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F A Henn

Publications and source records attributed to F A Henn.

At least 55 records · Page 3Linked to original sources
PubMed1999

Structural neuroimaging in schizophrenia. An integrative view of neuromorphology.

The use of structural magnetic resonance imaging (MRI) in studies of schizophrenia has resulted in a more detailed picture of anatomic areas which may be altered in this syndrome. Thus far, there have been over 130 studies of schizophrenia using MRI and, taken together, they present a clear picture of a group of disorders with altered brain structure. Their major finding is a confirmation of the older pneumoencephalography and computertomography studies showing an enlargement of lateral ventricles and a volume reduction seen in the temporal lobe. When structural studies are carried out in other cortical and subcortical regions, however, the volume reduction is not so uniform, but rather restricted to certain areas in a given patient. In addition medication effects can be seen especially in the caudate nucleus which tend to increase in volume after long-term neuroleptic drug usage and again normalize under the atypical drug clozapine. These data are consistent with a neurodevelopmental model of schizophrenia and with some kind of progressive neurodegenerative process. This review suggests that an integrative model with initial developmental errors may underlie the majority of cases of schizophrenia, but that cases of chronic schizophrenia appear to involve progressive neurodegeneration. In assessing the scatter in available data, it appears that there is no consistent neuropathology across all cases of schizophrenia and preferential areas of dysfunction can be determined. Thus, there seems a collection of subtle neurodevelopmental errors which can lead to various forms of schizophrenia and that at least some types of schizophrenia most probably also involve a neurodegenerative process which could in fact be a consequence of the initial developmental defect.

Brain↗
PubMed1999

Reduced activation and altered laterality in two neuroleptic-naive catatonic patients during a motor task in functional MRI.

BACKGROUND: Catatonia, a symptom complex with motor, affective and cognitive symptoms seen in a variety of psychotic conditions and with organic disease, was examined using a motor task using functional magnetic resonance imaging (fMRI). METHODS: Two acute catatonic patients and two age- and sex-matched healthy controls performed sequential finger opposition (SFO) after being medicated with 2 mg of lorazepam (i.v.). Functional magnetic resonance images were collected using a gradient echo pulse sequence (EPI). RESULTS: Patients with catatonia showed reduced motor activation of the contralateral motor cortex during SFO of the right hand, ipsilateral activation was similar for patients and controls. There were no differences in the activation of the SMA. During left hand activation the right-handed catatonic patients showed more activation in the ipsilateral cortex, a reversal from the normal pattern of activation in which the contralateral side shows four to five times more activation than the ipsilateral side. CONCLUSIONS: In catatonic patients there is a decreased activation in motor cortex during a motor task compared to matched medicated healthy controls. In addition activation of the non-dominant side, left-handed activity in right-handed patients, results in a total reversal of the normal pattern of lateral activation suggesting a disturbance in hemispheric localization of activity during a catatonic state.

Acute Disease↗
PubMed1997

Real-time direct volume rendering in functional magnetic resonance imaging.

Direct volume rendering is a visualization method that allows display of all information hidden in three-dimensional data sets of, for example, computed tomography or magnetic resonance imaging (MRI). In contrast to commonly used surface rendering methods, these algorithms need no preprocessing but suffer from a high computational complexity. A real-time rendering system, VIRIM (Vitec: Visualization Technology GmbH, Mannheim, Germany), cuts down rendering times of minutes on normal workstations to an interactive rate of 1 second or less. The immediate visual feedback allows interactive steering of the visualization process to achieve insight into the internal three-dimensional structure of objects. Additional information is obtained by using an interactive gray-value segmentation tool that both allows segmentation of the data set according to bone, tissue, and liquor and display of multifunctional data sets (e.g., functional MRI [fMRI] data sets). Thus, real-time direct volume rendering allows segmentation and volume data processing of functional and anatomical MR data sets simultaneously. As this method can be integrated in the clinical routine, it is of great importance for real-time motion artifact detection and the interpretation of fMRI data acquired during cognitive experiments with normal subjects and psychiatric patients. Because of the free programmability of VIRIM, more complex matching procedures are currently being investigated for future implementation.

Brain↗
PubMed1995

[Neurobiology of schizophrenia].

In this paper schizophrenia is taken to be a collection of diseases with similar pathological features, including the core Bleulerian symptoms. The aim is to see how far current research can specify the anatomical regions which are functionally defective in schizophrenia and what transmitter systems may be involved. It appears schizophrenic brains show a tendency toward fewer cells in the temporal region, including limbic system as well as the thalamus. Functional deficits are seen in the dorsolateral frontal cortex, as well as thalamus suggesting a cortical-thalamic-striatal pathway. It is clear that Dopamine disregulation in this pathway leads to psychotic symptoms but probably does not account for the ambivalence, affective blunting or asocial behavior. GABA lesions prenatally could lead to glutamate over activity with potential toxic consequences after puberty leading to a plausible hypothesis as to the central neurochemical defect in schizophrenia, this hypothesis is elaborated.

Brain↗
PubMed1994

Diminished cerebral metabolic response to motor stimulation in schizophrenics: a PET study.

Positron emission tomography (PET) and the deoxyglucose method were used to measure cerebral metabolism in 14 normals and 13 schizophrenics at rest and during performance of simple and complex finger-movement sequences. The normals, but not the schizophrenics, showed significant metabolic activation in mesial frontal and contralateral sensorimotor and premotor regions during the complex movement. The relative metabolism of schizophrenics was significantly lower than normal in frontal regions and higher than normal in thalamus and basal ganglia under all scanning conditions. The results suggest that schizophrenics may have a brain dysfunction which limits their capacity to produce a focal metabolic response to stimulation in several functionally distinct brain regions.

Adult↗
PubMed1993

Effects of the antiglucocorticoid RU 38486 on the induction of learned helpless behavior in Sprague-Dawley rats.

Learned helplessness (LH) is induced by exposure to an inescapable or uncontrollable stressor which results in an inability to escape or avoid the same stressor when subsequently presented in a different context. In order to understand which central mechanisms may influence the expression of the learned helpless phenotype, we have pursued an experimental approach that seeks to elucidate the behavioral effects of glucocorticoid (GC) hormones in this animal model of depression. We have previously shown that the induction of LH behavior is enhanced by adrenalectomy, an effect that is reversed by corticosterone. In this study, our aim was to attempt to locate CNS sites responsible for the observed effects of glucocorticoids on learned helpless behavior by introducing the type II GC receptor antagonist, RU 38486 to discrete brain regions. We did not observe a significant effect in LH with acute systemic, acute dentate gyrus or intracerebroventricular injection of RU 38486 in contrast to previous studies using the Porsolt swim test, another animal model of depression. However, we were able to observe a significant change upon chronic administration to the dentate gyrus. These findings suggest that glucocorticoids exert a long-term influence on stress-induced behavior, presumably by affecting glucocorticoid responsive genes in the dentate gyrus.

Animals↗
PubMed1993

Alterations in glucocorticoid inducible RNAs in the limbic system of learned helpless rats.

Glucocorticoids (GC) have an important effect on mood in humans and influence learned helplessness, an escape avoidance paradigm that is considered one of the best animal models of depression. A strong genetic component underlies the development of learned helplessness as shown by the emergence of a line of highly vulnerable rats (LH strain) through selective inbreeding. In addition, hormonal factors play a role. Adrenalectomy (adx) for example is known to increase the vulnerability to acquire learned helplessness, an effect that is reversed by glucocorticoids (GC). Since GC function primarily by modulating gene expression, hormone mediated alterations in mRNAs expressed in the brain may be important in the development of an adequate escape avoidance response. Conversely, we postulate that the deficit in escape avoidance behavior exhibited by the LH strain may be associated with an alteration in GC-mediated gene expression in the brain. To test this hypothesis, we analyzed GC-responsive mRNAs that are expressed in the hippocampus. Control Sprague-Dawley (SD) rats showed consistent alterations in mRNAs that are modulated by GC, such as type II GC receptor (GR) and metallothionein-1 (MT-1). Under our experimental conditions, both GR and MT-1 mRNA are significantly increased in the hippocampus of hormone-treated SD rats. An increase in hypothalamic GR mRNA was also observed. However, under the same experimental conditions, LH rats showed more selective hormone induced changes since GC had no effect on hypothalamic and hippocampal GR mRNA whereas a significant increase in MT-1 mRNA was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1992

Presynaptic serotonin mechanisms in rats subjected to inescapable shock.

After exposure to uncontrollable shock training, two distinct groups of rats can be defined in terms of their performance in learning to escape from a controllable stress. Learned helpless rats do not learn to terminate the controllable stress, whereas non-learned helpless rats learn this response as readily as naive control rats do. The present studies were designed to examine the correlations between the behavioral differences and the changes of presynaptic serotonergic activity, seen in these groups of rats. The major findings concerned presynaptic serotonergic effects in the hippocampus and hypothalamus of learned helpless rats. In the hippocampus, these included a statistically significant increase in three presynaptic 5-hydroxytryptamine (5-HT) mechanisms: K(+)-induced release of [3H]serotonin, high affinity uptake of [3H]serotonin and maximum density of binding sites for uptake of 5-HT, measured with [3H]paroxetine. In the hypothalamus, there was a differential modulation of all three presynaptic 5-HT mechanisms. A significant decrease in: K(+)-induced release of [3H]serotonin, in high affinity uptake of [3H]serotonin and the maximum binding site density of [3H]paroxetine binding was observed. No changes in uptake site binding was seen in other regions of the brain examined. These results implicate presynaptic serotonin mechanisms in the behavioral deficit caused by uncontrollable shock. In addition, a limbic-hypothalamic pathway may serve as a control center for the behavioral response to stress.

Analysis of Variance↗
PubMed1992

Hippocampal neuropeptide Y mRNA is reduced in a strain of learned helpless resistant rats.

The learned helpless rat is considered to be one of the better animal models of depression. A genetically inbred strain with a high vulnerability to develop helplessness (LH), as well as a highly resistant strain (NLH) have both been developed. Since the brain peptide neuropeptide Y (NPY) is involved in the regulation of a number of behaviors known to be altered in clinical depression as well as in learned helplessness, we measured the relative level of NPY mRNA in the hippocampus and cortex of control Sprague Dawley (SD), LH and NLH rats. We find that NLH rats have approximately a 30-35% decrease in basal hippocampal NPY mRNA compared with SD and LH rats. By contrast, cortical NPY mRNA and hippocampal pre-proenkephalin and somatostatin mRNA levels were not significantly different in the 3 strains. The data suggest that the regulation of NPY gene expression may be involved in the reduced vulnerability of NLH rats to develop learned helplessness.

Amino Acid Isomerases↗
PubMed1992

In vitro neurotransmitter release in an animal model of depression.

Sprague-Dawley rats exposed to uncontrollable shock can be separated by a subsequent shock escape test into two groups: a "helpless" (LH) group which demonstrates a deficit in escape behavior, and a "nonlearned helpless" (NLH) group which shows no escape deficit and acquires the escape response as readily as naive control rats (NC) do. The present studies were designed to examine the correlations between the behavioral differences and the changes of in vitro neurotransmitter release seen in these three groups of rats. The major finding concerned a significant increase in endogenous and K(+)-stimulated serotonin (5-HT) release in the hippocampal slices of LH rats. There were no apparent differences in acetylcholine, dopamine and noradrenaline release in the hippocampus of LH rats as compared to NLH and NC rats. These results add further support to previous studies in our laboratory which implicate presynaptic 5-HT mechanisms in the behavioral deficit caused by uncontrollable shock.

Acetylcholine↗
PubMed1991

Brain morphology in first-episode schizophrenic-like psychotic patients: a quantitative magnetic resonance imaging study.

Brain morphology was examined using magnetic resonance imaging in 30 first-episode patients with a schizophreniclike psychosis, 15 chronic schizophrenics, and 20 neurological controls. Statistical analyses of computer-generated measurements of regions of interest were controlled for gender, age, social class, and total brain volume. Lateral ventricular size was increased in both first-episode and chronic schizophrenic patients, with greater significance on the left than on the right side. Only the chronic patients, however, had reduced temporal lobe size, which also was greater on the left side. No major correlations of regional brain morphological measurements with cognitive functioning were found, although some measurements of verbal memory were correlated with parahippocampal size. This is a report of a preliminary study that suggests that some morphological brain changes may be present at the time of first treatment for a psychotic illness, whereas others may occur later in the course of illness. Future prospective studies may determine the clinical significance of these changes and whether they progress with the development of illness chronicity.

Adolescent↗
PubMed1991

5-HT1b receptors in an animal model of depression.

After exposure to a 0.8 mA course of uncontrollable shocks, Sprague-Dawley rats can be differentiated into two distinct groups defined in term of their performance in a shock escape paradigm. Learned helpless (LH) rats do not learn to escape a controllable shock while non-helpless (NLH) rats learn this response as quickly as naive controls (NC) rats do. The current experiments were designed to extend our studies of 5-HT receptors in these three groups of rats. The major finding in the present study concerned post-synaptic 5-HT receptor effects in the cortex, hippocampus, septum and hypothalamus of LH rats. These included an up regulation of 5-HT1b receptors in the cortex, hippocampus and septum in LH rats. In contrast, 5-HT1b receptors in the hypothalamus of LH rats were down-regulated. These results implicate serotonergic mechanisms in the behavioral deficit caused by uncontrollable shock with a limbic-hypothalamic circuit serving as a center for adaptation to stress.

Animals↗
PubMed1990

Monoamine receptors in an animal model of affective disorder.

After a relatively mild course of uncontrollable shocks, two distinct groups of rats can be defined in terms of their performance in learning to escape from a controllable stressor. Response-deficient (RD) rats do not learn to terminate the controllable stressor, whereas nondeficient (ND) rats learn this response as readily as do untreated control rats. The current studies were designed to determine the neurochemical correlates of the behavioral differences between these groups of rats. The major findings concerned postsynaptic beta-adrenergic effects in the hippocampus of RD rats. These included an up-regulation of beta-adrenergic receptors and, in parallel experiments, an increase in the sensitivity of adenylyl cyclase to stimulation by norepinephrine. There was no difference in brain levels of catecholamines between the three groups of rats. A statistically significant increase in levels of 5-hydroxytryptamine was noted in the hippocampus and hypothalamus of RD rats as compared to levels in ND rats, but no significant differences were measured between groups of rats in terms of S1 or S2 serotonergic receptor binding. These results implicate both beta-adrenergic and serotonergic mechanisms in the behavioral deficit caused by uncontrollable shock.

Adenylyl Cyclases↗
PubMed1986

Neurochemical and behavioral consequences of mild, uncontrollable shock: effects of PCPA.

The present experiments examined the role of the serotonergic system in the behavioral deficit produced by uncontrollable shock. In Experiment 1: Establishment of model, the behavioral potential of the Sprague-Dawley rat was defined. When exposed to mild uncontrollable stress such as a 0.8 mA electric footshock, a significant percentage of rats developed a shock escape deficit which was evident when subsequently placed in a shock escape paradigm. Serotonin depletion was produced by chronic treatment with p-chlorophenylalanine. Biogenic amine levels and 5-HT levels were monitored in various brain areas using HPLC. Following chronic treatment with PCPA, the shock escape capability of the Sprague-Dawley rat was assessed. The severe depletion of 5-HT in various brain regions was highly correlated with a dramatic improvement in the shock escape scores. Thus, the detrimental effects of exposure to a mild course of inescapable shock can be prevented by chronic treatment with PCPA. These experiments implicate the serotonergic system as a possible mediator of the "learned helplessness" phenomenon.

Animals↗