Accessory abducens nucleus and conditioned eye retraction/nictitating membrane extension in rabbit

Disterhoft, JF; Kj, Quinn; Weiss, Craig; Shipley, MT

doi:10.1523/jneurosci.05-04-00941.1985

Cited by 83 publications

(49 citation statements)

References 27 publications

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“…Substantial lesions in the region of the accessory abducens nucleus cause virtual abolition of the NM extension response for both the CR and the UR, but the NM CR shows much greater recovery over time than does the NM UR (Disterhoft et al 1985;Steinmetz et al 1992a). Importantly, lesions of the cerebellum that completely and permanently abolish all components of the CR (see below) have no lasting effect on any component of the UR, at any level of US intensity, including threshold (Steinmetz et al 1992a;Ivkovich et al 1993).…”

Section: The Ur Pathwaysmentioning

confidence: 96%

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

561

473

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Classical conditioning of the eyeblink reflex to a neutral stimulus that predicts an aversive stimulus is a basic form of associative learning. Acquisition and retention of this learned response require the cerebellum and associated sensory and motor pathways and engage several other brain regions including the hippocampus, neocortex, neostriatum, septum, and amygdala. The cerebellum and its associated circuitry form the essential neural system for delay eyeblink conditioning. Trace eyeblink conditioning, a learning paradigm in which the conditioned and unconditioned stimuli are noncontiguous, requires both the cerebellum and the hippocampus and exhibits striking parallels to declarative memory formation in humans. Identification of the neural structures critical to the development and maintenance of the conditioned eyeblink response is an essential precursor to the investigation of the mechanisms responsible for the formation of these associative memories. In this review, we describe the evidence used to identify the neural substrates of classical eyeblink conditioning and potential mechanisms of memory formation in critical regions of the hippocampus and cerebellum. Addressing a central goal of behavioral neuroscience, exploitation of this simple yet robust model of learning and memory has yielded one of the most comprehensive descriptions to date of the physical basis of a learned behavior in mammals.

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Section: The Ur Pathwaysmentioning

confidence: 96%

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

561

473

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“…Movement of the nictitating membrane is a passive response to eyeball retraction generated by motor neurons in the abducens and accessory abducens nucleus (Harvey and Gormezano 1981;Harvey et al 1984;Marek et al 1984;Disterhoft et al 1985;Weiss and Disterhoft 1985). The accessory abducens nucleus receives sensory relay input from the trigeminal nuclei and reticular brainstem .…”

Section: Response Output Circuitrymentioning

confidence: 99%

Neural circuitry and plasticity mechanisms underlying delay eyeblink conditioning

Freeman¹,

Steinmetz²

2011

Learn. Mem.

177

162

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Pavlovian eyeblink conditioning has been used extensively as a model system for examining the neural mechanisms underlying associative learning. Delay eyeblink conditioning depends on the intermediate cerebellum ipsilateral to the conditioned eye. Evidence favors a two-site plasticity model within the cerebellum with long-term depression of parallel fiber synapses on Purkinje cells and long-term potentiation of mossy fiber synapses on neurons in the anterior interpositus nucleus. Conditioned stimulus and unconditioned stimulus inputs arise from the pontine nuclei and inferior olive, respectively, converging in the cerebellar cortex and deep nuclei. Projections from subcortical sensory nuclei to the pontine nuclei that are necessary for eyeblink conditioning are beginning to be identified, and recent studies indicate that there are dynamic interactions between sensory thalamic nuclei and the cerebellum during eyeblink conditioning. Cerebellar output is projected to the magnocellular red nucleus and then to the motor nuclei that generate the blink response(s). Tremendous progress has been made toward determining the neural mechanisms of delay eyeblink conditioning but there are still significant gaps in our understanding of the necessary neural circuitry and plasticity mechanisms underlying cerebellar learning.Eyeblink conditioning is an associative learning paradigm that was first developed for use in human participants in the 1920s (Cason 1922). It was initially valued as a method for studying learning and higher nervous system function without confounds associated with verbal reports, introspection, or prior experience with similar associations. The procedure involves presentation of a conditioned stimulus (CS), typically a tone or light, which is paired with an unconditioned stimulus (US) that reliably elicits eyelid closure, such as an air puff or brief electrical stimulation near the eye. Humans will often show a short-latency lowamplitude unconditioned (alpha) response to an auditory CS. After repeated CS-US trials, conditioned eyelid closure (conditioned response [CR]) occurs during the CS. Maximum eyelid closure for the CR typically occurs near the onset time of the US. Several shortcomings of the paradigm were later identified, most notably, the presence of alpha responses and voluntary responses among human participants who became explicitly aware of the stimulus contingency. These shortcomings and the need for an animal model for invasive neuroscience research led to the development of the rabbit eyeblink and nictitating membrane paradigms Schneiderman et al. 1962;Gormezano 1966). Rabbits tolerate restraint well, do not exhibit alpha responses, and precise measures of eyelid closure and nictitating membrane movement are obtained readily (Gormezano 1966). Most of the initial work on the neural mechanisms underlying eyeblink conditioning was conducted using rabbits, but the paradigm has been applied to frogs, turtles, mice, rats, ferrets, sheep, dogs, monkeys, and cats. A concern with using species other...

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“…It is unlike the pathway described in cats and rabbits. In those species, the nictitating membrane/eyeblink reflex is disynaptic, having an interneuron located in the nucleus pars oralis of the trigeminal complex intercalated in the pathway from sensory fibers to accessory abducens motoneurons [Baker et al, 1980;Durand et al, 1983;Berthier and Moore, 1983;Disterhoft et al, 1985].…”

Section: Labeled Pathways Following Trigeminal Nerve Injectionsmentioning

confidence: 99%

Central Trigeminal and Posterior Eighth Nerve Projections in the Turtle <i>Chrysemys picta</i> Studied in vitro

Herrick

Keifer²

1998

Brain Behav Evol

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Recent electrophysiological studies in the turtle Chrysemys picta have suggested that a neural correlate of the eye-blink reflex can be evoked in an in vitro brainstem-cerebellum preparation by electrical rather than natural stimulation of the cranial nerves. Discharge recorded in the abducens nerve, which is similar to EMG recordings from extraocular muscles during eye retraction, is triggered by a brief electrical stimulus applied to the ipsilateral trigeminal nerve. Evidence also suggests that pairing a one-second electrical stimulus applied to the posterior eighth nerve immediately prior to a single shock to the trigeminal nerve results in classically conditioned abducens nerve discharge in response to the previously neutral eighth nerve stimulus. In view of these physiological findings, the aim of the present study was to examine the central projections of trigeminal and posterior eighth nerve inputs to elucidate the anatomical substrates that may underlie the in vitro eye-blink reflex and possible pathways involved in reflex conditioning. Neurobiotin (NB) or fluorescein dextran (FD) was pressure injected into the cut end of either the trigeminal or posterior eighth nerve of the in vitro brainstem-cerebellum. Following trigeminal nerve injections, both tracers showed label in the ipsilateral trigeminal nuclear complex. Direct projections to the ipsilateral principal and accessory abducens motor nuclei were observed, suggesting that the eye-blink reflex is monosynaptic. Trigeminal nerve axons were also observed to terminate in the ipsilateral cerebellar cortex. The results of the posterior eighth nerve injections showed axonal projections and terminals in the cochlear, vestibular and principal sensory trigeminal nuclei. Terminal label was also observed in the ipsilateral cerebellar cortex, deep cerebellar nuclei, and in the principal and accessory abducens motor nuclei. Results from the NB cases suggested transneuronal transport of this tracer substance, whereas the FD cases did not. The present findings suggest that convergence of trigeminal and posterior eighth nerve inputs occurs in the ipsilateral cerebellar cortex, the principal sensory trigeminal nucleus, and the principal and accessory abducens motor nuclei. These regions of convergence may therefore be considered as potential sites of synaptic modification during in vitro studies of the conditioned abducens nerve reflex.

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Accessory abducens nucleus and conditioned eye retraction/nictitating membrane extension in rabbit

Cited by 83 publications

References 27 publications

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Neural circuitry and plasticity mechanisms underlying delay eyeblink conditioning

Central Trigeminal and Posterior Eighth Nerve Projections in the Turtle <i>Chrysemys picta</i> Studied in vitro

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