Influence of the superior colliculus on the primate blink reflex

Gnadt, James W.; Lu, Shao‐Ming; Breznen, Boris; Basso, Michele A.; Henriquez, Victor M.; Evinger, Craig

doi:10.1007/pl00005767

Cited by 38 publications

(25 citation statements)

References 38 publications

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“…Although the exact nature of how the BG influence the blink reflex remains uncertain, Basso (Basso and Evinger, 1996) postulated the sequential chain depicted in Figure 2, namely that increased SNr activity leads to increased inhibition of SC, leading to decreased excitation of the nucleus raphe magnus and decreased inhibition of trigeminal blink reflex circuits. This is consistent with evidence showing that SC stimulation suppresses the blink reflex (Gnadt et al, 1997) and that the SC is hypometabolic on FDG-PET in BEB (Emoto et al, 2010). Indeed, the pathway from SNr to the trigeminal nucleus has long been suspected to be involved in BEB (Hotson and Boman, 1991).…”

Section: Dynamic Circuit Hypothesis For the Pathogenesis Of Bebsupporting

confidence: 91%

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Peterson

Sejnowski

2017

Front. Comput. Neurosci.

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Blepharospasm (sometimes called “benign essential blepharospasm,” BEB) is one of the most common focal dystonias. It involves involuntary eyelid spasms, eye closure, and increased blinking. Despite the success of botulinum toxin injections and, in some cases, pharmacologic or surgical interventions, BEB treatments are not completely efficacious and only symptomatic. We could develop principled strategies for preventing and reversing the disease if we knew the pathogenesis of primary BEB. The objective of this study was to develop a conceptual framework and dynamic circuit hypothesis for the pathogenesis of BEB. The framework extends our overarching theory for the multifactorial pathogenesis of focal dystonias (Peterson et al., 2010) to incorporate a two-hit rodent model specifically of BEB (Schicatano et al., 1997). We incorporate in the framework three features critical to cranial motor control: (1) the joint influence of motor cortical regions and direct descending projections from one of the basal ganglia output nuclei, the substantia nigra pars reticulata, on brainstem motor nuclei, (2) nested loops composed of the trigeminal blink reflex arc and the long sensorimotor loop from trigeminal nucleus through thalamus to somatosensory cortex back through basal ganglia to the same brainstem nuclei modulating the reflex arc, and (3) abnormalities in the basal ganglia dopamine system that provide a sensorimotor learning substrate which, when combined with patterns of increased blinking, leads to abnormal sensorimotor mappings manifest as BEB. The framework explains experimental data on the trigeminal reflex blink excitability (TRBE) from Schicatano et al. and makes predictions that can be tested in new experimental animal models based on emerging genetics in dystonia, including the recently characterized striatal-specific D1R dopamine transduction alterations caused by the GNAL mutation. More broadly, the model will provide a guide for future efforts to mechanistically link multiple factors in the pathogenesis of BEB and facilitate simulations of how exogenous manipulations of the pathogenic factors could ultimately be used to prevent and reverse the disorder.

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Section: Dynamic Circuit Hypothesis For the Pathogenesis Of Bebsupporting

confidence: 91%

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Peterson

Sejnowski

2017

Front. Comput. Neurosci.

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“…Functionally, the rostral pole of layer 4 may subserve the suppression of saccades during visual fixation (Bü ttner-Ennever et al, 1999). Physiological recordings in the monkey SC showed that microstimulation of the deeper layers resulted in suppression of the blink reflex (Gnadt et al, 1997) or of blink-perturbed saccades (Goossens and van Opstal, 2000b).…”

Section: Trigeminocollicular Connectionsmentioning

confidence: 99%

Organization of trigeminocollicular connections and their relations to the sensory innervation of the eyelids in the rat

Ndiaye¹,

Pinganaud²,

Buisseret-Delmas³

et al. 2002

J of Comparative Neurology

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Relationships between the trigeminal component of blinking and the superior colliculus (SC) were studied in rats. To localize primary afferent eyelid projections in the sensory trigeminal complex, neuronal tracing experiments were performed as well as analysis of c-Fos protein expression after supraorbital (SO) nerve stimulation. Labelled nerve fibers were found to enter ventrally within the ipsilateral sensory trigeminal complex. Labelled boutons were observed at the junction of the principal nucleus (5P) and the pars oralis (5o) and in the pars caudalis (5c). The c-Fos immunoreactivity was observed in neurons located in the ipsilateral ventral parts of 5P, 5o, and the pars interpolaris (5i) and bilaterally in 5c. Injections in 5P, 5o, 5i, and 5c resulted in anterogradely labelled fibers, with a contralateral preponderance, within the intermediate and deeper SC layers. Injections in 5P or 5o showed anterogradely labelled nerve fibers, profusely terminating in small patches in the medial and central portions of SC layer 4. Subsequently, dense labelling was found in the lateral portion of SC layers 4-7, without patch-like organization. Injections in SC showed retrogradely labelled neurons predominantly within the contralateral part of the sensory trigeminal complex (28% in 5P, 20% in 5o, 50% in 5i, and 2% in 5c). Colocalization of the retrograde tracer after SC injections and c-Fos immunoreactivity in neurons demonstrated that some 5P, 5o, and 5i neurons receive SO nerve inputs and project to SC. This implies that intermediate and deeper SC layers receive sensory information from the eyelids and may be directly involved in the regulation of eye-eyelid coordination.

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“…It also receives afferent input from the trigeminal sensory nucleus (important for corneal and other trigeminally mediated blink reflexes) and dorsal midbrain (where reflexive blinking to light is mediated). Inhibitory microstimulation of the SC in primates has been shown to both suppress spontaneous blinking and increase sensitivity to blink reflexes (44, 45). …”

Section: Decreased Blinkingmentioning

confidence: 99%

“…In one study, for example, when the supraorbital nerve was stimulated twice over a period of 250 ms, the second R2 was 84% smaller in amplitude and 50% shorter in duration compared to the first R2 among healthy controls. By contrast, PD patients off therapy had only a 60% smaller and 10% shorter second R2 response (44). Dopaminergic therapy and STN DBS in both humans (61) and animals (62) restores blink reflex excitability to normal levels.…”

Section: Decreased Blinkingmentioning

confidence: 99%

Eyelid Dysfunction in Neurodegenerative, Neurogenetic, and Neurometabolic Disease

Hamedani

Gold

2017

Front. Neurol.

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Eye movement abnormalities are among the earliest clinical manifestations of inherited and acquired neurodegenerative diseases and play an integral role in their diagnosis. Eyelid movement is neuroanatomically linked to eye movement, and thus eyelid dysfunction can also be a distinguishing feature of neurodegenerative disease and complements eye movement abnormalities in helping us to understand their pathophysiology. In this review, we summarize the various eyelid abnormalities that can occur in neurodegenerative, neurogenetic, and neurometabolic diseases. We discuss eyelid disorders, such as ptosis, eyelid retraction, abnormal spontaneous and reflexive blinking, blepharospasm, and eyelid apraxia in the context of the neuroanatomic pathways that are affected. We also review the literature regarding the prevalence of eyelid abnormalities in different neurologic diseases as well as treatment strategies (Table 1).

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Influence of the superior colliculus on the primate blink reflex

Cited by 38 publications

References 38 publications

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Organization of trigeminocollicular connections and their relations to the sensory innervation of the eyelids in the rat

Eyelid Dysfunction in Neurodegenerative, Neurogenetic, and Neurometabolic Disease

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