Mechanisms Underlying LTP of Inhibitory Synaptic Transmission in the Deep Cerebellar Nuclei

Ouardouz, Mohamed; Sastry, B.R.

doi:10.1152/jn.2000.84.3.1414

Cited by 99 publications

(95 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…High-frequency stimulation in the DCN has been shown to produce an NMDAR-dependent enhancement of mIPSC frequency but not amplitude (Ouardouz and Sastry, 2000). This phenomenon was blocked with postsynaptic infusions of BAPTA and tetanus toxin, suggesting that trafficking of GABA A Rs and/or release of postsynaptic agents that regulate GABA A R function could be triggered by NMDARs (Ouardouz and Sastry, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Many forms of plasticity at excitatory synapses have been characterized, including NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) and long-term depression (LTD), which are mediated by insertion or removal of AMPA-type glutamate receptors (AMPARs) from the postsynaptic membrane (Malenka and Bear, 2004). Numerous types of plasticity at inhibitory synapses have also been identified (for review, see Gaiarsa et al, 2002), including several thought to be expressed postsynaptically (Kano et al, 1992;Morishita and Sastry, 1996;Ouardouz and Sastry, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…GABA A Rs can be removed from the neuronal surface in the hippocampus after status epilepticus (Naylor et al, 2005), in the amygdala during fear conditioning (Chhatwal et al, 2005), and by treatment with phorbol esters (Connolly et al, 1999), the GABA A R agonist muscimol (Barnes, 1996), or tumor necrosis factor ␣ (Stellwagen et al, 2005). In the hippocampus, NMDARs couple to changes in GABAergic transmission in a manner consistent with membrane removal of GABA A Rs (Wang et al, 2003), whereas in the deep cerebellar nuclei (DCN) NMDARs increase GABAergic transmission, possibly through insertion of GABA A Rs (Ouardouz and Sastry, 2000). However, there has been no direct evidence that glutamatergic signaling regulates GABA A Rs trafficking despite reports of cross talk between excitatory and inhibitory synapses.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors

Marsden¹,

Beattie²,

Friedenthal³

et al. 2007

J. Neurosci.

171

203

View full text Add to dashboard Cite

The trafficking of postsynaptic AMPA receptors (AMPARs) is a powerful mechanism for regulating the strength of excitatory synapses. It has become clear that the surface levels of inhibitory GABA A receptors (GABA A Rs) are also subject to regulation and that GABA A R trafficking may contribute to inhibitory plasticity, although the underlying mechanisms are not fully understood. Here, we report that NMDA receptor activation, which has been shown to drive excitatory long-term depression through AMPAR endocytosis, simultaneously increases

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors

Marsden¹,

Beattie²,

Friedenthal³

et al. 2007

J. Neurosci.

171

203

View full text Add to dashboard Cite

show abstract

“…Finally, a distinction between sensory responses associated with welltrained sensorimotor tasks and sensory responses to novel stimuli is likely to be important. Identified mechanisms of plasticity in the DCN include synaptically driven changes in excitability (Aizenman and Linden 2000), and LTP/LTD of the Purkinje cell-DCN synapses (Aizenman et al 1998;Ouardouz and Sastry 2000). Such plasticity in conjunction with cerebellar cortical LTD/LTP is likely to lead to an experience-based shaping of sensory responses in the DCN.…”

Section: Sensory Coding In the Dcnmentioning

confidence: 99%

Coding of Tactile Response Properties in the Rat Deep Cerebellar Nuclei

Rowland¹,

Jaeger²

2005

Journal of Neurophysiology

View full text Add to dashboard Cite

Rowland, Nathan C. and Dieter Jaeger. Coding of tactile response properties in the rat deep cerebellar nuclei. J Neurophysiol 94: 1236 -1251, 2005; doi:10.1152/jn.00285.2005. In the lateral hemispheres of the cerebellar cortex, somatosensory responses are represented in a finely grained fractured somatotopy. It is unclear, however, how these responses contribute to the ultimate output of the cerebellum from the deep cerebellar nuclei (DCN). Robust responses of DCN neurons to somatosensory stimuli have been described, but a detailed examination of their somatotopic arrangement and stimulus coding properties is lacking. To address these questions, we recorded extracellular, single-unit activity in the DCN of ketamine-anesthetized rats in response to air-puff stimuli aimed at six different orofacial and forelimb locations. In additional experiments, the duration and intensity of air-puff stimuli to the ipsilateral upper lip were systematically varied. Overall, we found that DCN neuron responses to air puff stimuli showed combinations of three distinct response components: a short-latency spike response, a pronounced inhibition, and a longlatency increase in firing. Individual neurons responsive to air-puff stimulation exhibited any combination of just one, two, or all three of these response components. The inhibitory response was most common and frequently consisted of a complete cessation of spiking despite a high spontaneous rate of baseline firing. In contrast to published findings from cerebellar cortical recordings, the receptive fields of all responsive neurons in the DCN were large. In fact, the receptive field of most neurons covered the ipsi-and contralateral face as well as forepaws. Response properties of individual neurons did not reliably indicate stimulus intensity or duration, although as a population DCN neurons showed significantly increasing response amplitudes as air-puff intensity or duration increased. Overall, the responses were characterized by a distinct temporal profile in each neuron, which remained unchanged with changes in stimulus condition. We conclude that the responses in the DCN of rats to air-puff stimuli differ substantially from cerebellar cortical responses in their receptive field properties and do not provide a robust code of tactile stimulus properties. Rather, the characteristic temporal response profile of each neuron may be tuned to control the timing of a specific task to which its output is linked.

show abstract

“…Although in most models of motor learning, only the parallel fiber-Purkinje cell synapse is plastic, in fact, many of the other synapses in the cerebellar network, as well as the synapse between the Purkinje cell and its postsynaptic target (Kano 1996;Aizenman et al 1998;Ouardouz and Sastry 2000), are capable of long-term changes (for review, see Hansel et al 2001). Many such sites have been excluded from models because they yield no obvious behavioral advantage, but the sheer number of types of synaptic plasticity discovered so far indicates the need for more flexible thinking on this issue.…”

Section: Cerebellar Mechanismsmentioning

confidence: 99%

Learning in a Simple Motor System

Broussard¹,

Kassardjian²

2004

Learn. Mem.

View full text Add to dashboard Cite

Motor learning is a very basic, essential form of learning that appears to share common mechanisms across different motor systems. We evaluate and compare a few conceptual models for learning in a relatively simple neural system, the vestibulo-ocular reflex (VOR) of vertebrates. We also compare the different animal models that have been used to study the VOR. In the VOR, a sensory signal from the semicircular canals is transformed into a motor signal that moves the eyes. The VOR can modify the transformation under the guidance of vision. The changes are persistent and share some characteristics with other types of associative learning. The cerebellar cortex is directly linked to the VOR reflex circuitry in a partnership that is present in all vertebrates, and which is necessary for motor learning. Early theories of Marr, Albus, and Ito, in which motor memories are stored solely in the cerebellar cortex, have not explained the bulk of the experimental data. Many studies appear to indicate a site of learning in the vestibular nuclei, and the most successful models have incorporated long-term memory storage in both the cerebellar cortex and the brainstem. Plausible cellular mechanisms for learning have been identified in both structures. We propose that short-term motor memory is initially stored in the cerebellar cortex, and that during consolidation of the motor memory the locus of storage shifts to include a brainstem site. We present experimental results that support our hypothesis.In many situations, inaccurate movements are worse than useless. If the movement is slow, errors can be corrected online by visual or other sensory feedback. However, rapid movements must be intrinsically accurate. This could be accomplished by hard-wiring an accurate movement, which has the obvious disadvantage that the movement cannot be readjusted for changes in downstream motor centers or (in the case of a reflex) for changes in sensory sensitivity. A better solution is to calibrate the movement by trial and error, that is, by motor learning. For our purposes, motor learning is defined as the process by which we acquire precise, coordinated movements, like those that are required in order to run, serve a tennis ball, and type accurately. Because accurate movements are necessary whenever predators must be avoided or prey captured, we can speculate that motor learning may have been one of the earliest types of associative learning to evolve. It has been demonstrated in the ventral nerve cord of insects (Horridge 1962) and is probably universal in freely-moving animals. Furthermore, because its substrate can be relatively simple and well understood, there is a real possibility of understanding motor learning both on the molecular level and on the level of brain circuitry.Motor learning is classified as procedural learning. Errors are monitored and used to guide adaptive changes without conscious awareness. Instead of learning a concept, the subject learns an accurate and appropriate motor response. Distinctions have also been made b...

show abstract

Mechanisms Underlying LTP of Inhibitory Synaptic Transmission in the Deep Cerebellar Nuclei

Cited by 99 publications

References 36 publications

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors

Coding of Tactile Response Properties in the Rat Deep Cerebellar Nuclei

Learning in a Simple Motor System

Contact Info

Product

Resources

About

Mechanisms Underlying LTP of Inhibitory Synaptic Transmission in the Deep Cerebellar Nuclei

Cited by 99 publications

References 36 publications

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABAAReceptors

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABAAReceptors

Coding of Tactile Response Properties in the Rat Deep Cerebellar Nuclei

Learning in a Simple Motor System

Contact Info

Product

Resources

About

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors

NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABA_AReceptors