Biomedical subjects

Kimberlei A Richardson

Publications and source records attributed to Kimberlei A Richardson.

4 recordsLinked to original sources

PubMed2006

Neonatal animal models of opiate withdrawal.

The symptoms of opiate withdrawal in infants are defined as neonatal abstinence syndrome (NAS). NAS is a significant cause of morbidity in term and preterm infants. Factors, such as polysubstance abuse, inadequate prenatal care, nutritional deprivation, and the biology of the developing central nervous system contribute to the challenge of evaluating and treating opiate-induced alterations in the newborn. Although research on the effects of opiates in neonatal animal models is limited, the data from adult animal models have greatly contributed to understanding and treating opiate tolerance, addiction, and withdrawal in adult humans. Yet the limited neonatal data that are available indicate that the mechanisms involved in these processes in the newborn differ from those in adult animals, and that neonatal models of opiate withdrawal are needed to understand and develop effective treatment regimens for NAS. In this review, the behavioral and neurochemical evidence from the literature is presented and suggests that mechanisms responsible for opiate tolerance, dependence, and withdrawal differ between adult and neonatal models. Also reviewed are studies that have used neonatal rodent models, the authors' preliminary data based on the use of neonatal rat and mouse models of opiate withdrawal, and other neonatal models that have been proposed for the study of neonatal opiate withdrawal.

Age Factors↗

PubMed2005

Genioglossal hypoglossal muscle motoneurons are contacted by nerve terminals containing delta opioid receptor but not mu opioid receptor-like immunoreactivity in the cat: a dual labeling electron microscopic study.

This study has investigated (1) the distribution of delta opioid receptor (DOR) or mu opioid receptor (MOR) containing elements in the hypoglossal nucleus of the adult cat; and (2) the association of these processes with retrogradely labeled genioglossus muscle motoneurons. Cholera toxin B conjugated to horseradish peroxidase (CTB-HRP) was injected into the genioglossus muscle on the right side of four isoflurane-anesthetized cats. Forty-four to 52 h later, the animals were sacrificed. Motoneurons containing HRP were labeled with a histochemical reaction utilizing tetramethylbenzidine (TMB) as the chromogen. The tissues were then processed for immunocytochemistry, using an antiserum raised against DOR or MOR using diaminobenzidine (DAB) as the chromogen. At the light microscopic level, retrogradely labeled cells were observed primarily ipsilaterally in ventral and ventrolateral subdivisions of the hypoglossal nucleus. The majority of these labeled cells were observed immediately caudal to obex. DOR-like immunoreactive processes were apparent at the light microscopic level in the hypoglossal nucleus, but MOR-like immunoreactive processes were not. Both DOR and MOR-like immunoreactive processes were observed in other brainstem areas such as the spinal trigeminal nucleus. At the electron microscopic level, DOR-like immunoreactive nerve terminals formed synaptic contacts with retrogradely labeled genioglossus muscle motoneuronal dendrites and perikarya in the hypoglossal nucleus. Nineteen (19) percent of the DOR terminals contacted retrogradely labeled genioglossus muscle motoneurons. DOR-immunoreactive terminals also synapsed on unlabeled dendrites and somata. Few MOR-like immunoreactive terminals were found at the EM level in the hypoglossal nucleus, and none of these terminals contacted retrogradely labeled neuronal profiles from the GG muscle. These are the first ultrastructural studies demonstrating synaptic interactions between functionally identified hypoglossal motoneurons and DOR terminals, and that enkephalins most likely act presynaptically to modulate the release of other neurotransmitters that affect GG motoneuron activity. These studies demonstrate that hypoglossal motoneurons which innervate the major protruder muscle of the tongue, the genioglossus muscle, are modulated by terminals containing DOR, and that enkephalins acting on DOR but not MOR in the hypoglossal nucleus may play a role in the control of tongue protrusion.

Animals↗

PubMed2004

Cannabinoid receptor expression in peripheral arterial chemoreceptors during postnatal development.

Prenatal exposure to tobacco smoke increases risk of sudden infant death syndrome (SIDS). Marijuana is frequently smoked in conjunction with tobacco, and perinatal exposure to marijuana is associated with increased incidence of SIDS. Abnormalities in peripheral arterial chemoreceptor responses during sleep may be operative in infants at risk for SIDS, and nicotine exposure adversely affects peripheral arterial chemoreceptor responses. To determine whether marijuana could potentially affect the activity of peripheral arterial chemoreceptors during early postnatal development, we used in situ hybridization histochemistry to characterize the pattern and level of mRNA expression for cannabinoid type 1 receptor (CB1R) in the carotid body, superior cervical ganglia (SCG), and nodose-petrosal-jugular ganglia (NG-PG-JG) complex in newborn rats. We used immunohistochemistry and light, confocal, and electron microscopy to characterize the pattern of CB1R and tyrosine hydroxylase protein expression. CB1R mRNA expression was intense in the NG-PG-JG complex, low to moderate in the SCG, and sparse in the carotid body. With maturation, CB1R gene expression significantly increased (P < 0.01) in the NG-PG-JG complex. CB1R immunoreactivity was localized to nuclei of ganglion cells in the SCG and NG-PG-JG complex, whereas tyrosine hydroxylase immunoreactivity was localized to the cytoplasm. Exposure to marijuana during early development could potentially modify cardiorespiratory responses via peripheral arterial chemoreceptors. The novel finding of nuclear localization of CB1Rs in peripheral ganglion cells suggests that these receptors may have an, as yet, undetermined role in nuclear signaling in sensory and autonomic neurons.

Animals↗

PubMed2003

Genioglossal hypoglossal motoneurons contact substance P-like immunoreactive nerve terminals in the cat: a dual labeling electron microscopic study.

This study investigated the synaptic interactions between hypoglossal motoneurons that project to the genioglossus muscle and substance P (SP) containing immunoreactive nerve terminals. Cholera toxin B conjugated to horseradish peroxidase (CTB-HRP) was injected into the right half of the genioglossus muscle in four anesthetized cats. Two days later, the animals were perfused with acrolein fixative. Tetramethylbenzidine (TMB) was the chromogen used to detect retrogradely labeled cells containing CTB-HRP. The tissues were then processed for immunocytochemistry using an antiserum raised against SP with diaminobenzidine (DAB) as the chromogen. At the light microscopic level, labeled cells were observed primarily ipsilaterally in ventral and ventrolateral subdivisions of the hypoglossal nucleus. The majority of these labeled cells were observed at the level of the area postrema. At the electron microscopic level, SP-like immunoreactive nerve terminals formed synaptic contacts with retrogradely labeled dendrites and perikarya. Nineteen percent of the terminals that contacted retrogradely labeled cells contained SP. These are the first ultrastructural studies demonstrating synaptic interactions between protruder hypoglossal motoneurons and SP terminals. These studies demonstrate that hypoglossal motoneurons which innervate the major protruder muscle of the tongue, the genioglossus muscle, may be modulated by SP. Thus, SP may play a role in the control of protrusive movements of the tongue acting via neurokinin receptors.

Afferent Pathways↗