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Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 307 records · Page 17Linked to original sources
PubMed1983

Further studies of the cytopathic effect in tissue cultures inoculated with CSF from patients with schizophrenia and other nervous system diseases.

Tissue cultures were inoculated with CSF from patients with schizophrenia and some other psychiatric and neurological illnesses. The CPE was readily seen in all 13 strains of human skin fibroblasts examined but could not be serially passaged. The results of retesting many specimens, either by the same worker or under full double blind conditions, usually agreed and thus indicate that the CPE was due to the CSF and not to non specific changes in the cultures. CPE was seen in cultures in which mycoplasmas could not be detected. Degenerated cultures show polymorphous nuclei with condensed nuclear chromatin and enlarged mitochondria with few cristae but virus particles were not identified. The physical properties of the agent in the CSF that induced the CPE were the same as those reported earlier for CSF from schizophrenic patients.

Adult↗
PubMed1982

Behavioural and biochemical effects of chronic amphetamine treatment in the vervet monkey.

Five vervet monkeys were administered increasing doses (4--12 mg/kg/day) of d-amphetamine over a period of 35 days. Three phases od behavioural change were discerned: phase 1 during which animals exhibited repetitive stereotyped action sequences with rapid head movements, occasional abnormal grooming, picking at the cage, hand-staring and snatching; phase 2 in which behaviour became progressively more restricted and animals became markedly unresponsive to auditory, visual and tactile stimuli; phase 3 was characterised by the abrupt development of gross over-responsiveness to environmental stimuli, ataxia and tremor. At post-mortem, by comparison with controls, amphetamine-treated monkeys showed marked depletions of the monoamines dopamine (DA), noradrenaline (NA) and serotonin (5-HT) in corpus striatum and cerebral cortex and reductions in the activities of tyrosine hydroxylase and dopa decarboxylase in striatum. Turnover of these monoamines, assessed by high-performance liquid chromatography determinations of their respective metabolites, was also reduced. These findings are interpreted as evidence of monoamine neurone destruction, most severely in the case of DA neurones. Though there was a non-significant reduction in 3H-spiperone binding (reaching almost 50% in nucleus accumbens), numbers of receptors for the monoamines nA and 5-HT were not significantly changed, and the activities of the enzymes choline acetyltransferase and glutamine decarboxylase were similar in experimental and control animals. The contrast of these findings with those seen in post-mortem brains in schizophrenia is discussed.

Animals↗
PubMed1982

Distribution of neuropeptides in the limbic system of the rat: the amygdaloid complex.

The distribution of six neuropeptides (vasoactive intestinal polypeptide, cholecystokinin octapeptide, substance P, neurotensin, methionine-enkephalin and somatostatin) has been mapped in the amygdala using immunocytochemical methods. Cell bodies containing each peptide showed a differential distribution throughout the various subnuclei. Large numbers of vasoactive intestinal polypeptide and cholecystokinin-octapeptide-containing cell bodies were located in the lateral and cortical nuclei respectively, neurotensin-and methionine enkephalin-containing cell bodies in the central nucleus, and substance P-containing cell bodies primarily in the medial nucleus. Somatostatin-containing cell bodies were found in all nuclei. Neuropeptide-containing fibres were also differentially distributed. Substance P and cholecystokinin fibres formed dense plexuses in the medial nucleus whilst the greatest concentration of vasoactive intestinal polypeptide, neurotensin and methionine enkephalin fibres were seen in the central nucleus. Close observation of serial sections showed that all the neuropeptides studied had extensive intra-amygdaloid pathways and connections with other brain areas. The central nucleus and stria terminalis have particular importance in the organisation of peptides within the amygdala. The central nucleus acts as a focus for a number of converging/diverging peptide pathways and incoming catecholaminergic afferents. The stria terminalis contains all six peptides and represents the major efferent peptidergic system. The amygdala is thought to control a number of endocrine responses and to regulate complex behavioural functions. The abundance of neuropeptides within the amygdala and their complex pattern imply that they may act to regulate endocrine responses to external events (e.g. stress) or alter emotional tone functions thought to be controlled by the amygdala.

Amygdala↗
PubMed1982

Gonadotropin secretion abnormalities in chronic schizophrenia.

LH, FSH, PRL and testosterone were estimated by radioimmunoassay in serial venous samples from 20 male chronic schizophrenic patients, 17 age-matched controls, 3 patients in remission from acute schizophrenia, and in single samples from age-sex matched populations. LH and FSH, but not testosterone or PRL, were significantly reduced in patients with chronic schizophrenia. There was an associated reduction in the frequency, but not amplitude, of LH secretory episodes in patients with chronic schizophrenia. No abnormalities of LH secretion were detected in those patients in remission from acute schizophrenia. Fourteen of the chronic schizophrenic patients were retested at a later date with similar results, except in the case of the few patients who had been started on neuroleptic medication. Some relationships were established between hormonal secretion and the clinical features of these patients. The possible significance of these findings is discussed in the context of the complex control of gonadotropin secretion from the anterior pituitary and the natural history and nature of chronic schizophrenia.

Adult↗
PubMed1982

Skin conductance habituation during acute episodes of schizophrenia: qualitative differences from anxious and depressed patients.

Skin conductance habituation was measured in schizophrenic patients (N = 41) during an acute episode and compared with neurotic patients (N = 86) who were either predominantly anxious or predominantly depressed. All patients were tested before the onset of drug treatment. Between the 14th and 15th tone of the 17 tone simple habituation series a loud 'dishabituating' tone was inserted. In terms of traditional measures based on response frequency, non-habituation was most frequent in the anxious patients and least frequent in the depressed patients, with schizophrenic patients being intermediate. However, in terms of response amplitude the schizophrenic patients showed significantly faster habituation than either neurotic group. This paradox seems to be a consequence of the frequency of spontaneous fluctuations which was highly related to habituation status in the schizophrenic group, but not in the neurotic groups. When habituation was defined in terms of response amplitudes falling below spontaneous fluctuation amplitudes (rather than zero) the schizophrenic group showed the lowest frequency of non-habituation. None of the groups showed any evidence of dishabituation after the loud tone, but the schizophrenics showed a significantly smaller response to the loud tone itself. Following Groves & Thompson (1970), this is interpreted as showing that the loud tone induced a greater response because of its perceived difference from the other tones rather than a sensitization effect because of its loudness. In these terms the schizophrenic patients showed greater response generalization than the neurotic patients.

Acute Disease↗
PubMed1982

Reduced nocturnal melatonin secretion in chronic schizophrenia: relationship to body weight.

Melatonin was estimated by RIA in samples taken at 24.00 h and 08.00 h from twenty-one male chronic schizophrenics and twelve age--sex matched controls and subsequently in more frequent nocturnal samples from nine of the chronic schizophrenics. The 24.00 h melatonin level and the 24.00/08.00 h melatonin ratio were significantly reduced in the chronic schizophrenic patients. Similar results, with no evidence of subsidiary peaks of melatonin secretion, were obtained in those patients who were retested. No relationships between melatonin secretion and age or anterior pituitary hormone secretion were demonstrated, but an effect of body weight was noted which accounted, in part, for the difference between schizophrenics and controls. These results suggest that the low levels of melatonin noted in studies on depressed patients may not be specific and that body weight must be controlled in subsequent studies of melatonin secretion in patients with psychiatric disease.

Adult↗
PubMed1982

Familial cerebral amyloidosis and spongiform encephalopathy.

Clinical and neuropathological investigations are presented of the "W" family in which there is a dominant inheritance of slowly progressive cerebellar ataxia and dementia. The disease is of insidious onset and its average duration more than 4 years. Pathological findings included amyloid deposition in cerebellar and cerebral tissue; vascular amyloid in one case; and spongiform encephalopathy and astrocytic hyperplasia typical of Creutzfeldt-Jakob disease. Neuritic plaques of the senile (Alzheimer) type were present to a lesser extent. This study confirms the familial association between cerebral amyloidosis and spongiform encephalopathy.

Adult↗
PubMed1982

Abnormal involuntary movements in schizophrenia: are they related to the disease process or its treatment? Are they associated with changes in dopamine receptors?

Abnormal involuntary movements indistinguishable from those now described as tardive dyskinesia were reported in schizophrenic patients by Kraepelin long before the introduction of neuroleptic drugs. Two large surveys of mental hospital patients including patients who had never received neuroleptics also revealed involuntary movements; indeed, the incidence was not substantially different from that in drug-treated patients. This fact casts doubt on the widely held assumption that these movements are persistent and irreversible effects of neuroleptic drugs. In an animal model of dyskinesia, abnormal movements were seen after administration of a phenothiazine and a thioxanthene but not after haloperidol. The syndrome appeared to be unrelated to dopamine receptor blockade or to changes in dopamine receptors. In postmortem striatal tissue from patients with schizophrenia, ligand binding to D-1 and D-2 dopamine receptors was not increased in patients who had been found to have abnormal involuntary movements in comparison with those who did not have such movements; as previously reported, binding to D-2 receptors was increased in patients with schizophrenia in comparison with controls. It is concluded that dyskinetic changes occur as a consequence of the process of schizophrenia and perhaps other diseases. Whether or not persistent and irreversible changes can be caused either in animals or humans by neuroleptic administration has yet to be clearly established. Whether they occur as a manifestation of the disease process or a consequence of drug administration, such dyskinesias are unassociated with changes in D-1 or D-2 receptors.

Adult↗
PubMed1981

Reduced dopamine-beta-hydroxylase activity in Alzheimer's disease.

The activity of the noradrenergic marker enzyme dopamine-beta-hydroxylase was measured in brains removed postmortem from control patients and patients with Alzheimer's disease. Enzyme activity was decreased in the frontal and temporal cortices and hippocampus in patients with Alzheimer's disease, but was within the normal range in patients with depression, multiinfarct dementia, and terminal coma.The decrease in enzyme activity in Alzheimer's disease may reflect an abnormality of cortical noradrenergic fibres in some patients with the disease.

Aged↗
PubMed1981

Tritiated LSD binding in frontal cortex in schizophrenia.

It has been reported that the binding of tritiated LSD (at 2 or 4 nm) to frontal cortex is reduced in schizophrenia, a finding that has been interpreted as a reduction in the number of serotonin receptors. The present study, however, reveals in a Scatchard analysis of tritiated LSD binding in frontal cortex in the brains of 13 schizophrenic patients that there was no decrease in binding by comparison with eight control brains. Quantities of neuroleptic remaining in the brain after death cannot be readily washed out and could have led to the previous report of reduced LSD binding. A decrease in affinity of LSD binding sites consistent with this possibility has been demonstrated in chlorpromazine-treated rats. In the brains of five patients who had probably been neuroleptic-free for the year before death, tritiated LSD binding was significantly increased. This result needs to be replicated in larger samples.

Antipsychotic Agents↗
PubMed1981

Effect of chronic amphetamine administration on central dopaminergic mechanisms in the vervet.

A biochemical study of central dopaminergic mechanisms was carried out in brain tissue from vervet monkeys who had been subjected to chronic amphetamine administration. The brain concentrations of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) were markedly reduced. Significant reductions were also observed in the activities of dopa-decarboxylase (DDC) and tyrosine hydroxylase (TH). A kinetic study of TH revealed a 60% reduction in maximum reaction velocity, consistent with destruction of DA neurones. However, homovanillic acid (HVA) concentrations were only moderately reduced, suggesting a nearly normal production of DA. Hence despite the large depletions in DA concentrations, high affinity binding of 3H-spiperone binding to striatal DA receptors was no different from controls. The results are discussed in relation to the amphetamine psychosis in humans.

3,4-Dihydroxyphenylacetic Acid↗