Trigeminal pathways for hypertonic saline- and light-evoked corneal reflexes

Area of Science:

• Neuroscience
• Ophthalmology
• Sensory Physiology

Background:

• Cornea-evoked eyeblinks are vital for maintaining ocular surface health and protection.
• The central neural pathways for protective eyeblinks triggered by natural stimuli are not fully understood.

Purpose of the Study:

• To investigate the role of the trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition and subnucleus caudalis/upper cervical cord (Vc/C1) junction in mediating eyeblink responses.
• To determine the neural pathways involved in orbicularis oculi electromyographic (OOemg) activity evoked by ocular surface hypertonic saline and bright light stimuli.

Main Methods:

• Urethane-anesthetized male rats were used to record OOemg activity.
• Stimuli included hypertonic saline applied to the ocular surface and bright light exposure.
• Pharmacological interventions (lidocaine, cobalt chloride) were employed to block neural pathways.

Main Results:

• OOemg activity increased with stimulus intensity for both hypertonic saline and bright light.
• Lidocaine blocked responses to hypertonic saline when applied to the ocular surface, and blocked both stimuli when applied to the trigeminal ganglion.
• Cobalt chloride blockade of Vi/Vc or Vc/C1 regions significantly reduced OOemg responses.

Conclusions:

• The trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition and subnucleus caudalis/upper cervical cord (Vc/C1) junction are critical relay sites for protective eyeblinks.
• These findings elucidate the central neural circuitry underlying eyeblink reflexes evoked by natural ocular irritants.