Connections between the lacrimal gland and sensory trigeminal neurons: a WGA/HRP study in the cynomolgous monkey

Baljet, B.; VanderWerf, Frans

doi:10.1111/j.1469-7580.2005.00374.x

Cited by 10 publications

(9 citation statements)

References 56 publications

(65 reference statements)

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“…Middle portions of Vc and more rostral regions of the TBSC receive sparse input from corneal afferent fibers, although conjunctival afferents also terminate in rostral TBSC. 130 A restricted projection pattern as seen for corneal afferents also is seen for TG neurons that supply the eyelids, 131,132 lacrimal gland, 133,134 and meibomian gland. 128,135 The significance of multiple zones of termination for corneal afferents in the TBSC is not known and may simply reflect the need for redundancy in a system critical to preserve retinal function.…”

Section: Neurophysiology and Sensationmentioning

confidence: 89%

The TFOS International Workshop on Contact Lens Discomfort: Report of the Subcommittee on Neurobiology

Stapleton

Marfurt

Golebiowski

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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This report characterizes the neurobiology of the ocular surface and highlights relevant mechanisms that may underpin contact lens-related discomfort. While there is limited evidence for the mechanisms involved in contact lens-related discomfort, neurobiological mechanisms in dry eye disease, the inflammatory pathway, the effect of hyperosmolarity on ocular surface nociceptors, and subsequent sensory processing of ocular pain and discomfort have been at least partly elucidated and are presented herein to provide insight in this new arena. The stimulus to the ocular surface from a contact lens is likely to be complex and multifactorial, including components of osmolarity, solution effects, desiccation, thermal effects, inflammation, friction, and mechanical stimulation. Sensory input will arise from stimulation of the lid margin, palpebral and bulbar conjunctiva, and the cornea.

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Section: Neurophysiology and Sensationmentioning

confidence: 89%

The TFOS International Workshop on Contact Lens Discomfort: Report of the Subcommittee on Neurobiology

Stapleton

Marfurt

Golebiowski

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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“…A WGA/HRP tracer applied to the lacrimal gland in cynomolgus monkeys labelled not only several sensory neurons in the ophthalmic and maxillary ganglionic sections, but also the ipsilateral mesencephalic trigeminal nucleus [20]. A retrograde trans-synaptic tracer (tetanus toxin fragment C or BII(b)) applied into the levator muscle of macaque monkeys labelled a small circumscribed group of premotor neurons (the M-group) in the central gray of the rostral mesencephalon.…”

Section: Discussionmentioning

confidence: 99%

Cell bodies of the trigeminal proprioceptive neurons that transmit reflex contraction of the levator muscle are located in the mesencephalic trigeminal nucleus in rats

Fujita¹,

Matsuo²,

Yuzuriha³

et al. 2012

Journal of Plastic Surgery and Hand Surgery

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Since the levator and frontalis muscles lack interior muscle spindles despite being antigravity mixed muscles to involuntarily sustain eyelid opening and eyebrow lifting, this study has proposed a hypothetical mechanism to compensate for this anatomical defect. The voluntary contraction of fast-twitch fibres of the levator muscle stretches the mechanoreceptors in Müller's muscle to evoke proprioception, which continuously induces reflex contraction of slow-twitch fibres of the levator and frontalis muscles. This study confirmed the presence of cell bodies of the trigeminal proprioceptive neurons that transmit reflex contraction of the levator and frontalis muscles. After confirming that severing the trigeminal proprioceptive fibres that innervate the mechanoreceptors in Müller's muscle induced ipsilateral eyelid ptosis, Fluorogold was applied as a tracer to the proximal stump of the trigeminal proprioceptive nerve in rats. Fluorogold labelled the cell bodies of the trigeminal proprioceptive neurons, not in any regions of the rat brain including the trigeminal ganglion, but in the ipsilateral mesencephalic trigeminal nucleus neighbouring the locus ceruleus. Some Fluorogold particles accumulated in the area of the locus ceruleus. The trigeminal proprioceptive neurons could be considered centrally displaced ganglion cells to transmit afferent signal from the mechanoreceptors in Müller's muscle to the mesencephalon, where they may be able to make excitatory synaptic connections with both the oculomotor neurons and the frontalis muscle motoneurons for the involuntary coordination of the eyelid and eyebrow activities, and potentially to the locus ceruleus.

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“…The majority of ocular surface-responsive TG neurons terminate at two spatially discrete regions of the lower TBNC: the transition region between caudal Vi and Vc (ViVc transition) and at the Vc/upper cervical cord junction (VcC1 region); however, a smaller number of afferent fibers terminate in Vp and Vo [179,180]. TG neurons that supply the eyelids [16,182], lacrimal gland [183,184] and meibomian glands [177,185] display a similar terminal pattern in the TBNC. The significance of eye representation at multiple regions of the TBNC may reflect redundancy to preserve eye function or alternatively, may reflect cell groupings that serve different aspects of ocular function [186].…”

Section: Neurobiological Features In Normal/non Dry Eye Diseasementioning

confidence: 99%

TFOS DEWS II pain and sensation report

et al. 2017

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Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglia mechano- and polymodal nociceptor neurons while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of Meibonian gland secretion or mucins release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.

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Connections between the lacrimal gland and sensory trigeminal neurons: a WGA/HRP study in the cynomolgous monkey

Cited by 10 publications

References 56 publications

The TFOS International Workshop on Contact Lens Discomfort: Report of the Subcommittee on Neurobiology

The TFOS International Workshop on Contact Lens Discomfort: Report of the Subcommittee on Neurobiology

Cell bodies of the trigeminal proprioceptive neurons that transmit reflex contraction of the levator muscle are located in the mesencephalic trigeminal nucleus in rats

TFOS DEWS II pain and sensation report

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