Glutamate Neurotransmission in the Cerebellar Interposed Nuclei: Involvement in Classically Conditioned Eyeblinks and Neuronal Activity

Aksenov, Daniil P.; Serdyukova, Natalya A.; Bloedel, James R.; Bracha, Vlastislav

doi:10.1152/jn.00586.2004

Cited by 35 publications

(23 citation statements)

References 58 publications

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“…Cortical lesions and pharmacological corticonuclear disconnections have been reported to "unmask" short-latency CRs (Perrett et al, 1993;Bao et al, 2002;Ohyama et al, 2006;Vogel et al, 2009). Discrete inactivations of periocular microzone regions in our study were able to abolish CRs, but no short-latency responses were observed, in agreement with Attwell et al (2002) and Aksenov et al (2005).…”

Section: Periocular Microzones In Lobule Hvi Are Critical For Expresssupporting

confidence: 80%

“…Such small volumes are unlikely to have spread to the cerebellar nuclei. Moreover, nuclear blockade of glutamatergic transmission has little or no effect on CRs Aksenov et al, 2005). Cortical lesions and pharmacological corticonuclear disconnections have been reported to "unmask" short-latency CRs (Perrett et al, 1993;Bao et al, 2002;Ohyama et al, 2006;Vogel et al, 2009).…”

Section: Periocular Microzones In Lobule Hvi Are Critical For Expressmentioning

confidence: 99%

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Electrophysiological Localization of Eyeblink-Related Microzones in Rabbit Cerebellar Cortex

Mostofi¹,

Holtzman²,

Grout³

et al. 2010

Journal of Neuroscience

102

116

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The classically conditioned eyeblink response in the rabbit is one of the best-characterized behavioral models of associative learning. It is cerebellum dependent, with many studies indicating that the hemispheral part of Larsell's cerebellar cortical lobule VI (HVI) is critical for the acquisition and performance of learned responses. However, there remain uncertainties about the distribution of the critical regions within and around HVI. In this learning, the unconditional stimulus is thought to be carried by periocular-activated climbing fibers. Here, we have used a microelectrode array to perform systematic, high-resolution, electrophysiological mapping of lobule HVI and surrounding folia in rabbits, to identify regions with periocular-evoked climbing fiber activity. Climbing fiber local field potentials and single-unit action potentials were recorded, and electrode locations were reconstructed from histological examination of brain sections. Much of the sampled cerebellar cortex, including large parts of lobule HVI, was unresponsive to periocular input. However, short-latency ipsilateral periocular-evoked climbing fiber responses were reliably found within a region in the ventral part of the medial wall of lobule HVI, extending to the base of the primary fissure. Small infusions of the AMPA/kainate receptor antagonist CNQX into this electrophysiologically defined region in awake rabbits diminished or abolished conditioned responses. The known parasagittal zonation of the cerebellum, supported by zebrin immunohistochemistry, indicates that these areas have connections consistent with an essential role in eyeblink conditioning. These small eyeblink-related areas provide cerebellar cortical targets for analysis of eyeblink conditioning at a neuronal level but need to be localized with electrophysiological identification in individual animals.

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Section: Periocular Microzones In Lobule Hvi Are Critical For Expresssupporting

confidence: 80%

Section: Periocular Microzones In Lobule Hvi Are Critical For Expressmentioning

confidence: 99%

Electrophysiological Localization of Eyeblink-Related Microzones in Rabbit Cerebellar Cortex

Mostofi¹,

Holtzman²,

Grout³

et al. 2010

Journal of Neuroscience

102

116

View full text Add to dashboard Cite

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“…6). These observations are incompatible with notions that SLRs reflect nonassociative changes resulting from disinhibiting the AIN (Attwell et al, 2002), increases in tonic AIN activity levels (Aksenov et al, 2005), or cell-wide increases in the intrinsic excitability of AIN neurons (Aizenman and Linden, 2000;Zhang et al, 2004). Rather, they suggest that SLRs reflect an associative and input-specific form of AIN plasticity.…”

Section: Experiments 5: Slrs Are Learned and Associativementioning

confidence: 65%

“…3, top left, blue), as well as the failure of similar infusions to abolish the expression of normal conditioned responses (Attwell et al, 2002;Aksenov et al, 2005), appear to contradict the proposed hypothesis. However, glutamate blockade may be incomplete because of either low-drug concentrations or a wider area of inactivation required compared with muscimol.…”

Section: Functional Contributions Of Plasticity In the Ainmentioning

confidence: 95%

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Ohyama¹,

Nores²,

Medina³

et al. 2006

J. Neurosci.

139

131

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Evidence that cerebellar learning involves more than one site of plasticity comes from, in part, pavlovian eyelid conditioning, where disconnecting the cerebellar cortex abolishes one component of learning, response timing, but spares the expression of abnormally timed short-latency responses (SLRs). Here, we provide evidence that SLRs unmasked by cerebellar cortex lesions are mediated by an associative form of learning-induced plasticity in the anterior interpositus nucleus (AIN) of the cerebellum. We used pharmacological inactivation and/or electrical microstimulation of various sites afferent and efferent to the AIN to systematically eliminate alternative candidate sites of plasticity upstream or downstream from this structure. Collectively, the results suggest that cerebellar learning is mediated in part by plasticity in target nuclei downstream of the cerebellar cortex. These data demonstrate an instance in which an aspect of associative learning, SLRs, can be used as an index of plasticity at a specific site in the brain.

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“…These investigators interpret the first type to facilitate the lid closing orbicularis oculi (OO) muscle and the latter to promote activation of the lid opening levator palpebrae muscle with reflex blinks. In the rabbit, most anterior IP neurons exhibit elevated activity followed by a pause in activity starting ϳ50 ms after an air puff unconditioned stimulus (Aksenov et al, 2004(Aksenov et al, , 2005. In recordings from the anterior IP of rats, an intense periorbital shock generates a burst of activity (Freeman and Nicholson, 2000).…”

Section: Introductionmentioning

confidence: 99%

Cerebellar Modulation of Trigeminal Reflex Blinks: Interpositus Neurons

Chen

Evinger²

2006

J. Neurosci.

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Because of its simplicity, blinking is a prominent model system in analysis of adaptation and conditioning with the cerebellum. Nevertheless, data on the role of the cerebellum in modulation of normal reflex blinks are limited. We correlated the discharge of interpositus (IP) neurons with normal trigeminal reflex blinks and blink adaptation in urethane-anesthetized rats. Two groups of IP neurons responded to cornea stimulation. One group, pause neurons, showed a long cessation of their tonic discharge beginning 6 ms before the end of lid closure. The second group, burst neurons, exhibited a transient increase in firing frequency at a constant interval after the cornea stimulus. The cessation of pause neuron activity appeared to contribute to the termination of blinks. The tonic discharge rate increased and the cessation of pause neuron activity was delayed coincident with increased amplitude and duration of reflex blinks produced by blink adaptation. There was a coincident increase in the amplitude and duration of reflex blinks with increased tonic activity and delayed pause in pause neurons treated with the GABA A antagonist, gabazine. Burst neurons did not appear to modulate reflex blinks. Burst neuron discharge correlated neither with blink characteristics normally nor with blink adaptation. These findings indicated that pause neurons affect reflex blinks by providing a tonic excitatory input to facial motoneurons during lid closure and then disfacilitating those motoneurons to adjust the termination of lid closure. Burst neurons may play a role in eyelid conditioning.

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Glutamate Neurotransmission in the Cerebellar Interposed Nuclei: Involvement in Classically Conditioned Eyeblinks and Neuronal Activity

Cited by 35 publications

References 58 publications

Electrophysiological Localization of Eyeblink-Related Microzones in Rabbit Cerebellar Cortex

Electrophysiological Localization of Eyeblink-Related Microzones in Rabbit Cerebellar Cortex

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Cerebellar Modulation of Trigeminal Reflex Blinks: Interpositus Neurons

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