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Peter J Morgane

Publications and source records attributed to Peter J Morgane.

4 recordsLinked to original sources

The limbic brain: continuing resolution.

This paper presents an overview of the limbic brain and its distributed sub-systems. The extent of the limbic system has expanded in recent years. Among the brain areas that we now argue should be included in the extended limbic system are the medial prefrontal cortex, the insular cortex as well as the lower brainstem and spinal cord. In addition the limbic forebrain and limbic midbrain may be divided into medial and lateral divisions both anatomically and physiologically. This serves as an introduction to the papers that follow.

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A review of systems and networks of the limbic forebrain/limbic midbrain.

Evolutionarily older brain systems, such as the limbic system, appear to serve fundamental aspects of emotional processing and provide relevant and motivational information for phylogenetically more recent brain systems to regulate complex behaviors. Overall, overt behavior is, in part, determined by the interactions of multiple learning and memory systems, some seemingly complementary and some actually competitive. An understanding of limbic system function in emotion and motivation requires that these subsystems be recognized and characterized as extended components of a distributed limbic network. Behavioral neuroscientists face the challenge of teasing apart the contributions of multiple overlapping neuronal systems in order to begin to elucidate the neural mechanisms of the limbic system and their contributions to behavior. One major consideration is to bring together conceptually the functions of individual components of the limbic forebrain and the related limbic midbrain systems. For example, in the rat the heterogeneous regions of the prefrontal cortex (e.g., prelimbic, anterior cingulate, subgenual cortices and orbito-frontal areas) make distinct contributions to emotional and motivational influences on behavior and each needs consideration in its own right. Major interacting structures of the limbic system include the prefrontal cortex, cingulate cortex, amygdaloid nuclear complex, limbic thalamus, hippocampal formation, nucleus accumbens (limbic striatum), anterior hypothalamus, ventral tegmental area and midbrain raphe nuclei; the latter comprising largely serotonergic components of the limbic midbrain system projecting to the forebrain. The posterior limbic midbrain complex comprising the stria medullaris, central gray and dorsal and ventral nuclei of Gudden are also key elements in the limbic midbrain. Some of these formations will be discussed in terms of the neurochemical connectivity between them. We put forward a systems approach in order to build a network model of the limbic forebrain/limbic midbrain system, and the interactions of its major components. In this regard, it is important to keep in mind that the limbic system is both an anatomical entity as well as a physiological concept. We have considered this issue in detail in the introduction to this review. The components of these systems have usually been considered as functional units or 'centers' rather than being components of a larger, interacting, and distributed functional system. In that context, we are oriented toward considerations of distributed neural systems themselves as functional entities in the brain.

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Modulation of 5-HT release in the hippocampus of 30-day-old rats exposed in utero to protein malnutrition.

Previous in vivo microdialysis studies have shown increased spontaneous release of 5-HT in the hippocampus of adult behaving rats exposed to prenatal protein malnutrition. Furthermore, behavioral studies have shown that adolescent rats (PD30) that have been prenatally protein malnourished demonstrate an increased sensitivity to the benzodiazepine chlordiazepoxide (CDP). Given this altered sensitivity to benzodiazepines in adolescent malnourished rats, the present study was designed to test the hypothesis that the increased release of 5-HT in the hippocampus is present in adolescent rats and that this release is modulated by CDP. An altered release of 5-HT at PD30 would suggest an early developmental change associated with prenatal malnutrition. PD30 rats were implanted with microdialysis probes into the dorsal hippocampus and 5-HT release was monitored before and after administration of CDP. As previously reported in adult rats, release of 5-HT was significantly elevated in the dorsal hippocampus of PD30 rats as compared to well-nourished 30-day-old controls. Administration of CDP did not affect the release of 5-HT from the hippocampal formation of well-nourished rats but significantly decreased the elevated release of 5-HT in the malnourished rats. Following CDP, 5-HT release in the malnourished rats was at the same levels as release in well-nourished animals. Benzodiazepines have been reported to decrease extracellular 5-HT in stressed rats but not in unstressed rats. Thus, the elevated 5-HT release in the hippocampus in rats exposed to prenatal protein malnutrition may be associated with an increased response to stress. These data support other data that prenatal protein malnutrition alters the response to stressful stimuli possibly through changes in the GABAergic and/or serotonergic systems.

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Effects of prenatal protein malnutrition on the hippocampal formation.

In this review we have assessed the effects of prenatal protein malnutrition on the hippocampal formation of the developing brain. In investigating this insult in the hippocampal neuronal model we have concentrated on aspects of enhanced inhibition we have shown in our earlier studies. Since this involves particular attention to the GABAergic interneurons we have examined the complex interneuronal networks of the hippocampal formation and their neurotransmitter afferent inputs, particularly the serotonergic system from the midbrain raphé nuclei. A variety of combinations of specialized interneurons are discussed in terms of how malnutrition insults perturb function in these inhibitory and disinhibitory networks. Pathological enhancement of inhibition manifests itself by diminished plasticity, alterations in theta activity and deficits in long-term learning behaviors. Long-term inhibition in select GABA interneuron systems may form a major derangement seen following prenatal protein malnutrition. The focus of this study is to relate enhanced inhibition to the several forms of inhibitory systems present in the hippocampal formation and develop hypotheses as to the primary derangements that may account for pathological inhibition in prenatal malnutrition.

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