Adolescent transitions in reflexive and non-reflexive behavior: Review of fear conditioning and impulse control in rodent models.

Adolescence is a time of critical brain changes that pave the way for adult learning processes. However, the extent to which learning in adolescence is best characterized as a transitional linear progression from childhood to adulthood, or represents a period that differs from earlier and later developmental stages, remains unclear. Here we examine behavioral literature on associative fear conditioning and complex choice behavior with rodent models.

Adolescent and adult rats differ in the amnesic effects of acute ethanol in two hippocampus-dependent tasks: Trace and contextual fear conditioning.

Experience-produced deficits in trace conditioning and context conditioning have been useful tools for examining the role of the hippocampus in learning. It has also been suggested that learning in these tasks is especially vulnerable to neurotoxic effects of alcohol during key developmental periods such as adolescence. In five experiments we systematically examined the presence and source of age-dependent vulnerability to the memory-disrupting effects of acute ethanol in trace conditioning and contextual fear conditioning.

An animal model of fetal alcohol spectrum disorder: Trace conditioning as a window to inform memory deficits and intervention tactics.

Animal models of Fetal Alcohol Spectrum Disorders (FASD) afford the unique capacity to precisely control timing of alcohol exposure and alcohol exposure amounts in the developing animal. These models have powerfully informed neurophysiological alterations associated with fetal and perinatal alcohol. In two experiments presented here we expand use of the Pavlovian Trace Conditioning procedure to examine cognitive deficits and intervention strategies in a rat model of FASD.

Supplemental choline does not attenuate the effects of neonatal ethanol administration on habituation of the heart rate orienting response in rats.

Several studies using rodent subjects have now shown that extra dietary choline may prevent or even reverse the deleterious effects of pre- and early post-natal ethanol administration. Choline supplementation has been shown to attenuate many, although not all, of ethanol's effects on brain development and behavior. Our laboratory has consistently reported impaired habituation of the heart rate orienting response to a novel olfactory stimulus in animals exposed to ethanol on postnatal days (PD) 4-9.

Supplemental choline during the periweaning period protects against trace conditioning impairments attributable to post-training ethanol exposure in adolescent rats.

Supplemental choline during early stages of development can result in long-lasting improvements to memory function. In addition, pre- or postnatal choline has been shown to be protective against some of the adverse effects of early alcohol exposure. The present experiment examined whether supplemental choline given to rats would protect against the effects of posttraining alcohol administration on trace fear conditioning.

Deficits in trace fear conditioning induced by neonatal alcohol persist into adulthood in female rats.

The developing hippocampus is particularly vulnerable to the toxic effects of alcohol, and behavioral deficits on hippocampus-dependent tasks have been reported following neonatal alcohol exposure in rodents. Previously, we have found that trace fear conditioning (a hippocampus-dependent learning task) is disrupted in rats exposed to alcohol during postnatal days (PD) 4-9, although delay fear conditioning is not. The present study indicates that this impairment in trace fear conditioning, previously only measured during adolescence, persists into adulthood but only in females.

Adolescent nicotine exposure disrupts context conditioning in adulthood in rats.

Despite the prevalence of smoking among adolescents, few studies have assessed the effects of adolescent nicotine exposure on learning in adulthood. In particular, it remains unclear whether adolescent nicotine exposure has effects on hippocampus-dependent learning that persist into adulthood. The present experiment examined whether there were effects of adolescent nicotine exposure on context conditioning, a form of learning dependent on the integrity of the hippocampus, when tested during adulthood.

Deficits in trace fear conditioning in a rat model of fetal alcohol exposure: dose-response and timing effects.

In humans, prenatal alcohol exposure can result in significant impairments in several types of learning and memory, including declarative and spatial memory. Animal models have been useful for confirming that many of the observed effects are the result of alcohol exposure, and not secondary to poor maternal nutrition or adverse home environments. Wagner and Hunt (2006) reported that rats exposed to ethanol during the neonatal period (postnatal days [PDs] 4-9) exhibited impaired trace fear conditioning when trained as adolescents, but were unaffected in delay fear conditioning.

Persistent deficits in heart rate response habituation following neonatal binge ethanol exposure.

Background: We have previously shown that the rate of habituation of the heart rate orienting response to a novel odor in rats is negatively affected by neonatal ethanol exposure. Thus far, however, only young rats (16 days of age) have been tested. Given the persistence of attention and memory problems evident in humans exposed to ethanol in utero, the purpose of this experiment was to examine the longer-term consequences of ethanol exposure on response habituation.

Post-training ethanol disrupts trace conditioned fear in rats: effects of timing of ethanol, dose and trace interval duration.

Ethanol has complex effects on memory performance, although hippocampus-dependent memory may be especially vulnerable to disruption by acute ethanol intoxication occurring during or shortly after a training episode. In the present experiments, the effects of post-training ethanol on delay and trace fear conditioning were examined in adolescent rats. In Experiment 1, 30-day-old Sprague-Dawley rats were given delay or trace conditioning trials in which a 10s flashing light CS was paired with a 0.

Synapses, circuits, and the ontogeny of learning.

This article summarizes the proceedings of a symposium organized by Mark Stanton and Pamela Hunt and presented at the annual meeting of the International Society for Developmental Psychobiology. The purpose of the symposium was to review recent advances in neurobiological and developmental studies of fear and eyeblink conditioning with the hope of discovering how neural circuitry might inform the ontogenetic analyses of learning and memory, and vice versa. The presentations were: (1) Multiple Brain Regions Contribute to the Acquisition of Pavlovian Fear by Michael S.

Pharmacological dissociation of trace and long-delay fear conditioning in young rats.

In most studies comparing trace and delay conditioning, CS duration is kept constant across training conditions but the interstimulus interval (ISI), the time from CS onset to US onset, is confounded. In the infrequently used long-delay condition, however, ISI is kept constant across the trace and delay conditions but CS duration varies. A recent study reported that trace and long-delay fear conditioning have the same developmental trajectory, with both emerging later in development than standard-delay conditioning ().

The expression of fear-potentiated startle during development: integration of learning and response systems.

Relative to freezing, fear-potentiated startle (FPS) is developmentally delayed. Rats trained on Postnatal Day (PD) 18 expressed conditioned stimulus learning on PD 19 in freezing but not in FPS, whereas rats trained on PD 24 and tested on PD 25 expressed both freezing and FPS (Experiment 1). According to a neural maturation hypothesis, this delay results from functional immaturity of pathways mediating FPS.

Cholinergic modulation of trace conditioning trained in serial compound: A developmental analysis.

In four experiments the effects of serial compound conditioning on responding to a trace-conditioned CS were evaluated using a fear conditioning paradigm. The subjects were 18- and 25-day-old Sprague-Dawley rats, previously shown to exhibit little or no trace fear conditioning. Here, animals as young as 18 days of age were shown to be capable of trace conditioning between a visual CS1 and a shock US, provided the trace interval was filled with a non-target CS2 during serial conditioning trials (CS1-->CS2-->US).

Impaired trace fear conditioning following neonatal ethanol: reversal by choline.

Neonatal ethanol exposure in animals results in performance deficits on tests of hippocampus-dependent spatial memory, and recent studies have shown that extra dietary choline can ameliorate some of these impairments. In this experiment, rats were administered 5.25 g/kg ig ethanol per day or sham intubations on Postnatal Days (PD) 4-9 and choline (0.

Trace and long-delay fear conditioning in the developing rat.

In two experiments with rats, we examined the developmental emergence of conditioned freezing following trace and short-delay conditioning and also included a long-delay comparison group. In the short-delay and trace groups, a 10-sec conditioned stimulus (CS) was paired with shock; for the trace rats, a 10-sec trace interval followed CS termination. The long-delay groups received a 20-sec CS paired with shock, to equate for the longer interstimulus interval (ISI) in the trace group.

Neonatal treatment with a competitive NMDA antagonist results in response-specific disruption of conditioned fear in preweanling rats.

Rationale: The N-methyl-D-aspartate (NMDA) receptor has been implicated in processes of neurodevelopment, including cell proliferation, synaptogenesis, and apoptosis. Several studies have reported that administration of NMDA antagonists early in development can cause long-lasting changes in behavior. For example, Gould and Cameron [Behav Neurosci 111:49-56 (1997a)] have shown that a single injection of the competitive NMDA antagonist CGP 43487 on postnatal day (PD) 5 affected behavioral immobility in young rats exposed to the odor of a natural predator.

Postnatal ethanol exposure disrupts signal detection in adult rats.

Human prenatal ethanol exposure that occurs during a period of increased synaptogenesis known as the "brain growth spurt" has been associated with significant impairments in attention, learning, and memory. The present experiment assessed whether administration of ethanol during the brain growth spurt in the rat, which occurs shortly after birth, disrupts attentional performance. Rats were administered 5.

Early postnatal ethanol administration does not affect prepulse inhibition in rats.

Human prenatal ethanol exposure is associated with relatively widespread cognitive deficits but it is unclear whether general deficits in responsivity to sensory stimuli contribute to or underlie the deficits in later or more complex stages of information processing. The present experiment assessed the effects of early postnatal ethanol administration in rats on prepulse inhibition, with animals tested in adolescence (postnatal day (PD) 35) and early adulthood (PD 70). Animals were assigned to receive ethanol (5.