Developmental nicotine exposure alters potassium currents in hypoglossal motoneurons of neonatal rat.

We previously showed that nicotine exposure in utero and after birth via breast milk [developmental nicotine exposure (DNE)] is associated with many changes in the structure and function of hypoglossal motoneurons (XIIMNs), including a reduction in the size of the dendritic arbor and an increase in cell excitability. Interestingly, the elevated excitability was associated with a reduction in the expression of glutamate receptors on the cell body. Together, these observations are consistent with a homeostatic compensation aimed at restoring cell excitability.

Influence of developmental nicotine exposure on glutamatergic neurotransmission in rhythmically active hypoglossal motoneurons.

Developmental nicotine exposure (DNE) is associated with increased risk of cardiorespiratory, intellectual, and behavioral abnormalities in neonates, and is a risk factor for apnea of prematurity, altered arousal responses and Sudden Infant Death Syndrome. Alterations in nicotinic acetylcholine receptor signaling (nAChRs) after DNE lead to changes in excitatory neurotransmission in neural networks that control breathing, including a heightened excitatory response to AMPA microinjection into the hypoglossal motor nucleus. Here, we report on experiments designed to probe possible postsynaptic and presynaptic mechanisms that may underlie this plasticity.

Digital holographic microscopy discriminates sex differences in medial prefrontal cortex GABA neurons following amphetamine sensitization.

Sex differences have been noted in patterns of drug use and relapse, and in particular with amphetamine abuse, implicating estradiol in mediating female neurobehavioral responses. To investigate the interaction of estradiol with amphetamine-induced hyperactivity, we compared male, intact female (INTACT), ovariectomized (OVX) and ovariectomized estradiol-treated (OVX+EB) female rats receiving repeated amphetamine (AMPH) treatment. All rats received intermittent AMPH injections for three days, and baseline and post-injection locomotor activity as well as fine-motor movements were recorded.

Electrophysiology of arcuate neurokinin B neurons in female Tac2-EGFP transgenic mice.

Neurons in the arcuate nucleus that coexpress kisspeptin, neurokinin B (NKB), and dynorphin (KNDy neurons) play an important role in the modulation of reproduction by estrogens. Here, we study the anatomical and electrophysiological properties of arcuate NKB neurons in heterozygous female transgenic mice with enhanced green fluorescent protein (EGFP) under the control of the Tac2 (NKB) promoter (Tac2-EGFP mice). The onset of puberty, estrous cyclicity, and serum LH were comparable between Tac2-EGFP and wild-type mice.

Neurokinin B and the hypothalamic regulation of reproduction.

Loss-of-function mutations in the genes encoding either neurokinin B (NKB) or its receptor, NK3 (NK3R), result in hypogonadotropic hypogonadism, characterized by an absence of pubertal development and low circulating levels of LH and gonadal steroids. These studies implicate NKB and NK3R as essential elements of the human reproductive axis. Studies over the last two decades provide evidence that a group of neurons in the hypothalamic infundibular/arcuate nucleus form an important component of this regulatory circuit.