Morphology and electrophysiology of guinea-pig paratracheal neurones

Lees, G.J.; Pacitti, Elaine G.; Mackenzie, Gillian M.

doi:10.1002/(sici)1097-0185(199702)247:2<261::aid-ar13>3.0.co;2-n

Cited by 13 publications

(5 citation statements)

References 42 publications

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“…We injected NGF-␤ into the trachealis muscle, a primary site for innervation by cholinergic neurons located in tracheal ganglia (4) and, after 48 h, filled the ganglionic neurons with an intracellular dye. Control tracheal neurons had a similar size and dendritic complexity as previously reported (19). Neurons exposed to NGF-␤ showed an increase in dendritic length after 48 h compared with neurons exposed to vehicle and/or rhodamine-dextran alone (Fig.…”

Section: Discussionsupporting

confidence: 78%

“…Several studies have shown that NGF increases the length of dendrites on parasympathetic neurons in vitro (25) and on sympathetic neurons in vivo as well as enhancing neurite extension in vitro (20,40,44). Like neurons in rodent and guinea pig sympathetic ganglia (11), neurons in guinea pig lower airway parasympathetic ganglia have multiple and branching dendritic processes (19,30,35). We injected NGF-␤ into the trachealis muscle, a primary site for innervation by cholinergic neurons located in tracheal ganglia (4) and, after 48 h, filled the ganglionic neurons with an intracellular dye.…”

Section: Discussionmentioning

confidence: 99%

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Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia

Hazari

Pan

Myers³

2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hazari MS, Pan JH, Myers AC. Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia. Am J Physiol Lung Cell Mol Physiol 292: L992-L1001, 2007. First published December 28, 2006; doi:10.1152/ajplung.00216.2006.-Elevated levels of nerve growth factor (NGF) and NGF-mediated neural plasticity may have a role in airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). Although NGF is known to affect sensory and sympathetic nerves, especially during development, little is known regarding its effect on parasympathetic nerves, especially on adult neurons. The purpose of this study was to analyze the acute and chronic effects of NGF on the electrophysiological and anatomical properties of neurons in airway parasympathetic ganglia from adult guinea pigs. Using single cell recording, direct application of NGF caused a lasting decrease in the cumulative action potential afterhyperpolarization (AHP) and increased the amplitude of vagus nerve-stimulated nicotinic fast excitatory postsynaptic potentials. Neuronal responsiveness to nicotinic receptor stimulation was increased by NGF, which was blocked by the tyrosine kinase inhibitor, K-252a, implicating neurotrophin-specific (Trk) receptors. Neurotrophin-3 and brain-derived neurotrophic factor had no effect on the synaptic potentials, AHP, or nicotinic response; inhibition of cyclooxygenase with indomethacin inhibited the effect of NGF on the cumulative AHP. Forty-eight hours after in vivo application of NGF to the trachealis muscle caused an increase in dendritic length on innervating neurons. These results are the first to demonstrate that NGF increases the excitability of lower airway parasympathetic neurons, primarily through enhanced synaptic efficacy and changes to intrinsic neuron properties. NGF also had dramatic effects on the growth of dendrites in vivo. Such effects may indicate a new role for NGF in the regulation of parasympathetic tone in the diseased or inflamed lower airways.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia

Hazari

Pan

Myers³

2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The phasic neurons fire during the inspiratory phase in vivo and primarily project to the tracheobronchial smooth muscles, whereas tonic neurons fire tonically during the inspiratory intervals and primarily project to the intercartilaginous space (Mitchell et al 1987). Postganglionic neurons with similar phasic or tonic firing properties have also been identified in vitro , both in humans and in animals (Baker, 1986; Myers et al 1990; Lees et al 1997; Myers, 1998). It is thus reasonable to postulate that the phasic postganglionic neurons are preferentially innervated by the IA‐AVPNs in the eNA, whereas the tonic postganglionic neurons are preferentially innervated by the II‐AVPNs in the eNA.…”

mentioning

confidence: 99%

Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Zhou

Chen

et al. 2012

Experimental Physiology

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New Findings r What is the central question of this study?Airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons, which dominate the neural control of the airway physiologically and play critical roles in the pathogenesis of some common airway disorders. AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine or endogenous acetylcholine are unknown. r What is the main finding and its importance?Nicotine and endogenous acetylcholine both cause a postsynaptic excitatory current in inspiratory-activated AVPNs, and enhance both the excitatory and inhibitory synaptic inputs. The overall effect of nicotine on inspiratory-activated AVPNs is excitatory. The nicotinic effects on inspiratory-activated AVPNs are mediated presynaptically by activation of α4β2 type of nAChRs and postsynaptically by activation of multiple nAChRs including α7 and α4β2 types.The airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons and dominate the neural control of the airway both physiologically and pathophysiologically. The AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine and endogenous acetylcholine are unknown. This study examined the effects of nicotine and endogenous acetylcholine on retrogradely labelled, functionally identified inspiratory-activated AVPNs (IA-AVPNs) using the patchclamp technique. Nicotine (10 μmol l −1 ) significantly increased the frequency and amplitude of the spontaneous EPSCs of IA-AVPNs, and these effects were insensitive to methyllycaconitine (MLA, 100 nmol l −1 ), an antagonist of the α7 type of nAChR, but was prevented by dihydro-β-erythroidine (DHβE, 3 μmol l −1 ), an antagonist of the α4β2 type of nAChR. Nicotine caused a tonic inward current in IA-AVPNs, which was reduced by MLA or DHβE alone, but was not abolished by co-application of MLA and DHβE. Nicotine caused a significant increase in the frequency of GABAergic and glycinergic spontaneous IPSCs and significantly increased the amplitude of glycinergic spontaneous IPSCs, all of which were prevented by DHβE. Nicotine had no effects on the miniature EPSCs or miniature IPSCs following pretreatment with TTX. Under current clamp, nicotine caused depolarization and increased the firing rate of IA-AVPNs during inspiratory intervals. Neostigmine (10 μmol l −1 ), an acetylcholinesterase inhibitor, mimicked the effects of nicotine. These results demonstrate that nicotine and endogenous ACh enhance the excitatory and inhibitory synaptic inputs of IA-AVPNs and cause a postsynaptic excitatory

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“…On the other hand, non-ganglionic neurons that have comparatively more dendrite-like processes from the soma may be involved in the innervation of targets in proximity to their somata. Th is assumption is partly supported by the study on guinea pig paratracheal neurons where the soma morphology of neurons lying in the ganglionated plexus on trachealis muscle was more complex than of those positioned in more distant associated nerve trunks [5].…”

Section: Discussionmentioning

confidence: 94%

“…According to earlier studies, cranial and terminal autonomic ganglia of small vertebrates like the frog, the mouse or the hamster contain mostly non-dendritic neurons that are innervated by 1-2 preganglionic axons [2,13]. Th e complexity of the dendrites and the soma of autonomic neurons increases with the size of the species [13] or with closer distance to their innervation targets [5].…”

Section: Introductionmentioning

confidence: 99%

Ganglionic and non-ganglionic neurons in frog heart: do they differ?

Batulevičius

Skripkienė

Graužinytė

et al. 2017

PoA

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This study was designed to compare the morphology of neurons in relation to their distance from the major nerve trunks in the heart of the frog Rana temporaria. Seventy-nine intracardiac neurons were labelled intracellularly with fluorescent markers Lucifer Yellow CH and Alexa Fluor 568. The neurons located on the extensions of the vagus nerve were considered as ganglionic, while neurons spread loosely at further distance from these extensions were considered as non-ganglionic. The mean area of the soma in ganglionic neurons was about 25% larger than in non-ganglionic neurons. Ganglionic neurons had a higher soma area/nucleus area ratio than non-ganglionic neurons. Although both the total number and the total length of dendrite-like processes was similar between the two groups, ganglionic neurons had significantly fewer dendrite-like processes from the soma (1.5±0.3 vs. 3.9±1.0; P<0.05) and shorter total length of these processes from the soma (63±18 μm vs. 178±51 μm; P<0.05). In conclusion, ganglionic and non-ganglionic frog intracardiac neurons exhibit substantial morphological differences. We hypothesize that these differences may indicate different projections or variations in the number of their preganglionic inputs.

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Morphology and electrophysiology of guinea-pig paratracheal neurones

Cited by 13 publications

References 42 publications

Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia

Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia

Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Ganglionic and non-ganglionic neurons in frog heart: do they differ?

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