A developmental comparison of trace and delay eyeblink conditioning in rats using matching interstimulus intervals

Claflin, Dragana Ivkovich; Garrett, Teresa L.; Buffington, Michelle L.

doi:10.1002/dev.20068

Cited by 15 publications

(13 citation statements)

References 31 publications

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“…In normally developing rats, the emergence of reliable short-delay ECC using a 280-ms ISI occurs between postnatal days (PD) 17-24 (Stanton, Freeman, & Skelton, 1992), and rates of acquisition in 24-day-old rats [measured as percentage of eyeblink conditioned responses (CRs)] is faster using the 280-ms ISI than using ISIs of 560, 1120, or 1190 ms (Freeman, Spencer, Skelton, & Stanton, 1993). The slower conditioning imparted by longer delay intervals in 24-day-old rats has been recently confirmed and also extended to 30-day-old (periadolescent) rats (Claflin, Garrett, & Buffington, 2005); that study also showed that regardless of ISI, the 30-day-old rats conditioned better than 24-day-olds. The evidence that short ISIs are optimal for ECC in rats confirms earlier finding in rabbits (Schneiderman & Gormezano, 1966).…”

Section: Introductionmentioning

confidence: 61%

“…The slower conditioning imparted by longer delay intervals in 24-day-old rats has been recently confirmed and also extended to 30-day-old (periadolescent) rats (Claflin, Garrett, & Buffington, 2005); that study also showed that regardless of ISI, the 30-day-old rats conditioned better than 24-day-olds. The evidence that short ISIs are optimal for ECC in rats confirms earlier finding in rabbits (Schneiderman & Gormezano, 1966).…”

Section: Introductionmentioning

confidence: 81%

“…Alternatively, longer delay ISIs may produce even more severe ECC impairments in ethanol-exposed rats than for the short-delay ISIs, since the increased demands to control the precise timing of the conditioned response at a non-optimal interval is typically associated with the slower acquisition in intact rats. In the following two experiments, we evaluated the latter alternative by comparing the effects of binge neonatal alcohol exposure on ECC using two different interstimulus intervals-the optimal short-delay ISI used in our previous studies (280-ms), and a long-delay ISI (880-ms) used in previous studies of the development of ECC in rats (Claflin et al, 2005;Ivkovich, Paczkowski, & Stanton, 2000). Experiment 1 tested periadolescent rats (around 35 days old at the start of training), whereas Experiment 2 tested adults.…”

Section: Introductionmentioning

confidence: 99%

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Binge‐like ethanol exposure during the early postnatal period impairs eyeblink conditioning at short and long CS–US intervals in rats

Tran

Stanton

Goodlett

2007

Developmental Psychobiology

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Binge-like ethanol exposure on postnatal days (PD) 4-9 in rodents causes cerebellar cell loss and impaired acquisition of conditioned responses (CRs) during "short-delay" eyeblink classical conditioning (ECC), using optimal (280-350 ms) interstimulus intervals (ISIs). We extended those earlier findings by comparing acquisition of delay ECC under two different ISIs. From PD 4 to 9, rats were intubated with either 5.25 g/kg of ethanol (2/day), sham intubated, or were not intubated. They were then trained either as periadolescents (about PD 35) or as adults (>PD 90) with either the optimal short-delay (280-ms) ISI, a long-delay (880-ms) ISI, or explicitly unpaired CS and US presentations. Neonatal binge ethanol treatment significantly impaired acquisition of conditioning at both ages regardless of ISI, and deficits in the acquisition and expression of CRs were comparable across ISIs. These deficits are consistent with the previously documented ethanol-induced damage to the cerebellar-brainstem circuit essential for Pavlovian ECC.

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Section: Introductionmentioning

confidence: 61%

Section: Introductionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

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Binge‐like ethanol exposure during the early postnatal period impairs eyeblink conditioning at short and long CS–US intervals in rats

Tran

Stanton

Goodlett

2007

Developmental Psychobiology

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“…The reason for analyzing the adaptive CR is that it represents a well-timed eyeblink response just prior to (i.e., 200 ms before) US onset, which is mediated by the cerebellar cortex in delay ECC (Ivkovich, Paczkowski, & Stanton, 2000; Perrett, Ruiz, & Mauk, 1993) or hippocampus in trace ECC (Ivkovich & Stanton, 2001; Moyer et al, 1990). This method of comparing the same adaptive CR window between different ECC procedures has been utilized in many different studies (e.g., see Claflin et al, 2005; Ivkovich & Stanton, 2001). Furthermore, adaptive CRs that were expressed (as measured by frequency and amplitude) during CS-alone trials were analyzed.…”

Section: Methodsmentioning

confidence: 99%

Choline supplementation mitigates trace, but not delay, eyeblink conditioning deficits in rats exposed to alcohol during development

Thomas

Tran

2011

Hippocampus

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Children exposed to alcohol prenatally suffer from a range of physical, neuropathological and behavioral alterations, referred to as Fetal Alcohol Spectrum Disorders (FASD). Both the cerebellum and hippocampus are affected by alcohol exposure during development, which may contribute to behavioral and cognitive deficits observed in children with FASD. Despite the known neuropathology associated with prenatal alcohol exposure, many pregnant women continue to drink (heavy drinkers, in particular), creating a need to identify effective treatments for their children who are adversely affected by alcohol. We previously reported that choline supplementation can mitigate alcohol’s effects on cognitive development, specifically on tasks which depend on the functional integrity of the hippocampus. The present study examined whether choline supplementation could differentially mitigate ethanol’s effects on trace eyeblink classical conditioning (a hippocampal-dependent task) and delay eyeblink classical conditioning (a cerebellar-dependent task). Long-Evans rats were exposed to 5.25 g/kg/day alcohol via gastric intubation from postnatal days (PD) 4-9, a period of brain development equivalent to late gestation in humans. A sham-intubated control group was included. From PD 10-30, subjects received subcutaneous injections of 100 mg/kg choline chloride or vehicle. Beginning on PD 32-34, subjects were trained on either delay or trace eyeblink conditioning. Performance of subjects exposed to alcohol was significantly impaired on both tasks, as indicated by significant reductions in percentage and amplitude of conditioned eyeblink responses, an effect that was attenuated by choline supplementation on the trace, but not delay conditioning task. Indeed, ethanol-exposed subjects treated with choline performed at control levels on the trace eyeblink conditioning task. There were no significant main or interactive effects of sex. These data indicate that choline supplementation can significantly reduce the severity of trace eyeblink conditioning deficits associated with early alcohol exposure, even when administered after the alcohol insult is complete. These findings have important implications for the treatment of fetal alcohol spectrum disorders.

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“…The timing of CRs for a single CS has been well characterized across CS-US intervals ranging from a few hundred milliseconds in eyeblink conditioning in several species (Smith 1968;Claflin et al 2005;Kehoe et al 2008Kehoe et al , 2009b) through tens of seconds for appetitive conditioning in rats and pigeons (Cheng and Roberts 1991;Church et al 1994;Ludvig et al 2007). In all cases, peak responding occurred around the time that the reinforcer had been presented, and the variability in peak responding has tended to be proportional to the stimulus-reinforcer interval (Gibbon 1977;Cheng and Roberts 1991;Church et al 1994; Lejeune and Wearden 2006;Kehoe et al 2009b).…”

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confidence: 99%

Timing and cue competition in conditioning of the nictitating membrane response of the rabbit (Oryctolagus cuniculus)

2013

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Rabbits were classically conditioned using compounds of tone and light conditioned stimuli (CSs) presented with either simultaneous onsets (Experiment 1) or serial onsets (Experiment 2) in a delay conditioning paradigm. Training with the simultaneous compound reduced the likelihood of a conditioned response (CR) to the individual CSs ("mutual overshadowing") but left CR timing unaltered. CR peaks were consistently clustered around the time of unconditioned stimulus (US) delivery. Training with the serial compound (CSA CSB US) reduced responding to CSB ("temporal primacy/information effect") but this effect was prevented by prior CSB US pairings. In both cases, serial compound training altered CR timing. On CSA CSB test trials, the CRs were accelerated; the CR peaks occurred after CSB onset but well before the time of US delivery. Conversely, CRs on CSB-trials were decelerated; the distribution of CR peaks was variable but centered well after the US. Timing on CSB-trials was at most only slightly accelerated. The results are discussed with respect to processes of generalization and spectral timing applicable to the cerebellar and forebrain pathways in eyeblink preparations.The present experiments characterized the timing of eyeblink conditioned responses (CRs) in the rabbit during "cue competition" between two compounded stimuli (CSs) with either simultaneous onsets (Experiment 1) or serial onsets (Experiment 2) in advance of an unconditioned stimulus (US). The timing of CRs for a single CS has been well characterized across CS-US intervals ranging from a few hundred milliseconds in eyeblink conditioning in several species (Smith 1968;Claflin et al. 2005;Kehoe et al. 2008Kehoe et al. , 2009b) through tens of seconds for appetitive conditioning in rats and pigeons (Cheng and Roberts 1991;Church et al. 1994;Ludvig et al. 2007). In all cases, peak responding occurred around the time that the reinforcer had been presented, and the variability in peak responding has tended to be proportional to the stimulus-reinforcer interval (Gibbon 1977;Cheng and Roberts 1991;Church et al. 1994;Lejeune and Wearden 2006;Kehoe et al. 2009b).Less is known about timing when a compound of CSs signals the US. For stimulus-reinforcer intervals in the 10-90-sec range, peak responding during a compound and its component stimuli remains centered around the reinforcer. This pattern occurs even when compound training produces cue competition effects, most notably overshadowing of one or both stimuli and blocking of acquisition to an added stimulus (Jennings and Kirkpatrick 2006;Jennings et al. 2007;McMillan and Roberts 2010). The one exception appeared in McMillan and Roberts (2010). There, pretraining of a relatively short stimulus blocked the appearance of a systematic peak in responding. Responding was uniform across stimulus duration.The available findings from appetitive conditioning suggest that the mechanisms for timing in the 10-90-sec range are largely, although not wholly, separate from the mechanisms that govern cue competition. The...

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A developmental comparison of trace and delay eyeblink conditioning in rats using matching interstimulus intervals

Cited by 15 publications

References 31 publications

Binge‐like ethanol exposure during the early postnatal period impairs eyeblink conditioning at short and long CS–US intervals in rats

Binge‐like ethanol exposure during the early postnatal period impairs eyeblink conditioning at short and long CS–US intervals in rats

Choline supplementation mitigates trace, but not delay, eyeblink conditioning deficits in rats exposed to alcohol during development

Timing and cue competition in conditioning of the nictitating membrane response of the rabbit (Oryctolagus cuniculus)

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