PubMed · 2440768
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A Gorio. Spreading depression: metabolic and ionic implications.. https://pubmed.ncbi.nlm.nih.gov/2440768/
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SCHIZOPHRENIA: The long-standing dopaminergic hypothesis is based on well-established findings, mainly related to a dysfunction of the mesolimbic C2 and D3 receptors, negative signs of prefrontal hypodopaminergia concerning the D2 and D4 receptors. Immune disorders are also involved as well as a possible neurodevelopmental component. Finally genetic factors play an important role. DEPRESSIVE STATES: Three monoaminergic systems appear to be implicated: the catecholaminergic, serotaminergic and homovanilic systems. It is not known whether the disorder of the serotaminergic system results from pre-existing fragilization or a symptom-related modification. HYPOTHESES CONCERNING DEPRESSION: According to the chronobiology hypothesis, certain biological rhythms (cortisol, temperature, perhaps melatonin) are desynchronized, a disequilibrium which disappears after cure. The fragilization hypothesis is based on the progressive development of a stress-related pathological organization in the hippocampo-hypothalamo-adrenal axis. PERSPECTIVES: The development of new psychotropes remains a challenge to meet the unsatisfied demands in psychiatrics. Drugs with rapid action and minimal side effects are needed.
In our series of projects for accumulating sequence information on the coding sequences of unidentified human genes, we have newly determined the sequences of 100 cDNA clones from a set of size-fractionated human brain cDNA libraries, and predicted the coding sequences of the corresponding genes, named KIAA0711 to KIAA0810. These cDNA clones were selected according to their coding potentials of large proteins (50 kDa and more) in vitro. The average sizes of the inserts and corresponding open reading frames were 4.3 kb and 2.6 kb (869 amino acid residues), respectively. Sequence analyses against the public databases indicated that the predicted coding sequences of 78 genes were similar to those of known genes, 64% of which (50 genes) were categorized as proteins functionally related to cell signaling/communication, cell structure/motility and nucleic acid management. As additional information concerning genes characterized in this study, the chromosomal locations of the clones were determined by using human-rodent hybrid panels and the expression profiles among 10 human tissues were examined by reverse transcription-coupled polymerase chain reaction which was substantially improved by enzyme-linked immunosorbent assay.
Structural plasticity of nerve cells is a requirement for activity-dependent changes in the brain. The growth-associated protein GAP-43 is thought to be one determinant of such plasticity, although the molecular mechanism by which it mediates dynamic structural alterations at the synapse is not known. GAP-43 is bound by calmodulin when Ca2+ levels are low, and releases the calmodulin when Ca2+ levels rise, suggesting that calmodulin may act as a negative regulator of GAP-43 during periods of low activity in the neurons. To identify the function of GAP-43 during activity-dependent increases in Ca2+ levels, when it is not bound to calmodulin, we sought proteins with which GAP-43 interacts in the presence of Ca2+. We show here that rabaptin-5, an effector of the small GTPase Rab5 that mediates membrane fusion in endocytosis, is one such protein. We demonstrate that GAP-43 regulates endocytosis and synaptic vesicle recycling. Modulation of endocytosis by GAP-43, in association with rabaptin-5, may constitute a common molecular mechanism by which GAP-43 regulates membrane dynamics during its known roles in activity-dependent neurotransmitter release and neurite outgrowth.