Chronic, Episodic Nicotine Alters Hypoglossal Motor Neuron Function at a Critical Developmental Time Point in Neonatal Rats

Wollman, Lila Buls; Fregosi, Ralph F.

doi:10.1523/eneuro.0203-21.2021

Cited by 4 publications

(1 citation statement)

References 63 publications

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“…Nicotine triggered a robust inward ion current and excitation in GnRH neurons. The responses evoked by repeated application (90 - 120 s) of nicotine presented no desensitization at this period (Huang et al, 2011; Buls Wollman and Fregosi, 2021).…”

Section: Discussionmentioning

confidence: 91%

Cholinergic control of GnRH neuron physiology and luteinizing hormone secretion: involvement of ACh/GABA co-transmission

Vastagh,

Farkas,

Csillag

et al. 2023

Preprint

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Gonadotropin-releasing hormone (GnRH)-synthesizing neurons orchestrate reproduction centrally. They receive commands from various neuronal networks for regulation of the hypothalamo-pituitary-gonadal (HPG)-axis. Here we report acetylcholine (ACh) as a critical regulator of GnRH neurons and reproduction in mice. In acute brain slice preparation, the acetylcholine receptor (AChR) agonists, ACh and carbachol, evoked a biphasic effect on the firing rate in GnRH neurons, first increasing afterwards diminishing it. In the presence of tetrodotoxin, carbachol induced an inward current followed by a decline in frequency of mPSCs. RT-PCR and whole cell patch-clamp studies revealed that GnRH neurons expressed both muscarinic (M1-M5) and nicotinic (α4β2, α3β4 and α7) ACh receptors. Muscarine via M1 and M3 receptors increased, while via M2 and M4 reduced the frequency of both miniature postsynaptic currents (mPSCs) and firing. The identified nicotinic AChRs contributed to the nicotine-elicited inward current and the rise of firing rate. Optogenetic activation of channelrhodopsin-2-tagged cholinergic axons modified GnRH neuronal activity and evoked co-transmission of ACh and GABA from a subpopulation of boutons. 3DISCO immunocytochemistry and electron microscopy revealed innervation of GnRH neurons by cholinergic axons. Rabies retrograde viral labelling started from GnRH-Cre neurons identified the medial septum and the diagonal band of Broca as exclusive sites of origin for specific cholinergic afferents.In vivopharmacogenetic activation of cholinergic system resulted in an increased secretion of luteinizing hormone (LH) in gonadectomized mice. Our findings collectively corroborate that the central cholinergic system exerts an important regulatory influence upon GnRH neurons and activates the HPG-axis via ACh and ACh/GABA neurotransmissions.Graphical abstract

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Section: Discussionmentioning

confidence: 91%

Cholinergic control of GnRH neuron physiology and luteinizing hormone secretion: involvement of ACh/GABA co-transmission

Vastagh,

Farkas,

Csillag

et al. 2023

Preprint

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Impact of Electronic Cigarette Vaping on Cerebral Ischemia: What We Know So Far

Siegel

Patel

Mankaliye

et al. 2022

Transl. Stroke Res.

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Chronic, episodic nicotine exposure alters GABAergic synaptic transmission to hypoglossal motor neurons and genioglossus muscle function at a critical developmental age

Wollman

Flanigan

Fregosi

2022

Journal of Neurophysiology

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Regulation of GABAergic signaling through nicotinic acetylcholine receptor (nAChR) activation is critical for neuronal development. Here, we test the hypothesis that chronic, episodic developmental nicotine exposure (eDNE) disrupts GABAergic signaling, leading to dysfunction of hypoglossal motor neurons (XIIMNs), which innervate the tongue muscles. We studied control and eDNE pups at two developmentally vulnerable age ranges; postnatal days (P) 1-5, and P10-12. The amplitude and frequency of spontaneous and miniature inhibitory postsynaptic currents (sIPSCs/mIPSCs) at baseline were not altered by eDNE at either age. In contrast, eDNE increased GABAAR-a1 receptor expression on XIIMNs, and, in the older group, the postsynaptic response to muscimol (GABAA receptor agonist). Activation of nAChRs with exogenous nicotine increased the frequency of GABAergic sIPSCs in control and eDNE neurons at P1-5. By P10-12, acute nicotine increased sIPSC frequency in eDNE neurons but not control. In vivo experiments showed that the breathing-related activation of tongue muscles, which are innervated by XIIMNs, is reduced at P10-12. This effect was partially mitigated by subcutaneous muscimol, but only in the eDNE pups. Taken together, these data indicate that eDNE alters GABAergic transmission to XIIMNs at a critical developmental age, and this is expressed as reduced breathing-related drive to XIIMNs in vivo.

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Chronic, Episodic Nicotine Alters Hypoglossal Motor Neuron Function at a Critical Developmental Time Point in Neonatal Rats

Abstract: Title: Chronic, episodic nicotine alters hypoglossal motor neuron function at a critical developmental time point in neonatal rats.

Cited by 4 publications

References 63 publications

Cholinergic control of GnRH neuron physiology and luteinizing hormone secretion: involvement of ACh/GABA co-transmission

Cholinergic control of GnRH neuron physiology and luteinizing hormone secretion: involvement of ACh/GABA co-transmission

Impact of Electronic Cigarette Vaping on Cerebral Ischemia: What We Know So Far

Chronic, episodic nicotine exposure alters GABAergic synaptic transmission to hypoglossal motor neurons and genioglossus muscle function at a critical developmental age

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