Amygdala, deep cerebellar nuclei and red nucleus contribute to delay eyeblink conditioning in C57BL /6 mice

Sakamoto, Toshihiro; Endo, Shogo

doi:10.1111/j.1460-9568.2010.07406.x

Cited by 27 publications

(35 citation statements)

References 53 publications

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“…(2) We have used a very mild air-puff because it has been suggested recently that the much stronger periorbital stimulation typically employed for eyeblink conditioning in mice leads to a fear-related blink with a relatively fixed short-latency (Boele et al, 2010), and there is indirect evidence that in some cases this short-latency response can interfere with the adaptively timed component of the conditioned eyelid response (Aiba et al, 1994; Sakamoto and Endo, 2011). (3) We have developed a system that allows mice to be conditioned while they are actively engaged in one of their favorite activities: treadmill walking.…”

Section: Discussionmentioning

confidence: 99%

Adaptive Timing of Motor Output in the Mouse: The Role of Movement Oscillations in Eyelid Conditioning

Chettih¹,

McDougle²,

Ruffolo³

et al. 2011

Front. Integr. Neurosci.

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To survive, animals must learn to control their movements with millisecond-level precision, and adjust the kinematics if conditions, or task requirements, change. Here, we examine adaptive timing of motor output in mice, using a simple eyelid conditioning task. Mice were trained to blink in response to a light stimulus that was always followed by a corneal air-puff at a constant time interval. Different mice were trained with different intervals of time separating the onset of the light and the air-puff. As in previous work in other animal species, mice learned to control the speed of the blink, such that the time of maximum eyelid closure matched the interval used during training. However, we found that the time of maximum eyelid speed was always in the first 100 ms after movement onset and did not scale with the training interval, indicating that adaptive timing is not accomplished by slowing down (or speeding up) the eyelid movement uniformly throughout the duration of the blink. A new analysis, specifically designed to examine the kinematics of blinks in single trials, revealed that the underlying control signal responsible for the eyelid movement is made up of oscillatory bursts that are time-locked to the light stimulus at the beginning of the blink, becoming desynchronized later on. Furthermore, mice learn to blink at different speeds and time the movement appropriately by adjusting the amplitude, but not the frequency of the bursts in the eyelid oscillation.

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Section: Discussionmentioning

confidence: 99%

Adaptive Timing of Motor Output in the Mouse: The Role of Movement Oscillations in Eyelid Conditioning

Chettih¹,

McDougle²,

Ruffolo³

et al. 2011

Front. Integr. Neurosci.

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“…Amygdala lesions significantly slow the rate of CR acquisition depending on the conditioning parameters (Weisz et al 1992). However, damage of the amygdala reduces the asymptotic level of learning (Blankenship et al 2005; Sakamoto and Endo 2010), as it likely reduces the appreciation of the US (Christian and Thompson 2003; Whalen and Kapp 1991). This is a different pattern than obtained in the present study where intraseptal GAT1-SAP eventually reached the same level of performance, as sham-lesioned animals, during the second session.…”

Section: Discussionmentioning

confidence: 99%

GABAergic neurons in the medial septum-diagonal band of Broca (MSDB) are important for acquisition of the classically conditioned eyeblink response

Roland¹,

Janke

Servatius

et al. 2013

Brain Struct Funct

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The medial septum and diagonal band of Broca (MSDB) influence hippocampal function through cholinergic, GABAergic and glutamatergic septohippocampal neurons. Nonselective damage of the MSDB or intraseptal scopolamine impairs classical conditioning of the eyeblink response (CCER). Scopolamine preferentially inhibits GABAergic MSDB neurons suggesting that these neurons may be an important modulator of delay CCER, a form of CCER not dependent on the hippocampus. The current study directly examined the importance of GABAergic MSDB neurons in acquisition of delay CCER. Adult male Sprague-Dawley rats received either a sham (PBS) or GABAergic MSDB lesion using GAT1-saporin (SAP). Rats were given two consecutive days of delay eyeblink conditioning with 100 conditioned stimulus (CS)-unconditioned stimulus (US) paired trials. Intraseptal GAT1-SAP impaired acquisition of CCER. The impairment was observed on the first day with sham and lesion groups reaching similar performance by the end of the second day. Our results provide evidence that GABAergic MSDB neurons are an important modulator of delay CCER. The pathways by which MSDB neurons influence the neural circuits necessary for delay CCER are discussed.

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“…However, genetically modified mice with altered cerebellar functions constantly result in the incomplete loss of conditioned responses (CR) during delay eyeblink conditioning [9]–[14]. Furthermore, lesions or inactivation of deep cerebellar nuclei (DCN) did not impair the acquisition and expression of delay eyeblink conditioning [12], [15]. We revealed that mouse DCN play important roles in delay eyeblink conditioning with the low intensity CS [16], but not with high intensity CS [15].…”

Section: Introductionmentioning

confidence: 85%

Deep Cerebellar Nuclei Play an Important Role in Two-Tone Discrimination on Delay Eyeblink Conditioning in C57BL/6 Mice

Sakamoto

Endo

2013

PLoS ONE

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Previous studies have shown that deep cerebellar nuclei (DCN)-lesioned mice develop conditioned responses (CR) on delay eyeblink conditioning when a salient tone conditioned stimulus (CS) is used, which suggests that the cerebellum potentially plays a role in more complicated cognitive functions. In the present study, we examined the role of DCN in tone frequency discrimination in the delay eyeblink-conditioning paradigm. In the first experiment, DCN-lesioned and sham-operated mice were subjected to standard simple eyeblink conditioning under low-frequency tone CS (LCS: 1 kHz, 80 dB) or high-frequency tone CS (HCS: 10 kHz, 70 dB) conditions. DCN-lesioned mice developed CR in both CS conditions as well as sham-operated mice. In the second experiment, DCN-lesioned and sham-operated mice were subjected to two-tone discrimination tasks, with LCS+ (or HCS+) paired with unconditioned stimulus (US), and HCS− (or LCS−) without US. CR% in sham-operated mice increased in LCS+ (or HCS+) trials, regardless of tone frequency of CS, but not in HCS− (or LCS−) trials. The results indicate that sham-operated mice can discriminate between LCS+ and HCS− (or HCS+ and LCS−). In contrast, DCN-lesioned mice showed high CR% in not only LCS+ (or HCS+) trials but also HCS− (or LCS−) trials. The results indicate that DCN lesions impair the discrimination between tone frequency in eyeblink conditioning. Our results suggest that the cerebellum plays a pivotal role in the discrimination of tone frequency.

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Amygdala, deep cerebellar nuclei and red nucleus contribute to delay eyeblink conditioning in C57BL /6 mice

Cited by 27 publications

References 53 publications

Adaptive Timing of Motor Output in the Mouse: The Role of Movement Oscillations in Eyelid Conditioning

Adaptive Timing of Motor Output in the Mouse: The Role of Movement Oscillations in Eyelid Conditioning

GABAergic neurons in the medial septum-diagonal band of Broca (MSDB) are important for acquisition of the classically conditioned eyeblink response

Deep Cerebellar Nuclei Play an Important Role in Two-Tone Discrimination on Delay Eyeblink Conditioning in C57BL/6 Mice

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