Parallel nature of hippocampal synaptic plasticity.

This study demonstrates that the mechanisms involved in the production of long-term potentiation (LTP) in the hippocampus appear to be independent of those which generate shorter-lasting plasticity, but that both processes are activated concurrently following an LTP-inducing stimulus. Adult male Sprague-Dawley rats were anesthetized using either pentobarbital or secobarbital to record extracellular field potentials from the hippocampal CA1 pyramidal cell layer in response to stimulation of commissural afferents. Plasticity was generated by the delivery of a five-pulse patterned stimulus train, consisting of one priming pulse followed 170 milliseconds later by a burst of four pulses at 200 Hz. While similar LTP was observed in both groups, short-term plasticity was absent in the secobarbital-anesthetized animals. This result suggests that different plasticity mechanisms in the hippocampus are activated in parallel by the triggering stimulus.

Increased responsiveness of hippocampal pyramidal neurons to nicotine in aged, learning-impaired rats.

The effect of aging upon the responsiveness of hippocampal CA1 pyramidal neurons to nicotine was investigated using electrophysiological techniques in male Fischer 344 rats. Prior to electrophysiological recording, animals were behaviorally tested using the Morris water maze. All 3-6 and 18-21 month rats displayed rapid place learning in this task, while none of the 27-30 month animals learned within the 5-day test period. By contrast, rats of all age groups were able to learn a cue version of the water maze task. Following behavioral testing, the animals were anesthetized with sodium pentobarbital for acute recording. Nicotine was locally applied to electrophysiologically identified CA1 pyramidal neurons using pressure microejection from two-barreled glass microelectrodes. For each neuron, a dose of nicotine was found which elicited a 300-400% increase in basal firing rate. These data were used to construct cumulative dose response curves for populations of neurons tested in 3-6-, 18-21-, and 27-30-month-old animals. An age-related increase in the responsiveness of CA1 pyramidal neurons to locally applied nicotine was observed. The results of this study suggest that an increase in hippocampal CA1 pyramidal cell responsiveness to nicotine could be related to the impaired place learning ability seen with aging.

Modulation of hippocampal primed burst potentiation by anesthesia.

This study demonstrates that the anesthetics urethane and pentobarbital differentially affect a low threshold form of long-lasting synaptic plasticity, termed primed burst (PB) potentiation, in the CA1 area of rat hippocampus. PB potentiation was generated by the delivery of a 5-pulse patterned stimulus train, consisting of one priming pulse followed 170 ms later by a burst of 4 pulses at 200 Hz. PB potentiation could not be reliably generated in urethane-anesthetized rats unless stimulus currents were raised to 150% of baseline levels during the stimulus train. In pentobarbital-anesthetized rats, PB potentiation could always be evoked at baseline stimulus intensities. Differences between the anesthetics which could contribute to their varying effects upon PB potentiation are discussed.

Adrenalectomy reduces the threshold for hippocampal primed burst potentiation in the anesthetized rat.

Previously we demonstrated that the threshold for inducing hippocampal long-term potentiation (LTP) was reduced when the pattern of electrical stimulation mimicked physiological activity. This form of LTP, termed primed burst (PB) potentiation, is blocked by stress. In the present study, we tested the possibility that adrenal hormones contribute to the stress-related inhibition of PB potentiation. Our primary finding is that the amount of stimulation current necessary to induce PB potentiation was lower in adrenalectomized rats than in controls. This finding indicates that adrenal hormones exert an inhibitory influence on the induction of physiological plasticity in the hippocampus.