Trace eyeblink conditioning is hippocampally dependent in mice

Tseng, Wilbur; Guan, Ruili; Disterhoft, John F.; Weiss, Craig

doi:10.1002/hipo.10157

Cited by 124 publications

(139 citation statements)

References 47 publications

(53 reference statements)

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“…For instance, lesions of the visual cortex did not prevent acquisition of CRs with a light CS [73] , suggesting that the visual cortex is not involved in the process of CR acquisition, whereas stimulation of the visual cortex can be successfully used as a CS to establish CR [34] . Moreover, although lesions of the pretectal nuclei [73] and hippocampus [22][23][24]68] retarded acquisition of eyeblink conditioning, stimulation of the anterior pretectal nucleus [11] and of the CA1 layer of hippocampus [74] can not be served as effective CSs for establishing eyeblink conditioning. Therefore, the present results only suggest that electrical stimulation of mPFC is a very effective and sufficient CS for establishing eyeblink conditioning, and that it is dependent on the cerebellar interpositus nucleus, but can not be interpreted as providing evidence that mPFC is critically involved in DEC, short TEC, or long TEC.…”

Section: Discussionmentioning

confidence: 99%

Classical eyeblink conditioning using electrical stimulation of caudal mPFC as conditioned stimulus is dependent on cerebellar interpositus nucleus in guinea pigs

Yao

Fan

et al. 2012

Acta Pharmacol Sin

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Aim: To determine whether electrical stimulation of caudal medial prefrontal cortex (mPFC) as conditioned stimulus (CS) paired with airpuff unconditioned stimulus (US) was sufficient for establishing eyeblink conditioning in guinea pigs, and whether it was dependent on cerebellar interpositus nucleus. Methods: Thirty adult guinea pigs were divided into 3 conditioned groups, and trained on the delay eyeblink conditioning, short-trace eyeblink conditioning, and long-trace eyeblink conditioning paradigms, respectively, in which electrical stimulation of the right caudal mPFC was used as CS and paired with corneal airpuff US. A pseudo conditioned group of another 10 adult guinea pigs was given unpaired caudal mPFC electrical stimulation and the US. Muscimol (1 µg in 1 µL saline) and saline (1 µL) were infused into the cerebellar interpositus nucleus of the animals through the infusion cannula on d 11 and 12, respectively. Results: The 3 eyeblink conditioning paradigms have been successfully established in guinea pigs. The animals acquired the delay and short-trace conditioned responses more rapidly than long-trace conditioned responses. Muscimol infusion into the cerebellar interpositus nucleus markedly impaired the expression of the 3 eyeblink conditioned responses. Conclusion: Electrical stimulation of caudal mPFC is effective CS for establishing eyeblink conditioning in guinea pigs, and it is dependent on the cerebellar interpositus nucleus.

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Section: Discussionmentioning

confidence: 99%

Classical eyeblink conditioning using electrical stimulation of caudal mPFC as conditioned stimulus is dependent on cerebellar interpositus nucleus in guinea pigs

Yao

Fan

et al. 2012

Acta Pharmacol Sin

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“…We used a trace conditioning procedure with a short (300-ms) trace interval, which has been shown to be hippocampally-dependent in rats and mice (Tseng et al, 2004;Weiss et al, 1999), in order to produce a rate of learning that was not substantially slower than the rate of learning of delay conditioning. Animals that underwent delay conditioning showed somewhat poorer learning in the current study than in previous studies using the same parameters in our lab (unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

“…Trace eyeblink conditioning appears to require the same brainstem-cerebellar circuit for acquisition and retention as delay eyeblink conditioning (Takehara, Kawahara, & Kirino, 2003;Woodruff-Pak, Lavond, & Thompson, 1985) but, when the stimulus-free trace period is long enough (250-ms for rodents; Tseng, Guan, Disterhoft, & Weiss, 2004;Weiss, Bouwmeester, Power, & Disterhoft 1999; 500-ms for rabbits, Moyer, Deyo, & Disterhoft, 1990) the hippocampus is required as well. Lesion studies have indicated that the hippocampal formation is necessary for normal acquisition and/ or proper timing of trace eyeblink CRs (Beylin et al 2001;Ivkovich & Stanton, 2001;James, Hardiman, & Yeo, 1987;Kishimoto, Nakazawa, Tonegawa, Kirino, & Kano, 2006;Moyer et al, 1990;Port, Romano, Steinmetz, Mikhail, & Patterson, 1986;Solomon, Vander Schaaf, Thompson, & Weisz, 1986;Takehara et al, 2003;Tseng et al, 2004;Weiss et al, 1999) and for short-term retention (perhaps up to several weeks; Kim, Clark, & Thompson, 1995;Takehara, Kawahara, Takatsuki, & Kirino, 2002;Takehara et al, 2003) of trace eyeblink conditioning. However, recording studies of CA1 unit activity during trace eyeblink conditioning have yielded somewhat inconsistent results.…”

Section: Introductionmentioning

confidence: 99%

Hippocampal and cerebellar single-unit activity during delay and trace eyeblink conditioning in the rat

Green

Arenos

2007

Neurobiology of Learning and Memory

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In delay eyeblink conditioning, the CS overlaps with the US and only a brainstem-cerebellar circuit is necessary for learning. In trace eyeblink conditioning, the CS ends before the US is delivered and several forebrain structures, including the hippocampus, are required for learning, in addition to a brainstem-cerebellar circuit. The interstimulus interval (ISI) between CS onset and US onset is perhaps the most important factor in classical conditioning, but studies comparing delay and trace conditioning have typically not matched these procedures in this crucial factor, so it is often difficult to determine whether results are due to differences between delay and trace or to differences in ISI.In the current study, we employed a 580-ms CS-US interval for both delay and trace conditioning and compared hippocampal CA1 activity and cerebellar interpositus nucleus activity in order to determine whether a unique signature of trace conditioning exists in patterns of single-unit activity in either structure. Long-Evans rats were chronically implanted in either CA1 or interpositus with microwire electrodes and underwent either delay eyeblink conditioning, or trace eyeblink conditioning with a 300-ms trace period between CS offset and US onset. On trials with a CR in delay conditioning, CA1 pyramidal cells showed increases in activation (relative to a pre-CS baseline) during the CS-US period in sessions 1-4 that was attenuated by sessions 5-6. In contrast, on trials with a CR in trace conditioning, CA1 pyramidal cells did not show increases in activation during the CS-US period until sessions 5-6. In sessions 5-6, increases in activation were present only to the CS and not during the trace period. For rats with interpositus electrodes, activation of interpositus neurons on CR trials was present in all sessions in both delay and trace conditioning. However, activation was greater in trace compared to delay conditioning in the first half of the CS-US interval (during the trace CS) during early sessions of conditioning and, in later sessions of conditioning, activation was greater in the second half of the CS-US interval (during the trace interval). These results suggest that the pattern of hippocampal activation that differentiates trace from delay eyeblink conditioning is a slow buildup of activation to the CS, possibly representing encoding of CS duration or discrimination of the CS from the background context. Interpositus nucleus neurons show strong modeling of the eyeblink CR regardless of paradigm but show a changing pattern across conditioning that may be due to the necessary contributions of forebrain processing to trace conditioning.

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“…TEC engages a network of brain regions to support learning. In addition to PFC, the hippocampus, amygdala, and cerebellum also support TEC (Takehara et al, 2003;Tseng et al, 2004;Siegel et al, 2015). Using region-specific manipulations of FMRP, we were able to tease apart which behavioral deficits could be attributed to PFC dysfunction and which may be due to dysfunction in other brain regions.…”

Section: Brain Region-and Neuron-specific Differences In Fmrp Functionmentioning

confidence: 99%

Prefrontal Cortex Dysfunction in Fragile X Mice Depends on the Continued Absence of Fragile X Mental Retardation Protein in the Adult Brain

et al. 2017

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Fragile X Syndrome (FX) is generally considered a developmental disorder, arising from a mutation that disrupts the transcription of Fragile X Mental Retardation Protein (FMRP). However, FMRP regulates the transcription of other proteins and participates in an unknown number of protein-protein interactions throughout life. In addition to known developmental issues, it is thus likely that some dysfunction is also due to the ongoing absence of FMRP. Dissociating dysfunction due to developmental dysregulation from dysfunction due to the continued absence of FMRP is necessary to understand the different roles of FMRP and to treat patients effectively throughout life. We show here that FX model mice display substantial deficits in a PFC-dependent task. We then use conditional knock-out mice to eliminate FMRP only in the PFC alone of adult mice. We observe an increase in the proportion of nonlearners and a delay in the onset of learning in both FX and conditional knock-out mice. The results suggest that these deficits (1) are due to the absence of FMRP in the PFC alone and (2) are not the result of developmental dysregulation. Furthermore, PFC-associated deficits are rescued by initiating production of FMRP in adult conditional restoration mice, suggesting that PFC dysfunction may persist as long as FMRP is absent and therefore can be rescued after development. The data suggest that it is possible to dissociate the roles of FMRP in neural function from developmental dysregulation, and that PFC function can be restored in the adult FX brain.

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Trace eyeblink conditioning is hippocampally dependent in mice

Cited by 124 publications

References 47 publications

Classical eyeblink conditioning using electrical stimulation of caudal mPFC as conditioned stimulus is dependent on cerebellar interpositus nucleus in guinea pigs

Classical eyeblink conditioning using electrical stimulation of caudal mPFC as conditioned stimulus is dependent on cerebellar interpositus nucleus in guinea pigs

Hippocampal and cerebellar single-unit activity during delay and trace eyeblink conditioning in the rat

Prefrontal Cortex Dysfunction in Fragile X Mice Depends on the Continued Absence of Fragile X Mental Retardation Protein in the Adult Brain

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