title: Pre- and postnatal differences in membrane, action potential, and ion channel properties of rostral nucleus of the solitary tract neurons.
abstract: There is little known about the prenatal development of the rostral nucleus of the solitary tract (rNST) neurons in rodents or the factors that influence circuit formation. With morphological and electrophysiological techniques in vitro, we investigated differences in the biophysical properties of rNST neurons in pre- and postnatal rats from embryonic day 14 (E14) through postnatal day 20. Developmental changes in passive membrane and action potential (AP) properties and the emergence and maturation of ion channels important in neuron function were characterized. Morphological maturation of rNST neurons parallels changes in passive membrane properties. Mean soma size, dendritic branch points, neurite endings, and neurite length all increase prenatally. whereas neuron resting membrane potential, input resistance, and time constant decrease. Dendritic spines, on the other hand, develop after birth. AP discharge patterns alter in pre- and postnatal stages. At E14, neurons generated a single TTX-sensitive, voltage-gated Na(+) AP when depolarized; a higher discharge rate appeared at older stages. AP amplitude, half-width, and rise and fall times all change during development. Responses to current injection revealed a number of voltage-gated conductances in embryonic rNST, including a hyperpolarization-activated inward current and a low-threshold Ca(2+) current that initiated Ca(2+) spikes. A hyperpolarization-activated, transient outward potassium current was also present in the developing neurons. Although the properties of these channels change during development, they are present before synapses form and therefore, can contribute to initial establishment of neural circuits, as well as to the changing electrophysiological properties in developing rNST neurons.
authors.affiliation: Dept. of Biologic and Materials Sciences, School of Dentistry, Univ. of Michigan, Ann Arbor, MI 48109-1078, USA.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Suwabe
authors.forename: Charlotte M
authors.initials: CM
authors.lastname: Mistretta
authors.forename: Catherine
authors.initials: C
authors.lastname: Krull
authors.forename: Robert M
authors.initials: RM
authors.lastname: Bradley
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000367:Age Factors; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D048430:Cell Shape / Q000502:physiology; D054815:Cyclic Nucleotide-Gated Cation Channels / Q000502:physiology; D005260:Female; D005865:Gestational Age; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D016501:Neurites / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D017552:Solitary Nucleus / Q000196:embryology / Q000254:growth & development / Q000502:physiology; D013649:Taste / Q000502:physiology
chemical_list: D015220:Calcium Channels; D054815:Cyclic Nucleotide-Gated Cation Channels; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D007473:Ion Channels; D015221:Potassium Channels