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Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 271 records · Page 15Linked to original sources
PubMed1984

An involvement of acetylcholine in object discrimination learning and memory in the marmoset.

Five marmosets (Callithrix jacchus) were tested, using a Wisconsin General Test Apparatus, on a series of junk object visual discrimination tasks, including new learning, 24-hr reversal and 24-hr retention. The effects of administering the cholinergic receptor blocking agent, scopolamine either just before or immediately after the new learning task, or just before the 24-hr reversal and retention tasks, were assessed. Results suggest that scopolamine impairs new learning and impairs the encoding of new information in long term memory. Some evidence of a mild retrieval deficit under scopolamine was also seen, while state-dependent effects were not apparent.

Acetylcholine↗
PubMed1984

The effects of intravenous diazepam and hyoscine upon recognition memory.

Diazepam and hyoscine are known to have amnesic effects when administered intravenously. Nevertheless, they achieve these effects by entirely different neurochemical mechanisms, and so the question arises whether they can be differentiated in terms of their effects upon different categories of encoding operations. Sixteen normal volunteers received intravenous administrations of diazepam, hyoscine, and saline following a double-blind procedure. Both drugs completely eliminated the subjects' ability to discriminate between successive lists of words in a test of recognition memory. Moreover, both drugs also impaired the subjects' ability to reject homophones or synonyms of presented words. Thus, both diazepam and hyoscine appeared to impair the use of list tags, phonemic coding, and semantic coding in storing individual stimulus items in long-term memory.

Adult↗
PubMed1984

Distribution of neuropeptides in the limbic system of the rat: the hippocampus.

The distribution of several neuropeptides (vasoactive intestinal polypeptide, cholecystokinin octapeptide, substance P, neurotensin, methionine-enkephalin and somatostatin) in the hippocampal formation has been studied with immunocytochemical techniques. Numerous vasoactive intestinal polypeptide, cholecystokinin-octapeptide and somatostatin-positive cell bodies were found within the hippocampus and subiculum. Neurotensin-positive cell bodies were found within the subiculum, but no substance P or methionine-enkephalin-containing cell bodies were seen in either hippocampus proper or subiculum. Vasoactive intestinal polypeptide and cholecystokinin-octapeptide-positive cell bodies were predominantly located in the stratum moleculare and stratum radiatum of CA 1-2 regions and dentate gyrus, whilst somatostatin-containing cell bodies were found mainly in the stratum oriens. Nerve fibres containing each of the six peptides were found within the hippocampus. Large numbers of vasoactive intestinal polypeptide, cholecystokinin-octapeptide and somatostatin fibres innervated the pyramidal and granule cell layers, with smaller numbers in the stratum radiatum and fewer still in the stratum moleculare and stratum oriens. Other than a moderately dense neurotensin-positive fibre plexus in the dorsal subiculum, fewer neurotensin, substance P and methionine-enkephalin fibres were present. However, when present, these three peptides had a distribution restricted to a region close to the pyramidal layer in the CA 2/3 region and to the stratum moleculare of the CA 1 region. Peptide-containing fibres were identified entering or leaving the hippocampus in three ways, via (i) the fornix (all six peptides), (ii) the dorsal subiculum (neurotensin-positive fibres projecting to the cingulate cortex: somatostatin, vasoactive intestinal polypeptide, and cholecystokinin-octapeptide present in fibres running between the dorsal subiculum and occipito-parietal cortex) and (iii) the ventral subiculum (vasoactive intestinal polypeptide, cholecystokinin-octapeptide and somatostatin in fibres running between entorhinal cortex and hippocampus, and all six peptides in fibres crossing the amygdalo-hippocampal border). These findings indicate a major distinction between those peptides (vasoactive intestinal polypeptide, cholecystokinin-octapeptide, somatostatin, neurotensin) which are found in cell bodies intrinsic to the hippocampal formation and those peptides (substance P, methionine-enkephalin) which are found only in hippocampal afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Serotonin receptor changes in dementia of the Alzheimer type.

Serotonin receptors were assessed in post-mortem brains of control and Alzheimer-type dementia (ATD) patients using ligand binding techniques. Differential losses of serotonin S1 and S2 receptors were present in neocortex, hippocampus, and amygdala of ATD patients, whereas no significant changes were observed in basal forebrain and basal ganglia. Losses of S1 receptors were significantly age-related in the ATD group, suggesting they occurred at a later stage of the disease process. Losses of S2 receptors were considerably greater (with a reduction to 35% of control in temporal cortex) and were not age-related in ATD. Significant correlations were observed within the ATD group between S2 receptor binding and somatostatin immunoreactivity in temporal and frontal cortices. Thus the loss of S2 receptors in ATD may be a relatively early change in the disease process, and may precede the changes in ascending serotonergic neurones.

Aged↗
PubMed1984

Herpes simplex virus and Alzheimer's disease: a search for virus DNA by spot hybridisation.

A sensitive hybridisation screening technique (spot hybridisation) was used to search post-mortem brain DNA extracts for herpes simplex I virus sequences in non-neurological controls, Alzheimer's disease cases and Herpes simplex virus infected mice. A reconstruction experiment showed that 0.1 herpes genome equivalents per cell could be detected in 100 micrograms tissue extracts. Although herpes sequences were readily detected in infected mice, none of the human brains examined could be shown to contain such sequences.

Alzheimer Disease↗
PubMed1984

Age disorientation in chronic schizophrenia is associated with global intellectual impairment.

From a population of long-stay patients with a diagnosis of schizophrenia according to the St Louis criteria, a group of 21 patients with 'age disorientation' was selected, and compared on a series of tests of intellect and learning capacity with a matched control group of 21 schizophrenic patients without this feature. The age-disorientated patients demonstrated substantial impairments on tests of orientation and general knowledge, associational learning, the 'famous personality' test, tests of vocabulary and aphasia, Raven's matrices, the digit-symbol substitution test and the mental test score. We conclude that profound 'organic-type' psychological deficits (global impairment of intellectual function associated with temporal disorientation) undoubtedly occur in chronic schizophrenia. The findings on the 'famous personality' test and the Peabody vocabulary test did not exclude the possibility that such impairment arises early in life, at a time preceding the onset of the illness which leads to hospital admission.

Chronic Disease↗
PubMed1984

Clinical effects of apomorphine in schizophrenia.

There have been reports that low doses of the dopamine-agonist apomorphine, which may inhibit dopamine neurotransmission, are of therapeutic benefit in schizophrenia. We conducted a placebo-controlled study of acute and chronic schizophrenics in which videotaped interviews were blindly rated. No specific therapeutic effect was demonstrated for apomorphine other than a reduction in anxiety in acute schizophrenics. Furthermore, there was no difference in the frequency of side-effects of apomorphine between schizophrenic patients and controls, and no specific effect of apomorphine on blink-rates. These findings emphasize the importance of placebo-controlled studies in schizophrenia research.

Acute Disease↗
PubMed1984

Hormonal effects of apomorphine in schizophrenia.

The hormonal effects of apomorphine, a direct-acting dopamine receptor agonist, in schizophrenic patients are of interest in view of the therapeutic efficacy of dopamine receptor antagonists. In this study, apomorphine (0.75 mg s.c.) and placebo were administered to unmedicated acute and chronic schizophrenics and controls. Apomorphine-induced prolactin suppression did not discriminate between the groups. However, an inverse relationship between basal prolactin levels and the severity of positive symptoms was detected in the patients with acute schizophrenia, consistent with a role for dopamine in the genesis of these symptoms. Growth hormone increments after apomorphine administration were blunted in the chronic schizophrenic patients, particularly those with 'negative' symptoms. It is argued that this blunting is not due to previous neuroleptic therapy and may represent evidence of structural change in the hypothalamus in this group of patients.

Acute Disease↗
PubMed1984

A re-evaluation of the viral hypothesis: is psychosis the result of retroviral integration at a site close to the cerebral dominance gene?

The extent to which concordance rates for schizophrenia in monozygotic twins (between 36 and 58%) fall short of 100% is often taken as an index of the role of an environmental factor in schizophrenia, but such an agent remains elusive. That schizophrenic symptoms are observed in some viral illnesses suggests that schizophrenia might be due to a gene-virus interaction, but analysis of age of onset in pairs of siblings with the disease rules out horizontal transmission. An alternative hypothesis is proposed that onset of disease is due to the expression of a 'provirus', which is integrated in the genome, having been acquired either by prenatal infection or in the germ-line from an affected parent; this could explain why the season of birth effect is accentuated in, and perhaps confined to the group of patients without a family history of the disease. Germ-line integration is known to occur following infection with agents of the retrovirus class. Such agents can integrate at many sites in the host genome, but their interactions with proto-oncogenes (cellular genes which may act as growth factors) identify one type of integration site, and are associated with some of their pathogenic effects. Some characteristics of schizophrenic illness, particularly their selectivity for the dominant hemisphere, can be understood on the assumption that the virus (perhaps a retrovirus) responsible for the disease interacts with a proto-oncogene, which induces the asymmetrical brain growth responsible for laterality and cerebral dominance. The aetiologies of manic-depressive illness and schizophrenia may be related (the season of birth and onset effects are the same for the two conditions) and there is some evidence that the former transmutes into the latter in succeeding generations. The persistence of the functional psychoses may be due to the ability of the psychosis gene (or 'provirus') to induce change in the genetic mechanisms responsible for the development of laterality.

Bipolar Disorder↗
PubMed1984

Schizophrenic patients discharged from hospital--a follow-up study.

A cohort of 120 patients, comprising all those who met the St Louis criteria for a diagnosis of schizophrenia, discharged from a mental hospital over a five-year period, were followed-up in the community after an interval of five to nine years; 105 were traced and 94 were alive. Of those, 66 were living in UK, out of hospital, and willing to be seen. Their mental states, and social functioning and circumstances were assessed by interview with the patients and those with whom they lived; 18% had recovered to the extent that they had no significant symptoms and appeared to function satisfactorily. More than 50% had definite psychotic features. No patients and few relatives sought a return to hospital care, but severe emotional, social, and financial difficulties were commonplace; 27% of the sample had no contact with medical or social services, a further 14% saw only community nurses, and 24% only their general practitioners. The findings emphasise the limitations of community services in dealing with the chronicity and severity of the impairments resulting from schizophrenic illness.

Family↗
PubMed1983

Peptides, the limbic lobe and schizophrenia.

The human brain contains several peptides with probable synaptic actions, some of which form complex neuronal networks in the limbic lobe (amygdala, hippocampus and temporal cortex). A limbic lobe abnormality has been postulated in schizophrenia on the basis of similarities between schizophrenic symptoms and symptoms in cases of known limbic pathology. Cholecystokinin (CCK), somatostatin (SRIF), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and substance P (SP)-like immunoreactivities were measured by radioimmunoassay in 10 brain areas of 14 schizophrenics and 12 controls. In the schizophrenic group symptoms had been rated in life and the group was divided into Type I (n = 7) and Type II (n = 7) subgroups on the basis of the absence or presence of morbid negative symptoms. In control brains each peptide showed a characteristic distribution with high levels in cortex (CCK), limbic lobe (SOM, NT, VIP) or striatal areas (SP) and low levels of each of the peptides in thalamus. Significant (P less than 0.05) differences between groups were: reductions of CCK and SOM in hippocampus and CCK in amygdala in Type II schizophrenics, and CCK in the temporal cortex of the total schizophrenic group; and elevations of VIP in amygdala in Type I schizophrenics and of SP in the hippocampus in the total schizophrenic group. The findings could not be explained by variables such as age, delay between death and necropsy or to neuroleptic medication. These clinical-state related alterations in the peptide content of the limbic system in schizophrenia may illuminate the pathophysiological basis of the disease, particularly the distinction between Type I and II syndromes.

Brain↗
PubMed1983

[3H]R05-4864 and [3H]flunitrazepam binding in kainate-lesioned rat striatum and in temporal cortex of brains from patients with senile dementia of the Alzheimer type.

In agreement with other workers we report increased [3H]R05-4864 binding in kainate-lesioned rat striatum. [3H]R05-4864 binding, a possible glial marker, was also increased in temporal cortex obtained post-mortem from patients with Alzheimer's disease. [3H]Flunitrazepam binding was decreased in these brain samples, possibly indicative of neuronal cell loss. It is suggested that the poor binding characteristics of [3H]R05-4864 in human brain samples may limit its usefulness in assessing gliosis.

Aged↗
PubMed1983

Neurotransmitter receptors as glycoproteins.

Incubation of calf brain membrane preparations with the plant lectins, concanavalin A and wheat germ agglutinin did not inhibit neurotransmitter receptor binding sites directly. Plant lectins did however protect these sites against subsequent trypsin digestion suggesting that neurotransmitter binding sites may be associated with glycoprotein structures.

Animals↗
PubMed1983

Neuropeptide Y distribution in the rat brain.

A massive neuronal system was detected by immunocytochemistry and radioimmunoassay with antibodies to neuropeptide Y, the recently isolated peptide of the pancreatic polypeptide family. Immunoreactive cell bodies and fibers were most prevalent in cortical, limbic, and hypothalamic regions. Neuropeptide Y was extracted in concentrations higher than those of any other peptide hitherto discovered in the mammalian brain. Column chromatography of brain extracts and double immunostaining experiments indicate that neuropeptide Y is the endogenous brain peptide responsible for immunostaining of pancreatic polypeptide-like immunoreactivity in the mammalian brain.

Animals↗
PubMed1983

77Br-p-bromospiperone: a ligand for in vivo labelling of dopamine receptors.

A high striatum: cerebellum ratio of 77Br-p-bromospiperone (77Br-BrSp) was observed in rat brain following tail vein injection of the drug. Striatal 77Br-BrSp was stereospecifically displaced by the isomers of flupenthixol. After chronic haloperidol administration striatal dopamine receptor supersensitivity was demonstrated both by increased 3H-spiperone binding to striatal membranes in vitro and by increased striatal 77Br-BrSp content. These results confirm and extend previous findings and enhance interest in the use of 77Br-BrSp for the in vivo assessment of central dopamine receptors in man.

Animals↗