Pharmacological dissociation of memory: anisomycin, a protein synthesis inhibitor, and leupeptin, a protease inhibitor, block different learning tasks

Inhibition of protein synthesis by anisomycin for a short duration impairs memory of a one-trial inhibitory avoidance task in rats. Memory of escape conditioning involving eight trials is disrupted only if the duration of protein synthesis is prolonged by repeated injections. In marked contrast, olfactory memory of rats trained on two odor discriminations is not affected by anisomycin even if the duration of inhibition is prolonged and the number of trials is reduced to a minimum. In previous work, leupeptin, a thiol proteinase inhibitor, was shown to impair olfactory discrimination learning, but left inhibitory and avoidance conditioning intact. Together, these results provide a pharmacological double dissociation of memory, and suggest that the same chemistries, or mixtures of chemistries, may not be involved in all types of memory.     

Exploration and avoidance in rats with lesions in amygdala and piriform cortex

Lesions localized to specific areas of the amygdala and overlying cortex in rats produced differential effects in several behavioral tasks. Three different types of lesions were tested: central, basolateral, and cortex lateral to the amygdala. Lesions restricted to the central nucleus produced increased activity on all parameters studied in an open-field test, but the other two groups were not changed. In one-way active avoidance all three groups with lesions showed deficits. The most pronounced change was observed in the central group. All groups showed the same degree of retention loss, but in forced extinction of one-way active avoidance after retraining, the cortical and basolateral groups were most defective. A fear-reduction hypothesis is proposed for the central lesion. The basolateral and cortical areas may be more specifically involved in passive avoidance behavior.     

Differential indications for desipramine--results of a controlled multiclinical study]

The antidepressants desipramine and imipramine were compared within the framework of a multiclinical study performed under the conditions of a controlled clinical experiment. There has been found a time-different remission of affective symptoms, which was not detectable for the inhibition of drive. The tachythymoleptic action of desipramine is discussed with reference to these results. Evaluation of the possibility of controlling affects shows different ranges of activity of desipramine and imipramine, with desipramine influencing especially negative psychoenergetic symptoms in the area of drives and emotions and imipramine, restrictive symptoms in addition to differential phenomena of the psychomotor expression.     

Why child neuropsychiatry?]

The author gives a brief survey of the development of Child-Neuropsychiatry in the G.D.R. and subsequently gives reasons for the decision in favor of the unity of neurology and psychiatry as applied to children and juveniles, which is in contrast to developments in other countries. In addition to hygienic, economic, organizational, and medical considerations, this decision was also determined by the fact that a Child-Neuropsychiatrist must, in his practical work as a subspecialist, be able to head a multiprofessional team and, thus, help assure optimum development of a child's personality.     

Central deafness and subcortical motor aphasia

Clinical and autopsy studies were made on a right-handed man who had central deafness and subcortical motor aphasia, and the literature on central deafness and on subcortical motor aphasia was analyzed. Central deafness is due to bilateral destruction of the primary auditory cortex. It is sometimes difficult to distinguish from word deafness and from auditory agnosia, which are due to pathology in other parts of the temporal lobes. There is almost always some preserved hearing in central deafness, possibly from some auditory pathway other than the classical pathway. In this patient the subcortical motor aphasia was due to bilateral destruction of the motor cortex for the mouth and throat. In some other cases subcortical motor aphasia was due to the same pathology that usually causes Broca's aphasia; in these cases the unexpected preservation of writing was perhaps related to some difference in how language functions were organized in the brain.     

Production deficits in aphasia: A voice-onset time analysis

An experimental study was conducted to examine phonetic and phonemic deficits in the speech production of aphasics. Subjects included four Broca's aphasics, four Conduction aphasics, five Wernicke's aphasics, one nonaphasic dysarthric patient, and four normal controls. The subjects read a list of words containing word-initial stop consonants which were subsequently measured acoustically for voice-onset time. The results showed that Broca's aphasics exhibit a more severe production disorder than Conduction aphasics who in turn exhibit a more severe disorder than Wernicke's aphasics, in accord with clinical observations. In addition, although Broca's aphasics produced both phonetic and phonemic errors, the results showed that they have a pervasive phonetic disorder which affects their correct target productions as well as the total number of phonetic errors produced. This deficit however seems to be a speech deficit rather than a low-level motor control problem. In contrast, the Wernicke's aphasics show a deficit characterized by isolated phonemic mistargeting errors. Finally, the pattern of productions for the Conduction aphasics indicates that some patients show a predominantly phonetic disorder similar to the Broca's aphasics and others show predominantly a phonemic disorder similar to the Wernicke's aphasics.