Experiential Modification of the Trigeminal Reflex Blink Circuit

Dauvergne, Céline; Evinger, Craig

doi:10.1523/jneurosci.1152-07.2007

Cited by 17 publications

(15 citation statements)

References 51 publications

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“…Under general anesthesia (ketamine 90 mg/kg, xylazine 10 mg/kg), rats were prepared for chronic recording of the orbicularis oculi EMG (OOemg) and stimulation of the supraorbital branch of the trigeminal nerve (Dauvergne & Evinger, 2007). OOemg recordings were performed with a pair of Teflon-coated stainless steel wires (0.003 inch diameter bare, 0.0055 inch coated; A-M Systems, Everett, WA) implanted into the orbicularis oculi muscle near the lateral canthus.…”

Section: Methodsmentioning

confidence: 99%

Characterizing the Spontaneous Blink Generator: An Animal Model

Kaminer¹,

Powers²,

Horn³

et al. 2011

J. Neurosci.

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Although spontaneous blinking is one of the most frequent human movements, little is known about its neural basis. We developed a rat model of spontaneous blinking in order to identify and better characterize the spontaneous blink generator. We monitored spontaneous blinking for 55 min periods in normal conditions and after the induction of mild dry eye or dopaminergic drug challenges. The normal spontaneous blink rate was 5.3 ± 0.3 blinks/min. Dry eye or 1 mg/kg apomorphine significantly increased and 0.1 mg/kg haloperidol significantly decreased the blink rate. Additional analyses revealed a consistent temporal organization to spontaneous blinking with a median 750 s period that was independent of the spontaneous blink rate. Dry eye and dopaminergic challenges significantly modified the regularity of the normal pattern of episodes of frequent blinking interspersed with intervals having few blinks. Dry eye and apomorphine enhanced the regularity of this pattern, whereas haloperidol reduced its regularity. The simplest explanation for our data is that the spinal trigeminal complex is a critical element in the generation of spontaneous blinks; incorporating reflex blinks from dry eye and indirect basal ganglia inputs into the blink generator. Although human subjects exhibited a higher average blink rate (17.6 ± 2.4) than rats, the temporal pattern of spontaneous blinking was qualitatively similar for both species. These data demonstrate that rats are an appropriate model for investigating the neural basis of human spontaneous blinking and suggest that the spinal trigeminal complex is a major element in the spontaneous blink generator.

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Section: Methodsmentioning

confidence: 99%

Characterizing the Spontaneous Blink Generator: An Animal Model

Kaminer¹,

Powers²,

Horn³

et al. 2011

J. Neurosci.

Self Cite

156

136

View full text Add to dashboard Cite

show abstract

“…By contrast, eyeblink reflexes are critical for maintaining tear film integrity and can occur spontaneously, be evoked by diverse inputs of trigeminal or spinal origin as well as by conditioning stimuli (Evinger et al, 1991, Gruart et al, 1995, Delgado-Garcia et al, 2003, Dauvergne and Evinger, 2007, Kaminer et al, 2011). Although corneal reflexes and eyeblinks share several features and each results in excitation of orbicularis oculi (OO) motor units and lid closure, several lines of evidence suggest that the brain circuitry for corneal and blink reflexes are organized differently (Ongerboer de Visser, 1983, Berardelli et al, 1985, Cruccu et al, 1991).…”

mentioning

confidence: 99%

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

et al. 2014

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Cornea-evoked eyeblinks maintain tear film integrity on the ocular surface in response to dryness and protect the eye from real or potential damage. Eyelid movement following electrical stimulation has been well studied in humans and animals; however, the central neural pathways that mediate protective eyeblinks following natural nociceptive signals are less certain. The aim of this study was to assess the role of the trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition and subnucleus caudalis/upper cervical cord (Vc/C1) junction regions on orbicularis oculi electromyographic (OOemg) activity evoked by ocular surface application of hypertonic saline or exposure to bright light in urethane anesthetized male rats. The Vi/Vc and Vc/C1 regions are the main sites of termination for trigeminal afferent nerves that supply the ocular surface, while hypertonic saline (saline = 0.15-5M) and bright light (light = 5-20k lux) selectively activate ocular surface and intraocular trigeminal nerves, respectively, and excite second-order neurons at the Vi/Vc and Vc/C1 regions. Integrated OOemg activity, ipsilateral to the applied stimulus, increased with greater stimulus intensities for both modalities. Lidocaine applied to the ocular surface inhibited OOemg responses to hypertonic saline, but did not alter the response to light. Lidocaine injected into the trigeminal ganglion blocked completely the OOemg responses to hypertonic saline and light indicating a trigeminal afferent origin. Synaptic blockade by cobalt chloride of the Vi/Vc or Vc/C1 region greatly reduced OOemg responses to hypertonic saline and bright light. These data indicate that OOemg activity evoked by natural stimuli known to cause irritation or discomfort in humans depends on a relay in both the Vi/Vc transition and Vc/C1 junction regions.

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“…The platform was attached to the skull by four stainless‐steel screws. A silver wire connected to one of the stainless‐steel screws served as the ground (Evinger & Manning, ; Dauvergne & Evinger, ).…”

Section: Methodsmentioning

confidence: 99%

Frequency matters: beta‐band subthalamic nucleus deep‐brain stimulation induces Parkinsonian‐like blink abnormalities in normal rats

Kaminer

Thakur

Evinger

2014

Eur J of Neuroscience

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The synchronized beta band oscillations in the basal ganglia-cortical networks in Parkinson's disease (PD) may be responsible for PD motor symptoms or an epiphenomenon of dopamine loss. We investigated the causal role of beta band activity in PD motor symptoms by testing the effects of beta frequency subthalamic nucleus deep brain stimulation (STN DBS) on blink reflex excitability, amplitude, and plasticity in normal rats. Delivering 16 Hz STN DBS produced the same increase in blink reflex excitability and impairment in blink reflex plasticity in normal rats as occurs in rats with 6-OHDA lesions and PD patients. These deficits were not an artifact of STN DBS because when these normal rats received 130 Hz STN DBS, their blink characteristics were the same as without STN DBS. To demonstrate the blink reflex disturbances with 16 Hz STN DBS were frequency specific, we tested the same rats with 7 Hz STN DBS, a theta band frequency typical of dystonia. In contrast to beta stimulation, 7 Hz DBS exaggerated blink reflex plasticity as occurs in focal dystonia. Thus, without destroying dopamine neurons or blocking dopamine receptors, frequency specific STN DBS can be used to create PD- or dystonic-like symptoms in a normal rat.

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Experiential Modification of the Trigeminal Reflex Blink Circuit

Cited by 17 publications

References 51 publications

Characterizing the Spontaneous Blink Generator: An Animal Model

Characterizing the Spontaneous Blink Generator: An Animal Model

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

Frequency matters: beta‐band subthalamic nucleus deep‐brain stimulation induces Parkinsonian‐like blink abnormalities in normal rats

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