽  
Developmental Programming ◽  
Developmental Trajectory ◽  
Long Term Effects ◽  
Prenatal Growth ◽  
Underlying Mechanisms ◽  
The Right

Animal producers are well aware that a low-birthweight animal is more likely to die in the first few days of life, and, if it survives, it is likely to perform poorly. We are now coming to appreciate that early life events can permanently change an animal’s developmental trajectory, also often referred to as developmental programming. This is an area of current interest in biomedicine, where the concept is known as the ‘developmental origins of health and disease’ (DOHaD). Current gaps in understanding include many of the underlying mechanisms, and whether and how we might intervene and restore the potential for healthy and productive development. This review introduces the biomedical perspective of developmental programming, reviews some of the evidence for long-term effects of early life exposures on welfare and productivity in animal production, with a focus on prenatal growth and maternal stress in pig production, and discusses options for intervening to improve long-term outcomes.

Nociceptive signalling in the periphery and spinal cord

2013 ◽  
pp. 53-64
Author(s):  
Suellen M. Walker ◽  
Mark L. Baccei
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Afferent Input ◽  
Acute Response ◽  
Management Interventions ◽  
Age Related ◽  
Noxious Stimuli ◽  
Electrical Stimuli ◽  
Age Related Changes

Responses to painful or noxious stimuli are functional at birth. However, postnatal changes in the transmitters, receptors, and pathways involved in nociceptive signalling result in significant age-related changes in the nature and degree of response. Noxious mechanical, thermal, and chemical stimuli are detected by peripheral nociceptors, transduced into electrical stimuli, and transmitted to the spinal cord. Within the spinal cord, there are significant postnatal changes in the balance of inhibitory and excitatory signalling, that not only influence the acute response to afferent input, but can also underlie long-term alterations in sensory processing following tissue injury in early life. Evaluating age-related changes in nociceptive signalling is essential not only for understanding acute behavioural responses to noxious stimuli, but also for identifying the most appropriate and effective pain management interventions at different developmental ages.

Nociceptive signaling in the periphery and spinal cord

2021 ◽  
pp. 59-66
Author(s):  
Gareth Hathway ◽  
Charles M. Greenspon ◽  
Mark L. Baccei
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Afferent Input ◽  
Acute Response ◽  
Management Interventions ◽  
Age Related ◽  
Noxious Stimuli ◽  
Electrical Stimuli ◽  
Age Related Changes

Responses to painful or noxious stimuli are functional at birth. However, postnatal changes in the transmitters, receptors, and pathways involved in nociceptive signaling result in significant age-related changes in the nature and degree of response. Noxious mechanical, thermal, and chemical stimuli are detected by peripheral nociceptors, transduced into electrical stimuli, and transmitted to the spinal cord. Within the spinal cord, there are significant postnatal changes in the balance of inhibitory and excitatory signaling, that not only influence the acute response to afferent input, but can also underlie long-term alterations in sensory processing following tissue injury in early life. Evaluating age-related changes in nociceptive signaling is essential not only for understanding acute behavioral responses to noxious stimuli, but also for identifying the most appropriate and effective pain-management interventions at different developmental ages.

The Neurobiology of Pain

2019 ◽  
pp. 387-414
Author(s):  
Maria Fitzgerald ◽  
Michael W. Salter
Keyword(s):  
Early Life ◽  
Pain Perception ◽  
Long Term Effects ◽  
Male And Female ◽  
Functional Changes ◽  
Pain Pathways ◽  
Developmental Age ◽  
Short And Long Term ◽  
Age And Sex

The influence of development and sex on pain perception has long been recognized but only recently has it become clear that this is due to specific differences in underlying pain neurobiology. This chapter summarizes the evidence for mechanistic differences in male and female pain biology and for functional changes in pain pathways through infancy, adolescence, and adulthood. It describes how both developmental age and sex determine peripheral nociception, spinal and brainstem processing, brain networks, and neuroimmune pathways in pain. Finally, the chapter discusses emerging evidence for interactions between sex and development and the importance of sex in the short- and long-term effects of early life pain.

scholarly journals Melatonin Successfully Rescues the Hippocampal Molecular Machinery and Enhances Anti-oxidative Activity Following Early-Life Sleep Deprivation Injury

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 774
Author(s):  
Hung-Ming Chang ◽  
Hsing-Chun Lin ◽  
Hsin-Lin Cheng ◽  
Chih-Kai Liao ◽  
To-Jung Tseng ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Early Life ◽  
Cognitive Activity ◽  
Oxidative Activity ◽  
Protective Effects ◽  
Long Term Effects ◽  
Ionic Distribution ◽  
Melatonin Administration ◽  
Molecular Machinery ◽  
Underlying Mechanisms

Early-life sleep deprivation (ESD) is a serious condition with severe cognitive sequelae. Considering hippocampus plays an essential role in cognitive regulation, the present study aims to determine whether melatonin, a neuroendocrine beard with significant anti-oxidative activity, would greatly depress the hippocampal oxidative stress, improves the molecular machinery, and consequently exerts the neuro-protective effects following ESD. Male weanling Wistar rats (postnatal day 21) were subjected to ESD for three weeks. During this period, the animals were administered normal saline or melatonin (10 mg/kg) via intraperitoneal injection between 09:00 and 09:30 daily. After three cycles of ESD, the animals were kept under normal sleep/wake cycle until they reached adulthood and were sacrificed. The results indicated that ESD causes long-term effects, such as impairment of ionic distribution, interruption of the expressions of neurotransmitters and receptors, decreases in the levels of several antioxidant enzymes, and impairment of several signaling pathways, which contribute to neuronal death in hippocampal regions. Melatonin administration during ESD prevented these effects. Quantitative evaluation of cells also revealed a higher number of neurons in the melatonin-treated animals when compared with the saline-treated animals. As the hippocampus is critical to cognitive activity, preserving or even improving the hippocampal molecular machinery by melatonin during ESD not only helps us to better understand the underlying mechanisms of ESD-induced neuronal dysfunction, but also the therapeutic use of melatonin to counteract ESD-induced neuronal deficiency.

Long term effects of early life stress on HPA circuit in rodent models

2021 ◽  
Vol 521 ◽  
pp. 111125
Author(s):  
Lucy Babicola ◽  
Rossella Ventura ◽  
Sebastian Luca D'Addario ◽  
Donald Ielpo ◽  
Diego Andolina ◽  
...  
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Rodent Models ◽  
Long Term Effects

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

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