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M S Oitzl

Publications and source records attributed to M S Oitzl.

57 records · Page 4Linked to original sources

Electroencephalographic spreading depression and concomitant behavioral changes induced by intrahippocampal injections of ACTH1-24 and D-Ala2-Met-enkephalinamide in the rat.

ACTH1-24 (0.5 or 10 micrograms = 0.17 or 3.45 nmol) and D-Ala2-Met-enkephalinamide (DAME; 10 micrograms = 17.05 nmol) were injected unilaterally into the hippocampus of freely moving rats to examine their effects on EEG activity, DC potentials and behavior. In 85% of the rats DAME elicited spreading depression (SD) with epileptiform discharges preceding and following the wave of SD. The following behavioral changes were recorded. DAME- and KCl-induced SD were accompanied by an increase in locomotor activity and wet-dog shaking behavior, which occurred only during the period of SD. After a wave of SD induced by DAME a biphasic pattern of activity, consisting of an initial depression in locomotion followed by hyperactivity, appeared in 59% of the rats. ACTH1-24 elicited SD in 13% of the rats tested. Neither the dosage of ACTH1-24 nor the strain of rats influenced the occurrence of SD and the incidence of ACTH-induced grooming behavior. SD induced by KCl also resulted in excessive grooming comparable to that induced by ACTH1-24. In the case of KCl-induced SD, grooming began directly after the injection of KCl and was frequently interrupted by short periods of locomotion. ACTH-induced grooming had a later onset and episodes of stretching and yawning were observed. It can be concluded that the behavioral effects of the injection of DAME are unspecific responses to SD and seizure activity. However, ACTH-induced grooming is not solely a byproduct of SD, since it occurred also in the absence of SD.

Adrenocorticotropic Hormone↗

Spreading depression induced by microinjection of enkephalins into the hippocampus and neocortex.

The opioid peptides Leu-enkephalin, Met-enkephalin and D-Ala2-Met-enkephalinamide were injected at various concentrations into the neocortex and hippocampus of rats to examine their effects on EEG activity and DC potentials. All three compounds were found to elicit spreading depression (SD) in both structures. Higher doses of Met-enkephalin were required to elicit SD as well as seizure activity. In the hippocampus the wave of SD was frequently preceded by seizure activity which was antagonized by naloxone pretreatment (40 mg/kg i.p.). Naloxone also prevented Leu-enkephalin-induced SD in the neocortex (but not in the hippocampus) and Met-enkephalin-induced SD in the hippocampus (but not in the neocortex). It failed to block SD elicited by D-Ala2-Met-enkephalinamide in both structures. Some of the various reported behavioral effects of intracranial injections of enkephalins could be artefacts of hippocampal and/or cortical spreading depression.

Animals↗

The relationship between reinforcement and memory: parallels in the rewarding and mnemonic effects of the neuropeptide substance P.

A theory of reinforcement is presented which accounts for the backward action of a reinforcer on operant behavior in terms of its effect on memory traces left by the operant. Several possible ways in which a reinforcer could strengthen the probability of recurrence of an operant are discussed. Predictions from the model regarding general memory-promoting effects of reinforcers presented posttrial in various learning paradigms are outlined. The theory also predicts a parallelism in reinforcing and memory-promoting effects of stimuli, including drugs. The second part of the chapter outlines experiments investigating memory modulating and reinforcing effects of the neuropeptide substance P. In general, injection of SP is positively reinforcing when injected into parts of the brain where it has been shown to facilitate learning. Peripheral injection of SP is also reinforcing at the dose known to promote passive avoidance learning when presented posttrial.

Amino Acid Sequence↗