Biomedical subjects

D Ivkovich

Publications and source records attributed to D Ivkovich.

8 recordsLinked to original sources

PubMed2001

Effects of early hippocampal lesions on trace, delay, and long-delay eyeblink conditioning in developing rats.

The effects of bilateral hippocampal aspiration lesions on later acquisition of eyeblink conditioning were examined in developing Long-Evans rat pups. Lesions on postnatal day (PND) 10 were followed by evaluation of trace eyeblink conditioning (Experiment 1) and delay eyeblink conditioning (Experiment 2) on PND 25. Pairings of a tone conditioned stimulus (CS) and periocular shock unconditioned stimulus (US, 100 ms) were presented in one of three conditioning paradigms: trace (380 ms CS, 500 ms trace interval, 880 ms interstimulus interval [ISI]), standard delay (380 ms CS, 280 ms ISI), or long delay (980 ms CS, 880 ms ISI). The results of two experiments indicated that hippocampal lesions impaired trace eyeblink conditioning more than either type of delay conditioning. In light of our previous work on the ontogeny of trace, delay, and long-delay eyeblink conditioning (Ivkovich, Paczkowski, & Stanton, 2000) showing that trace and long-delay eyeblink conditioning had similar ontogenetic profiles, the current data suggest that during ontogeny hippocampal maturation may be more important for the short-term memory component than for the long-ISI component of trace eyeblink conditioning. The late development of conditioning over long ISIs may depend on a separate process such as protracted development of cerebellar cortex.

Animals↗

PubMed2001

Late positive ERP peaks observed in stimulus-response compatibility tasks tested under speed-accuracy instructions.

Speed-accuracy instructions were manipulated in two symbolic stimulus-response compatibility tasks in an event-related potential study with young adults. For both tasks, the stimuli were the words left and right written in upper and lower case. Three late positive peaks (early P3, P3b, and P4) were seen in one task (with compatibility type blocked) with an additional peak (P3c) in the task that required identifying two stimulus attributes (compatibility type signaled by case). In both tasks, stimulus-response incompatibility and an emphasis on accuracy increased reaction time, made the P4 more prominent and increased its latency. With very rapid responding, P4 was not prominent because of overlap with the preceding peak. Functional characteristics of the peaks are discussed as well as potential sources of latency and amplitude measurement error when P3b is measured in a temporal window broad enough to include the P4.

Adult↗

PubMed2000

Ontogeny of delay versus trace eyeblink conditioning in the rat.

The ontogeny of delay versus trace eyeblink conditioning was examined in 19-, 23-, and 30-day-old rat pups. Pairings of a tone conditioned stimulus (CS) and periocular shock unconditioned stimulus (US; 100-ms) were presented in one of three conditioning paradigms: standard delay [380-ms CS, 280-ms interstimulus interval (ISI)], trace (380-ms CS, 500-ms trace interval), or long-delay (980-ms CS, 880-ms ISI). The results of two experiments indicated that standard delay conditioning emerged between 19 and 23 days of age whereas trace and long-delay eyeblink conditioning emerged more slowly from postnatal Days 19 to 30. Because the acquisition profile for long-delay paralleled that of trace and not standard delay, it appears that the relative deficits in the emergence of trace eyeblink conditioning during development reflect difficulty in forming associations over long ISIs rather than the short-term memory demands of the trace conditioning paradigm.

Age Factors↗

PubMed1999

Ontogeny of eyeblink conditioning using a visual conditional stimulus.

The developmental emergence of associative learning in rodents is determined by interactions among sensory, motor, and associative systems that are engaged in a particular experimental preparation (Carter & Stanton, 1996; Hunt & Campbell, 1997; Rudy, 1992). In fear conditioning, chemosensory, auditory, and visual cues emerge successively as effective conditional stimuli (CS) during postnatal ontogeny. In the present study, we begin to examine the generality of this principle of sensory system development for eyeblink conditioning, a form of associative learning that develops substantially later than conditioned fear (Carter & Stanton, 1996). We asked whether the developmental emergence of eyeblink conditioning to a visual CS occurs at an age that is the same or different from conditioning to an auditory CS. In Experiment 1, rat pups were trained on postnatal Day 17 or 24 with experimental parameters (and design) that were identical to our previous studies of eyeblink conditioning except that presentation of a light rather than a tone served as the CS. The outcome was also identical: no eyeblink conditioning on Day 17 and strong conditioning on Day 24. In Experiment 2, conditioning to tone versus light was directly compared by means of a discrimination learning design on postnatal Days 19, 21, 23, and 31. There was no evidence for differential development of auditory versus visual eyeblink conditioning. The difference between this outcome and previous ones involving conditioned fear (Hunt & Campbell, 1997; Rudy, 1992) suggests that principles concerning sensory maturation and learning may be different for early- versus late-developing associative systems.

Amygdala↗

PubMed1997

Motor cortex lesions do not affect learning or performance of the eyeblink response in rabbits.

The possible modulatory role of motor cortex in classical conditioning of the eyeblink response was examined by ablating anterior neocortex in rabbits and training them with an auditory conditioned stimulus (CS) and an airpuff unconditioned stimulus (US) in either a delay (Experiment 1) or a trace (Experiment 2) conditioning paradigm. Topographic measures such as amplitude and onset latency were assessed during conditioning sessions for conditioned responses (CRs) and on separate test days for unconditioned responses (URs) by using a range of US intensities. No lesion effects were observed for learning or performance measures in acquisition or retention of either delay or trace conditioning. During trace conditioning, lesioned rabbits did, however, exhibit a trend toward impairment and demonstrated significantly longer CR latencies. Damage to motor and frontal cortex does not significantly affect eyeblink response performance or learning in either a delay or a trace conditioning paradigm.

Acoustic Stimulation↗

PubMed1994

Transfer of learning but not memory after unilateral cerebellar lesion in rabbits.

Unilateral lesion of the cerebellum in rabbits completely and permanently abolishes previous learning and prevents new learning ipsilateral to the lesion. However, when training continues on the contralateral side, there is substantial savings in that it takes few trials to learn. This observation may imply that the memory survives the lesion. Rabbits were classically conditioned for an eyelid response and then the ipsilateral interpositus nucleus of the cerebellum was lesioned. Then the rabbits were trained on the contralateral side. There is no savings on the contralateral side without first trying to train on the lesioned side. The authors conclude that the survival of a memory after the lesion probably does not account for the rapid transfer, but rather that the act of trying to train on the lesioned side in previous studies first induces a new memory on the contralateral side.

Animals↗

PubMed1993

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

Classical conditioning of the rabbit eyeblink response was used to study the effects of cerebellar lesions on performance in animals trained with low-intensity unconditioned stimuli (US). Animals were trained with 1 of 2 low-intensity corneal-airpuff USs paired with a tone-conditioned stimulus. This study confirms earlier findings demonstrating the differential effects of lesions of deep cerebellar nuclei on the conditioned (CR) and unconditioned responses (UR). Lesions of the anterior interpositus nucleus of the cerebellum in animals that were successfully conditioned abolished CRs without affecting UR performance.

Animals↗

PubMed1992

Disruption of classical eyelid conditioning after cerebellar lesions: damage to a memory trace system or a simple performance deficit?

Over the past 10 years, a number of laboratories have reported that classically conditioned skeletal muscle responses, such as conditioned nictitating membrane/eyelid responses, are critically dependent on activity in the cerebellum. For example, unilateral lesions of the cerebellar interpositus nucleus have been shown to prevent acquisition and abolish retention of the conditioned eyelid response on the side ipsilateral to the lesions without affecting conditioned responding (CR) on the contralateral side. Also, recording studies involving the interpositus nucleus have consistently revealed patterns of neuronal discharge that predict execution of the CR. The lesion and recording studies have generally been cited as evidence that plasticity in the cerebellum is critically involved in the learning and memory of classically conditioned responses. This interpretation was recently challenged by Welsh and Harvey (1989a), who claimed that cerebellar lesions simply produced a performance deficit and speculated that the role of the cerebellum was not in learning and memory processes associated with the CR but only in performance of the eye blink response. Presented here are three experiments that provide additional strong evidence for a critical role of the cerebellum in the learning and memory of the Pavlovian CR. These experiments include (1) demonstrations of complete and permanent CR abolition after appropriate interpositus lesions, (2) a failure to find systematic or persisting decrements in the unconditioned response amplitude (i.e., the eye blink reflex) after appropriate interpositus lesion, and (3) observations of differential effects on the CR and unconditioned response after lesions were placed in populations of motoneurons responsible for executing the eye blink response. These data are discussed in the context of performance versus learning issues; evidence presented here rules out the possibility that interpositus lesion abolition of the eye blink CR is simply due to lesion effects on performance.

Animals↗