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J A Oler

Publications and source records attributed to J A Oler.

6 recordsLinked to original sources

Differential behavioral state-dependence in the burst properties of CA3 and CA1 neurons.

Brief bursts of fast high-frequency action potentials are a signature characteristic of CA3 and CA1 pyramidal neurons. Understanding the factors determining burst and single spiking is potentially significant for sensory representation, synaptic plasticity and epileptogenesis. A variety of models suggest distinct functional roles for burst discharge, and for specific characteristics of the burst in neural coding. However, little in vivo data demonstrate how often and under what conditions CA3 and CA1 actually exhibit burst and single spike discharges. The present study examined burst discharge and single spiking of CA3 and CA1 neurons across distinct behavioral states (awake-immobility and maze-running) in rats. In both CA3 and CA1 spike bursts accounted for less than 20% of all spike events. CA3 neurons exhibited more spikes per burst, greater spike frequency, larger amplitude spikes and more spike amplitude attenuation than CA1 neurons. A major finding of the present study is that the propensity of CA1 neurons to burst was affected by behavioral state, while the propensity of CA3 to burst was not. CA1 neurons exhibited fewer bursts during maze running compared with awake-immobility. In contrast, there were no differences in burst discharge of CA3 neurons. Neurons in both subregions exhibited smaller spike amplitude, fewer spikes per burst, longer inter-spike intervals and greater spike amplitude attenuation within a burst during awake-immobility compared with maze running. These findings demonstrate that the CA1 network is under greater behavioral state-dependent regulation than CA3. The present findings should inform both theoretic and computational models of CA3 and CA1 function.

Action Potentials↗

Hippocampal and amygdalar involvement in discriminatory place learning.

A conflict task was developed that simultaneously examines place aversion learning and fear-motivated context discrimination. The task superimposed Pavlovian discriminative fear conditioning on an appetitively motivated instrumental response (alternation). Rats were trained to alternate along a high-walled, diamond-shaped runway between two chambers for food. On half of the trials, a tone CS signaled the fact that a fixed section at the apex of the runway was electrified. Both the tone and the shock were turned on at the beginning of, and remained on for the duration of, each tone trial. A new trial was initiated at the time the animal entered the subsequent food chamber. Therefore, during a tone trial, in order to attain additional food reinforcement, the animal had to cross over the electrified region at the runway apex. Behavioral performance of rats with small lesions of the amygdala or dorsal hippocampus (DH) was compared with that of sham-operated controls. All groups displayed significant discriminative responding, hesitating more on tone trials while in areas of the runway adjacent to the shock region. Animals with lesions of the DH were similar to controls with respect to the tone-mediated discrimination, yet were delayed in the initial expression of a location-specific fear response. Conversely, amygdala lesions did not affect place learning; however, these animals were impaired in their suppression of the fear response following repeated unpaired trials.

Acoustic Stimulation↗

Age-related deficits in the ability to encode contextual change: a place cell analysis.

Aging is known to impair the formation of episodic memory, a process dependent upon the integrity of the hippocampal region. To investigate this issue, hippocampal place cells were recorded from middle-aged and old F-344 male rats while running on a "figure-8" track. The top and bottom arcs of the track were removed, converting it into a plus maze, and the animals were required to conduct a working memory task. Following this change in task, the arcs were replaced and the animals again ran the figure-8 task. Analysis of place fields across the recording session demonstrated that both middle-aged and old rats had reliable representations of the figure-8 task. A comparison of place fields between different behavioral tasks (figure-8 and plus maze) demonstrated a change in the hippocampal representation of the environment in both age groups, despite the fact that the animals remained on the maze throughout the recording session. Notably, place cells in old animals were less affected by the change in task than those in middle-aged animals. The results suggest that hippocampal neurons reflect significant behavioral events within a given environment. Furthermore, the data indicate that age-related episodic memory deficits may result from decreased sensitivity of the hippocampal network to respond to meaningful changes in the environment.

Aging↗

Age-related deficits on the radial maze and in fear conditioning: hippocampal processing and consolidation.

Young adult, middle-aged, and old male F-344 rats were assessed for their hippocampal ability. This was accomplished by examining the animals on two different paradigms, each incorporating a simultaneous measure of hippocampal-dependent and -independent processing. The animals were fear conditioned and then tested for retention of the conditioning context and tone. This was followed by an 8-arm radial maze task which combined spatial working and cued reference memory elements. The two paradigms are compared in terms of task demands, potential confounds, and validity for aging studies. The results indicate that the performance of the animals on the two tasks is correlated. Age-related deficits limited to the hippocampal aspects of the above tasks were found, with no deficits found in the analogous but hippocampus-independent aspects of these tasks. The function of the hippocampus in incorporating new memories is time-related. Therefore, the possibility of age-related changes in consolidation was examined. It has previously been shown on the fear conditioning paradigm that the hippocampus is involved in retention of the aversive context for approximately 28 days. In the present study, an attempt was made to test the animals for retention of the conditioning context both early into the period of consolidation (10 days) and after consolidation should have been completed (52 days). The results indicate that, initially, the old animals show comparable retention to young rats. When examined later, young animals showed a stronger retention of the conditioning context than they had previously. The aged rats, however, did not seem to benefit from this additional period of time and in fact showed a decrease in retention of the conditioning context. The data are interpreted in terms of consolidation, alternative explanations of the data are presented, and suggestions are given for future research. Finally, the implications of such age-related changes in hippocampal consolidation on learning and memory are discussed.

Aging↗

Hippocampal dysfunction during aging I: deficits in memory consolidation.

Numerous ablation studies indicate a critical role for the hippocampal system in establishing or consolidating certain types of memory. Normal aging manifests by selective neurobiological changes in the hippocampal formation and on performance of tasks that require a functional hippocampus, including retention of contextual fear conditioning. To determine if impairments in the consolidation process contribute to memory dysfunction in aging, middle-aged and aged rats were fear conditioned and subsequently received dorsal hippocampal lesions or sham surgery after a 1, 7, 14, or 28-day interval. During retention tests, middle-aged rats exhibited a temporally graded retrograde amnesia of contextual fear conditioning, whereas aged rats manifested contextual memory impairments at all intervals. We postulate that the lack of consolidation in aged animals relates to previous findings of age-related changes in neuroanatomy and neurophysiological plasticity. The present findings suggest that impaired hippocampal consolidation contributes to age-related learning and memory deficits.

Aging↗