Abstract
By providing ~70% of the eye’s refractive power, the preocular tear film is essential for optimal vision. However, its integrity is often jeopardized by environmental and pathologic conditions that accelerate evaporation and cause sight-impairing dry eye. A key adaptive response to evaporation-induced tear film hyperosmolarity is the reflex-triggered release of tear-stabilizing mucin from conjunctival goblet cells. Here, we review progress in elucidating the roles of ion channels in mediating this important exocytotic response. Much is now known about the modulatory impact of ATP-sensitive potassium channels, nonspecific cation channels and voltage-gated calcium channels. Recently, we discovered that during unremitting extracellular hyperosmolarity, P2X7 receptor/channels also become activated and markedly impair goblet cell viability. However, our understanding of possible adaptive benefits of this P2X7 activation remains limited. In the present study, we utilized high-temporal resolution membrane capacitance measurements to monitor the exocytotic activity of single goblet cells located in freshly excised rat conjunctiva. We now report that activation of P2X7 purinoceptors boosts neural-evoked exocytosis and accelerates replenishment of mucin-filled granules after exocytotic depletion. Thus, P2X7 activation exerts a yin-yang effect on conjunctival goblet cells: the high-gain benefit of enhancing the supply of tear-stabilizing mucin is implemented at the high-risk of endangering goblet cell survival.
Highlights
Academic Editor: Hana ZemkovaReceived: 16 May 2021Accepted: 25 June 2021Published: 28 June 2021Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Visual perception begins at the preocular tear film where this interface between the external environment and the ocular surface plays a key role in focusing incoming light [1].To effectively perform this important optical function, stability of the tear film is essential.the integrity of this complex fluid layer is threatened by a multitude of processes that accelerate its evaporation
The aim of this study was to better understand how the activation of P2X7 purinoceptors affects the exocytotic response of conjunctival goblet cells to cholinergic input, which in vivo is a key parasympathetic effector triggering these cells to release of mucin-filled granules [5]
In conjunctival specimens freshly isolated from the rat, the magnitude of exocytosis evoked during exposure to the cholinergic agonist carbachol was quantified by high-temporal resolution monitoring of the membrane capacitance (Cm) of single goblet cells (Figure 1A)
Summary
Academic Editor: Hana ZemkovaReceived: 16 May 2021Accepted: 25 June 2021Published: 28 June 2021Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Visual perception begins at the preocular tear film where this interface between the external environment and the ocular surface plays a key role in focusing incoming light [1].To effectively perform this important optical function, stability of the tear film is essential.the integrity of this complex fluid layer is threatened by a multitude of processes that accelerate its evaporation. Visual perception begins at the preocular tear film where this interface between the external environment and the ocular surface plays a key role in focusing incoming light [1]. To effectively perform this important optical function, stability of the tear film is essential. The integrity of this complex fluid layer is threatened by a multitude of processes that accelerate its evaporation. Common environmental conditions such as the rapid movement of air and low ambient humidity cause transient preocular dryness. No matter the etiology of tear film instability, an evaporation-induced increase in the osmolarity of the preocular fluid is a universal feature of the uncomfortable sight-impairing condition of dry eye [2], which afflicts millions of individuals [3]
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