Secondhand tobacco smoke exposure differentially alters nucleus tractus solitarius neurons at two different ages in developing non-human primates
- Department of Pharmacology, University of California Davis, Davis, CA 95616 (United States)
- Department of Pediatrics, University of California Davis, Davis, CA 95616 (United States)
- Center for Health and the Environment, University of California Davis, Davis, CA 95616 (United States)
Exposing children to secondhand tobacco smoke (SHS) is associated with increased risk for asthma, bronchiolitis and SIDS. The role for changes in the developing CNS contributing to these problems has not been fully explored. We used rhesus macaques to test the hypothesis that SHS exposure during development triggers neuroplastic changes in the nucleus tractus solitarius (NTS), where lung sensory information related to changes in airway and lung function is first integrated. Pregnant monkeys were exposed to filtered air (FA) or SHS for 6 h/day, 5 days/week starting at 50-day gestational age. Mother/infant pairs continued the exposures postnatally to age 3 or 13 months, which may be equivalent to approximately 1 or 4 years of human age, respectively. Whole-cell recordings were made of second-order NTS neurons in transverse brainstem slices. To target the consequences of SHS exposure based on neuronal subgroups, we classified NTS neurons into two phenotypes, rapid-onset spiking (RS) and delayed-onset spiking (DS), and then evaluated intrinsic and synaptic excitabilities in FA-exposed animals. RS neurons showed greater cell excitability especially at age of 3 months while DS neurons received greater amplitudes of excitatory postsynaptic currents (EPSCs). Developmental neuroplasticity such as increases in intrinsic and synaptic excitabilities were detected especially in DS neurons. In 3 month olds, SHS exposure effects were limited to excitatory changes in RS neurons, specifically increases in evoked EPSC amplitudes and increased spiking responses accompanied by shortened action potential width. By 13 months, the continued SHS exposure inhibited DS neuronal activity; decreases in evoked EPSC amplitudes and blunted spiking responses accompanied by prolonged action potential width. The influence of SHS exposure on age-related and phenotype specific changes may be associated with age-specific respiratory problems, for which SHS exposure can increase the risk, such as SIDS and bronchiolitis in infants and asthma in older children.
- OSTI ID:
- 21344841
- Journal Information:
- Toxicology and Applied Pharmacology, Journal Name: Toxicology and Applied Pharmacology Journal Issue: 2 Vol. 242; ISSN TXAPA9; ISSN 0041-008X
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
AEROSOLS
AGE GROUPS
ANIMAL CELLS
ANIMALS
ASTHMA
BIOLOGICAL STRESS
BODY
CENTRAL NERVOUS SYSTEM
CHILDREN
CHRONIC EXPOSURE
CHRONIC IRRADIATION
COLLOIDS
DISEASES
DISPERSIONS
HAZARDS
INFANTS
IRRADIATION
LUNGS
MAMMALS
MAN
MONKEYS
NERVE CELLS
NERVOUS SYSTEM
ORGANS
PRIMATES
RESIDUES
RESPIRATORY SYSTEM
RESPIRATORY SYSTEM DISEASES
SMOKES
SOLS
SOMATIC CELLS
TOBACCO SMOKES
TOXICITY
VERTEBRATES