Interpositus lesion abolition of the eyeblink conditioned response is not due to effects on performance.

Ivkovich, Dragana; Lockard, J. M.; Thompson, Richard F.

doi:10.1037/0735-7044.107.3.530

Cited by 28 publications

(19 citation statements)

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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). The cerebellar circuitry thus plays no essential role in performance of the reflex response.…”

Section: The Ur Pathwaysmentioning

confidence: 99%

“…Steinmetz et al (1992a) investigated numerous parameters of the UR including amplitude, rise time, frequency, and latency in the same animals at several US intensities and found no significant lasting effects of interpositus lesions in any of these properties. Ivkovich et al (1993) lowered US intensity levels to threshold to control for discrepancies in the amplitude of prelesion CRs and URs, and it was again shown that interpositus lesions that completely abolished the CR had no significant effect on postlesion UR amplitude. Results from Kolb et al (1997) have shown similar transient effects on unconditioned limb withdrawal with interpositus inactivation following classical conditioning of this reflex in cats, but again only 130 trials were given during inactivation, and therefore the results cannot be interpreted as demonstrating a sustained involvement of the interpositus on UR expression.…”

Section: The Ur Pathwaysmentioning

confidence: 99%

“…Interpositus-lesioned animals were trained periodically for periods up to 8 mos; no CRs ever developed (Lavond et al 1984b;Steinmetz et al 1992b). In these and other interpositus lesion studies it was shown that lesions effective in completely abolishing the CR had no lasting effects on any properties of the UR, that is, no effects on performance of the response (Steinmetz et al 1992a;Ivkovich et al 1993; see also Welsh and Harvey 1989, and the reanalysis of their data in Steinmetz et al 1992a). Kainic acid lesions of the interpositus as small as about 1mm 3 in the anterior lateral region of the nucleus abolished the CR, indicating extreme localization of the critical region and ruling out the possibility that fibers of passage were involved (Lavond et al 1984a).…”

Section: Cerebellar Interpositus Nucleus Lesionsmentioning

confidence: 99%

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Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

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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: 99%

Section: The Ur Pathwaysmentioning

confidence: 99%

Section: Cerebellar Interpositus Nucleus Lesionsmentioning

confidence: 99%

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Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

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565

473

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“…Some investigators describe a CR loss with a smaller effect on reflex blinks (Bracha et al 1994;Jimenez-Diaz et al 2004;Welsh 1992;Welsh and Harvey 1989). Other investigators report a loss of CRs with no change in reflex blinks (Ivkovich et al 1993;McCormick and Thompson 1984;Steinmetz et al 1992). These divergent results may arise from differences in the anterior-posterior extent of IP lesions and the collection of data immediately after IP inactivation (Bracha et al 1994;Jimenez-Diaz et al 2004) rather than days after the lesion (Ivkovich et al 1993;McCormick and Thompson 1984;Steinmetz et al 1992 (Chen and Evinger 2006;Jimenez-Diaz et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Conditioned Eyelid Movement Is not a Blink

Powers

Coburn-Litvak

Evinger

2010

Journal of Neurophysiology

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Based on kinematic properties and distinct substrates, there are different classes of eyelid movement described as eyeblinks. We investigate whether the eyelid movements made in response to a conditioned stimulus (CS) are a category of eyelid movements distinct from blinks. Human subjects received 60 trials of classical eyelid conditioning with a tone as the CS and electrical stimulation of the supraorbital branch of the trigeminal nerve as the unconditioned stimulus (UCS). Before and after training, reflex blinks were elicited with the UCS. The kinematics of conditioned responses (CRs) differed significantly from those of reflex blinks. The slope of the amplitude-maximum velocity function was steeper for reflex blinks than for CRs, and reflex blink duration was significantly shorter than CR duration. Unlike reflex blinks, for which maximum velocity was independent of blink duration, the maximum velocity of CRs depended on CR duration. These quantitative and qualitative differences indicated that CRs were a unique class of eyelid movements distinct from blinks and eyelid movements with vertical saccadic gaze shifts.

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“…Lesions of the interpositus nucleus completely and permanently abolish previously learned conditioned responding (Steinmetz & Sengelaub, 1992) and block acquisition in naive animals (McCormick & Thompson, 1982), with no significant effects on performance of the reflex itself (Ivkovich, Lockard, & Thompson, 1993). Lesions of the cerebellar cortex disrupt conditioning, but small-amplitude, poorly timed conditioned responses do slowly develop across training (Lavond et al, 1987;Woodruff-Pak, Lavond, Logan, Steinmetz, & Thompson, 1993).…”

Section: The Cerebellum and Classical Conditioningmentioning

confidence: 99%

Cerebellar Substrates for Error Correction in Motor Conditioning

Gluck

Allen

Myers

et al. 2001

Neurobiology of Learning and Memory

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The authors evaluate a mapping of Rescorla and Wagner's (1972) behavioral model of classical conditioning onto the cerebellar substrates for motor reflex learning and illustrate how the limitations of the Rescorla-Wagner model are just as useful as its successes for guiding the development of new psychobiological theories of learning. They postulate that the inhibitory pathway that returns conditioned response information from the cerebellar interpositus nucleus back to the inferior olive is the neural basis for the error correction learning proposed by Rescorla and Wagner (Gluck, Myers, & Thompson, 1994;Thompson, 1986). The authors' cerebellar model expects that behavioral processes described by the Rescorla-Wagner model will be localized within the cerebellum and related brain stem structures, whereas behavioral processes beyond the scope of the Rescorla-Wagner model will depend on extracerebellar structures such as the hippocampus and related cortical regions. Simulations presented here support both implications. Several novel implications of the authors' cerebellar error-correcting model are described including a recent empirical study by Kim, Krupa, and Thompson (1998), who verified that suppressing the putative error correction pathway should interfere with the Kamin (1969) blocking effect, a behavioral manifestation of error correction learning. The authors also discuss the model's implications for understanding the limits of cerebellar contributions to associative learning and how this informs our understanding of hippocampal function in conditioning. This leads to a more integrative view of the neural substrates of conditioning in which the authors' realtime circuit-level model of the cerebellum can be viewed as a generalization of the long-term memory module of Gluck and Myers' (1993) trial-level theory of cerebellar-hippocampal interaction in motor conditioning. ᭧

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Interpositus lesion abolition of the eyeblink conditioned response is not due to effects on performance.

Cited by 28 publications

References 11 publications

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Conditioned Eyelid Movement Is not a Blink

Cerebellar Substrates for Error Correction in Motor Conditioning

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