The development of electrocortical activity in the fetal and neonatal guinea pig

Umans, Jason G.; Cox, Martha J.; Hinman, Donald J.; Dogramajian, Mary Ellen; Senger, Gretchen; Szeto, Hazel H.

doi:10.1016/0002-9378(85)90089-4

Cited by 22 publications

(5 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These experiments are particularly significant in light of the fact that they were performed using an altricial species at ages before the onset of sleep-related neocortical activity [1,2,3]. Consequently, these results may prove to be broadly applicable to our understanding of sleep mechanisms in other mammalian species at an analogous time in development, including the period before 120 d postconception in sheep [29,30], 50 d postconception in guinea pigs [31], approximately 32 wk postconception in preterm human infants [32], and P13–15 in kittens [28]. …”

Section: Discussionmentioning

confidence: 99%

The Neural Substrates of Infant Sleep in Rats

et al. 2005

View full text Add to dashboard Cite

Sleep is a poorly understood behavior that predominates during infancy but is studied almost exclusively in adults. One perceived impediment to investigations of sleep early in ontogeny is the absence of state-dependent neocortical activity. Nonetheless, in infant rats, sleep is reliably characterized by the presence of tonic (i.e., muscle atonia) and phasic (i.e., myoclonic twitching) components; the neural circuitry underlying these components, however, is unknown. Recently, we described a medullary inhibitory area (MIA) in week-old rats that is necessary but not sufficient for the normal expression of atonia. Here we report that the infant MIA receives projections from areas containing neurons that exhibit state-dependent activity. Specifically, neurons within these areas, including the subcoeruleus (SubLC), pontis oralis (PO), and dorsolateral pontine tegmentum (DLPT), exhibit discharge profiles that suggest causal roles in the modulation of muscle tone and the production of myoclonic twitches. Indeed, lesions in the SubLC and PO decreased the expression of muscle atonia without affecting twitching (resulting in “REM sleep without atonia”), whereas lesions of the DLPT increased the expression of atonia while decreasing the amount of twitching. Thus, the neural substrates of infant sleep are strikingly similar to those of adults, a surprising finding in light of theories that discount the contribution of supraspinal neural elements to sleep before the onset of state-dependent neocortical activity.

show abstract

Section: Discussionmentioning

confidence: 99%

The Neural Substrates of Infant Sleep in Rats

et al. 2005

View full text Add to dashboard Cite

show abstract

“…For example, the neocortical EEG does not exhibit state‐dependent differentiation, including slow wave activity, until 115–120 days postconception in sheep (Clewlow et al. , 1983; Szeto and Hinman, 1985), 50 days postconception in guinea pigs (Umans et al. , 1985), approximately 32 weeks postconception in preterm human infants (Dreyfus‐Brisac, 1975), and until 12 days of age (P12) in rats (Frank and Heller, 1997; Gramsbergen, 1976; Mirmiran and Corner, 1982).…”

Section: Sleep Not Presleepmentioning

confidence: 99%

The ontogeny of mammalian sleep: a response to Frank and Heller (2003)

Blumberg

Karlsson

Seelke

et al. 2005

Journal of Sleep Research

View full text Add to dashboard Cite

SUMMAR Y In a recent review, Frank and Heller (2003) provided support for their Ôpresleep theoryÕ of sleep development. According to this theory, rapid eye movement (REM) and non-rapid eye movement (Non-REM) sleep in rats emerge from a common ÔdissociatedÕ state only when the neocortical EEG differentiates at 12 days of age (P12). Among the assumptions and inferences associated with this theory is that sleep before EEG differentiation is only Ôsleep-likeÕ and can only be characterized using behavioral measures; that the neural mechanisms governing presleep are distinct from those governing REM and Non-REM sleep; and that the presleep theory is the only theory that can account for developmental periods when REM and Non-REM sleep components appear to overlap. Evidence from our laboratory and others, however, refutes or casts doubt on these and other assertions. For example, infant sleep in rats is not Ôsleep-likeÕ in that it satisfies nearly every criterion used to characterize sleep across species. In addition, beginning as early as P2 in rats, myoclonic twitching occurs only against a background of muscle atonia, indicating that infant sleep is not dissociated and that electrographic measures are available for sleep characterization. Finally, improved techniques are leading to new insights concerning the neural substrates of sleep during early infancy. Thus, while many important developmental questions remain, the presleep theory, at least in its present form, does not accurately reflect the phenomenology of infant sleep.k e y w o r d s active sleep, atonia, myoclonic twitching, rat, rem sleep, slow-wave sleep

show abstract

“…; Umans et al . ). This neurodevelopmental correlation, along with the high proportion of rapid eye movement‐like behavioural activity during early life, supports a role for behavioural state activity in the brain's development and more so in guinea pigs and humans prenatally in response to conditions during pregnancy than in rats (Richardson et al .…”

Section: Introductionmentioning

confidence: 97%

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Morrison

Botting

Darby

et al. 2018

The Journal of Physiology

114

108

View full text Add to dashboard Cite

Over 30 years ago Professor David Barker first proposed the theory that events in early life could explain an individual's risk of non-communicable disease in later life: the developmental origins of health and disease (DOHaD) hypothesis. During the 1990s the validity of the DOHaD hypothesis was extensively tested in a number of human populations and the mechanisms underpinning it characterised in a range of experimental animal models. Over the past decade, researchers have sought to use this mechanistic understanding of DOHaD to develop therapeutic interventions during pregnancy and early life to improve adult health. A variety of animal models have been used to develop and evaluate interventions, each with strengths and limitations. It is becoming apparent that effective translational research requires that the animal paradigm selected mirrors the tempo of human fetal growth and development as closely as possible so that the effect of a perinatal insult and/or therapeutic intervention can be fully assessed. The guinea pig is one such animal model that over the past two decades has demonstrated itself to be a very useful platform for these important reproductive studies. This review highlights similarities in the in utero development between humans and guinea pigs, the strengths and limitations of the guinea pig as an experimental model of DOHaD and the guinea pig's potential to enhance clinical therapeutic innovation to improve human health.

show abstract

The development of electrocortical activity in the fetal and neonatal guinea pig

Cited by 22 publications

References 10 publications

The Neural Substrates of Infant Sleep in Rats

The Neural Substrates of Infant Sleep in Rats

The ontogeny of mammalian sleep: a response to Frank and Heller (2003)

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Contact Info

Product

Resources

About