The functional parcellation of the motor thalamus of primates has suffered from serious historical and technical drawbacks, which have led to extreme confusion. This is a problem when thalamic stereotaxy is again being use clinically. The cause usually imputed is the historical conflict between two main schools, the Vogt and the 'Anglo-American' (Michigan), which used different nomenclatures. In fact, the reasons are more profound and serious. A combination of them led to: an archaic, rigid conception of the 'thalamic nucleus'; overexploitation of cytoarchitectonic technique, comparative anatomy and cortical connections; underexploitation of subcortical afferent territories; recent misuse of these territories; hesitations in the use of the VA-VL system; and opposition between ventral ('relay') and dorsal ('associative') 'nuclei'. Previous and current parcellations and nomenclatures for the lateral region finally appeared inappropriate. Before presenting a new parcellation and nomenclature for the lateral region, we explain why we did not adopt one of most common or of recently proposed nomenclatures, and were led to make our own. This is established according to rational and historically grounded rules. Precise definition of thalamic elements is provided. A thalamic 'region' is a gross topographic division corresponding to the former nuclei. A 'territory' is defined as the cerebral space filled by afferent endings from one source. When having a distinct topography in a region, a given territory makes a 'subregion'. For each of the studied 'motor' territories a review was made of its known cortical projections. The thalamic space where neurons project to a given cortical target constitutes a 'source space'. Topographical comparison of the sources spaces with territories reveals that there is often no coincidence between different (afferent or efferent) neuronal set spaces. It appears that source spaces are coincident in the pallidal and nigral territories but not in the cerebellar territory where two topographically distinct source spaces could be distinguished. A 'thalamic nucleus' is defined as the intersection of a thalamocortical source space with one territory. A rapid review of the general anatomy of the diencephalon is made. The ('dorsal') thalamus is divided into 'allo-' and 'isothalamus', the latter with 'bushy' and 'microneurons'. The lateral region is isothalamic. The 'motor thalamus' makes the anterior part of the lateral region. The present work aims to analyse the functional anatomy of the 'motor thalamus' by using precise topography and three-dimensional analyses of the subcortical territories receiving from the cerebellar nuclei (part II), the medial nucleus of the pallidum (part III) and the pars reticulata and mixta of the substantia nigra (part IV). Large injections were used to obtain the maximal extent of each territory. A major deficiency of previous studies was inadequate catography. Reliance on ventricular (CA-CP) lan
Lithium has been hypothesised to exert its therapeutic effects in the treatment of bipolar disorder by attenuating phosphatidylinositol (PI) cell signalling pathways that are presumably hyperactive in this disorder. More specifically, lithium has been proposed to inhibit inositol monophosphatase (IMPase) thereby causing a depletion of intracellular inositol which results in a reduction in the synthesis of the PI required to sustain this signalling pathway. In the present article this 'inositol depletion' hypothesis will be reviewed and pathological, pharmacodynamic, developmental and anatomical aspects of IMPase as well as inhibitors of this enzyme will be described.
Recent studies have demonstrated that neuropeptide expression in forebrain neurons is responsive to changes in physiological activity. This is particularly true in the hippocampus where the expression of various neuropeptides has been reported to change in distinct neuronal populations in response to seizure activity. The aim of this work is to review and integrated the information on the pathological changes and functional modifications in neuropeptide systems of the hippocampal formation in kindling and other models of limbic epilepsy. This will be done by presenting a study in which we investigated the changes in the expression of somatostatin, neuropeptide Y (NPY), neurokinin B (NKB) and cholecystokinin-octapeptide (CCK) in the rat hippocampal principal neurons during and after kindling of the hippocampus using immunocytochemistry and in situ hybridization analysis of mRNA. NPY-IR was transiently expressed in the granule cells/mossy fibres after the preconvulsive stage 2 and 2 days but not 1 week after three consecutive tonic-clonic seizures (stage 5). A more pronounced increase was observed in NKB-IR lasting 1 week after kindling acquisition. Only the NKB mRNA expression was enhanced in granule cells at these intervals. At stages 2 and 5, somatostatin- and NPY-IR and their mRNA levels were markedly increased in interneurons in the deep hilus and in the polymorphic cell layer and their presumed projections to the outer molecular layer of the dentate gyrus. NKB- and CCK-IR and their mRNAs were highly expressed in basket cells at both stages of kindling. Their IR was increased in the inner molecular layer of the dentate gyrus in the ventral hippocampus. Peptide-containing neurons in the hilus appeared well preserved in spite of a reduction of Nissl stained cells by 24 % in the stimulated and contralateral hippocampus at stage 5. In the hippocampus proper, somatostatin and NPY-IR were enhanced in the stratum lacunosum molecular while CCK-IR fibres and its mRNA were particularly expressed in the pyramidal cell layer. The number of Somatostatin-, NKB- and CCK-IR cells was increased in the subiculum. The intensity of these changes was similar 2 days after stages 2 or 5 of kindling. Less pronounced effects were observed 1 week after kindling completion. These results, in the frame of the literature data, suggest that lasting functional changes occur in distinct neuropeptide-containing neurons during limbic epileptogenesis. This may have profound effects on synaptic transmission and contribute to modulate hippocampal excitability.
Aromatase cytochrome P45 (P450AROM) enzyme activity catalyzes the conversion of androgens to estrogens in specific brains areas. During central nervous system development local estrogen formation influences the sexual differentiation of neural structures (i.e., by increasing neurite growth and establishing neural circuitry) and modulates neuroendocrine/reproductive functions and sexual behavior. More than 20 years ago, in 1970, Naftolin et al. provided preliminary direct evidence for the aromatization of androgens by central neuroendocrine tissues. This work created the foundation for the brain aromatase hypothesis. A review of past and recent data reveals the importance of brain aromatase in the development and function of the central nervous system. This review re-examines the aromatase hypothesis in light of recent data and a theoretical proposal is presented in reference to the aromatase mechanism. The metabolic pathway of androgen metabolism by the aromatase cytochrome P450 pathway, cell type, distribution, developmental profile, and regulation of brain aromatase is also presented. The complex nature of brain aromatase is exemplified by recent molecular biology studies examining the expression of aromatase cytochrome P450 during prenatal/postnatal development. Data derived from these studies provide insight into the regulation of the brain aromatase cytochrome P450 gene and suggest an additional level of control for the expression of brain aromatase. These findings present evidence for the utilization of alternative promoter(s) in man and rodents in driving aromatase gene expression in brain. It is clear that molecular mechanism(s) account for the diverse expression of aromatase in different neural tissue sites and during various physiological states or developmental periods. Therefore, further study is necessary in order to understand the significance of the regulation of local estrogen biosynthesis by the aromatase cytochrome P450 gene during prenatal and postnatal development due to the dramatic impact these estrogen molecules have on neural development and their influence on reproductive function and behavior.