Temporal specificity of long-term depression in parallel fiber--Purkinje synapses in rat cerebellar slice.

Chen, C; Thompson, R. F.

doi:10.1101/lm.2.3-4.185

Cited by 171 publications

(89 citation statements)

References 45 publications

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“…The precise interval of time between granule cell and climbing fiber activation that is required for induction of LTD remains under investigation. Reported effective intervals have ranged from presynaptic first by 250 msec (Chen and Thompson, 1995) to climbing fiber first by 125 msec (Ekerot and Kano, 1989). Because we find that the results do not differ significantly for this range of intervals, our choice of a 0 msec interval (i.e., simultaneous activity in gr3Pk j synapse and climbing fiber input) represents a consensus interval that allows induction of LTD under a variety of experimental conditions (Ekerot and Kano, 1989;Karachot et al, 1994;Chen and Thompson, 1995).…”

Section: Methodsmentioning

confidence: 99%

“…Reported effective intervals have ranged from presynaptic first by 250 msec (Chen and Thompson, 1995) to climbing fiber first by 125 msec (Ekerot and Kano, 1989). Because we find that the results do not differ significantly for this range of intervals, our choice of a 0 msec interval (i.e., simultaneous activity in gr3Pk j synapse and climbing fiber input) represents a consensus interval that allows induction of LTD under a variety of experimental conditions (Ekerot and Kano, 1989;Karachot et al, 1994;Chen and Thompson, 1995). The reversibility of plasticity at gr3Pk j synapses is at present an assumption of the simulation because the evidence to date suggests that LTP-LTD at this synapse are not mutually reversible because the expression of the former seems to be presynaptic (Salin et al, 1996), whereas that of the later is clearly postsynaptic (Linden, 1994).…”

Section: Methodsmentioning

confidence: 99%

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A Mechanism for Savings in the Cerebellum

2001

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The phenomenon of savings (the ability to relearn faster than the first time) is a familiar property of many learning systems. The utility of savings makes its underlying mechanisms of special interest. We used a combination of computer simulations and reversible lesions to investigate mechanisms of savings that operate in the cerebellum during eyelid conditioning, a well characterized form of motor learning. The results suggest that a site of plasticity outside the cerebellar cortex (possibly in the cerebellar nucleus) can be protected from the full consequences of extinction and that the residual plasticity that remains can later contribute to the savings seen during relearning.Key words: plasticity; learning; memory; eyelid conditioning; simulation; LTD; LTP; extinction Riding a bicycle, playing the piano, and typing are examples of motor skills that illustrate our capacity for relearning that is much more rapid than the original learning. In the laboratory, this rapid relearning is known as savings and has been frequently studied in the context of Pavlovian conditioning of motor responses. During conditioning of eyelid responses for example, paired presentations of a tone [the conditioned stimulus (CS)] and a reinforcing unconditioned stimulus (US), such as periorbital electrical stimulation, promote the acquisition of a conditioned motor response (closing the eyelid in response to the tone). These conditioned responses can be unlearned during extinction training in which the CS is not paired with the US (Schneiderman et al., 1962). During reacquisition training, savings is apparent because relearning occurs much faster than original learning (Frey and Ross, 1968;Napier et al., 1992). The existence of savings is among the evidence supporting the notion that extinction training leaves behind residual excitatory strength (Reberg, 1972;Schactman et al., 1985;Kehoe, 1988). Here we present evidence for this residual-plasticity hypothesis in eyelid conditioning and characterize basic mechanisms involved in the savings observed with this form of motor learning.A variety of evidence indicates that the cerebellum is a necessary component of the neural pathways that mediate eyelid conditioning (Thompson, 1986;Thompson and Krupa, 1994;Raymond et al., 1996;Kim and Thompson, 1997). This evidence, combined with the well characterized synaptic organization and physiology of the cerebellum (Eccles et al., 1967;Llinas, 1981;Ito, 1984;Voogd and Glickstein, 1998), makes it possible to build large-scale computer simulations of the cerebellum and to test their capacity to display eyelid conditioning. We have shown previously that, by incorporating the evidence for plasticity at two sites (one in the cerebellar cortex and one in the cerebellar interpositus nucleus), these simulations can emulate the acquisition and extinction of conditioned responses (Medina et al., 2000). Here we report that these same simulations also display savings, even after extensive extinction training. In the simulations, the rules for plasticity combine...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

A Mechanism for Savings in the Cerebellum

2001

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“…Paired stimulation of parallel and climbing fibers induces LTD (Chen & Thompson, 1995;Schreurs, Oh, & Alkon, 1996;Freeman, Shi, & Schreurs, 1998), but parallel fiber stimulation without climbing fiber stimulation can induce LTP (Sakurai, 1987;Salin, Malenka, & Nicoll, 1996). It is possible that the parallel fiber-alone stimulation that presumably occurs during the non-reinforced compound stimulus in conditioned inhibition training induces LTP in Purkinje cells.…”

Section: Introductionmentioning

confidence: 99%

“…Several models argue that long-term depression (LTD) of parallel fiber inputs to Purkinje cells is a learning mechanism involved in excitatory conditioning (Albus, 1971;Gluck, Reifsnider, & Thompson, 1990;Kim & Thompson, 1997;Mauk, 1997;Mauk et al, 1998;Mauk & Donegan, 1997;Thompson & Krupa, 1994;Thompson, 2000;Yeo & Hesslow, 1998). LTD has been demonstrated in vitro using parallel fiber stimulation followed by climbing fiber stimulation, a protocol which resembles delay conditioning (Chen & Thompson, 1995;Freeman, Shi, & Schreurs, 1998;Schreurs, Oh, & Alkon, 1996). Moreover, several studies have shown changes in Purkinje cell simple spike activity that are consistent with the LTD hypothesis (Foy, Krupa, Tracy, & Thompson, 1992;Gilbert & Thach, 1977;Hesslow & Ivarsson, 1994).…”

Section: Introductionmentioning

confidence: 99%

Blockade of GABAA receptors in the interpositus nucleus modulates expression of conditioned excitation but not conditioned inhibition of the eyeblink response

Nolan

Nicholson

Freeman

2002

Integrative Physiological & Behavioral Science

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The cerebellum and related brainstem structures are essential for excitatory eyeblink conditioning. Recent evidence indicates that the cerebellar interpositus and lateral pontine nuclei may also play critical roles in conditioned inhibition (CI) of the eyeblink response. The current study examined the role of GABAergic inhibition of the interpositus nucleus in retention of CI. Male Long-Evans rats were implanted with a cannula positioned just above or in the anterior interpositus nucleus before training. The rats were trained with two different tones and a light as conditioned stimuli, and a periorbital shock as the unconditioned stimulus. CI training consisted of four phases: 1) excitatory conditioning (8 kHz tone paired with shock); 2) feature-negative discrimination (2 kHz tone paired with shock or 2 kHz tone concurrent with light); 3) summation test (8 kHz tone or 8 kHz tone concurrent with light); and 4) retardation test (light paired with shock). After reaching a criterion level of performance on the feature-negative discrimination (40% discrimination), 0.5 μl picrotoxin (a GABA A receptor antagonist) was infused at one of four concentrations, each concentration infused during separate test sessions. Picrotoxin transiently impaired conditioned responses during trials with the excitatory stimulus (tone) in a dose-dependent manner, but did not significantly impact responding to the inhibitory compound stimulus (tone-light). The results suggest that expression of conditioned inhibition of the eyeblink conditioned response does not require GABAergic inhibition of neurons in the anterior interpositus nucleus.

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“…This mechanism of decremental plasticity might contribute to Pavlovian learning through disinhibition of neurons of the NI that, as we have seen, seem to be the central role of plasticity. In a study by Chen and Thompson (1995), using an in vitro preparation, maximum LTD was observed after stimulation of parallel fibers was preceded by 250 ms stimulation of climbing fibers. These temporal parameters are similar to those effective for behavioral learning or for the neurophysiological conditioning previously described.…”

Section: Two Forms Of Synaptic Plasticity Mediate Eyelid Conditioningmentioning

confidence: 99%

Neuroscience of Pavlovian Conditioning: A Brief Review

Aguado

2003

Span. J. Psychol.

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Current knowledge on the neuronal substrates of Pavlovian conditioning in animals and man is briefly reviewed. First, work on conditioning in aplysia, that has showed amplified pre-synaptic facilitation as the basic mechanism of associative learning, is summarized. Then, two exemplars of associative learning in vertebrates, fear conditioning in rodents and eyelid conditioning in rabbits, are described and research into its neuronal substrates discussed. Research showing the role of the amygdala in fear conditioning and of the cerebellum in eyelid conditioning is reviewed, both at the circuit and cellular plasticity levels. Special attention is given to the parallelism suggested by this research between the neuronal mechanisms of conditioning and the principles of formal learning theory. Finally, recent evidence showing a similar role of the amygdala and of the cerebellum in human Pavlovian conditioning is discussed. Keywords: Pavlovian conditioning, neural mechanisms, learning theoriesEl artículo revisa brevemente los conocimientos actuales acerca de los substratos neuronales del condicionamiento pavloviano en los animales y en el hombre. En primer lugar, se resume la investigación sobre condicionamiento en aplysias, que ha demostrado la importancia de la facilitación sináptica amplificada como mecanismo básico del aprendizaje asociativo. A continuación, se describen dos ejemplos de aprendizaje asociativo en vertebrados, el condicionamiento del miedo en roedores y el condicionamiento del parpadeo en conejos, con referencias a la investigación sobre sus substratos neuronales. Se revisa la investigación que muestra el papel de la amígdala en el condicionamiento del miedo y del cerebelo en el condicionamiento del parpadeo, al nivel tanto de circuitos como de la plasticidad celular. Se presta especial atención a los paralelismos que esta área de investigación sugiere entre los mecanismos neuronales del condicionamiento y los principios de las teorías formales del aprendizaje. Por último, se comentan diversas pruebas recientes que demuestran un papel semejante de la amígdala y del cerebelo en el condicionamiento pavloviano humano. Palabras clave: condicionamiento pavloviano, mecanismos neurales, teorias del aprendizaje

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Temporal specificity of long-term depression in parallel fiber--Purkinje synapses in rat cerebellar slice.

Cited by 171 publications

References 45 publications

A Mechanism for Savings in the Cerebellum

A Mechanism for Savings in the Cerebellum

Blockade of GABAA receptors in the interpositus nucleus modulates expression of conditioned excitation but not conditioned inhibition of the eyeblink response

Neuroscience of Pavlovian Conditioning: A Brief Review

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