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Biomedical subjects

F E Bloom

Publications and source records attributed to F E Bloom.

480 records · Page 27Linked to original sources
PubMedDate not supplied

Interferon-alpha and transforming growth factor-beta 1 regulate corticotropin-releasing factor release from the amygdala: comparison with the hypothalamic response.

Interferon-alpha (IFN-alpha) and transforming growth factor-beta 1 (TGF-beta 1) have been reported in different brain regions. The amygdala contains high levels of corticotropin releasing factor (CRF) and has been implicated as a central site for its stress-related autonomic and behavioral response. IFN-alpha will release arginine vasopressin (AVP) from both amygdala and hypothalamus, which further supports a role for the amygdala in neuroimmune interactions. In the present study, we compared the effects of these cytokines on the in vitro release of CRF from the amygdala and hypothalamus. In addition, we evaluated the possible involvement of guanylate cyclase-mediated signaling in CRF release. IFN-alpha stimulates CRF release from both amygdala and hypothalamus. The CRF release by IFN-alpha, Interleukin-2 (IL-2) and acetylcholine is blocked by guanylate cyclase inhibitors, indicating a role for cGMP accumulation in this CRF release. TGF-beta 1 had no effect on basal release of CRF, nor on the CRF-release induced by IL-2, but selectively blocked the acetylcholine-induced release in both amygdala and hypothalamus. Taken with a previous report that TGF-beta 1 specifically inhibits AVP release by acetylcholine, these results suggest that TGF-beta 1 may modulate HPA axis activation, by antagonizing (acetylcholine-evoked) CRF and AVP release. These data further support a role for the amygdala in the bidirectional communication between neuroendocrine and immune system.

Acetylcholine↗
PubMedDate not supplied

Noradrenergic receptor function and aging: beyond the binding.

Quantitative studies of noradrenergic binding sites with aging probably underestimate the functional alterations in this, and other, central synaptic systems. Transmitters like norepinephrine, whose actions are based on amplification and interaction of interneuronal signalling capacity, rely on interactions among receptor subtypes for their complete effect. Thus, slight losses of one or both receptor subtypes with normal aging may have far more devastating effects.

Aging↗
PubMedDate not supplied

Naloxone augments electrophysiological signs of selective attention in man.

Previous research on the behavioural functions of endogenous opioid systems in rodents suggested a possible opioid role in the regulation of attention. This proposal was consistent with reports that opiate administration in man impairs the ability to concentrate while opiate antagonists augment behavioural and electrophysiological indices of arousal and attention. We examined the effects of the opiate antagonist naloxone on electrophysiological measures of attention in normal human subjects, using a paradigm which dissociates selective information processing from concurrent processes of general arousal or alertness that may be present. We now report electrophysiological evidence that naloxone improves the selectivity of auditory attention in the presence of competing sources of stimuli. These findings indicate a role for the endogenous opioid systems in the regulation of selective attention in man.

Acoustic Stimulation↗
PubMedDate not supplied

Somatostatin immunoreactivity in neuritic plaques of Alzheimer's patients.

Senile dementia of the Alzheimer's type can be diagnosed with certainty only by examining neurofibrillary tangles and neuritic plaques under the microscope. Recently, it has been suggested that the condition is linked to specific neurotransmitter systems, with a decline of cortical acetylcholine, choline acetyltransferase, cholinergic neurones projecting to the cortex, cortical noradrenaline content, locus coeruleus neurones and cortical somatostatic content. Using immunocytochemical methods, we here report that somatostatin-immunoreactive processes are present in neuritic plaques in human Alzheimer's specimens. These data, as well as other reports of non-cholinergic changes, strongly imply that Alzheimer's disease cannot be linked exclusively to cortical cholinergic elements, as proposed previously. Rather, our data on plaque and somatostatin co-localization and distribution patterns suggest that Alzheimer's neuropathology may involve primarily the loss of selective cortical neurones that are targets of the implicated transmitter systems and that plaque formation may result from the degeneration of presynaptic and postsynaptic neurites of large projection neurones in layers III and V. Given the neurochemically heterogeneous input to these cells, it is not surprising that several neurotransmitter systems, one of which is somatostatin, are implicated in the pathology of Alzheimer's disease.

Alzheimer Disease↗
PubMedDate not supplied

Stimulation of food intake in rats by centrally administered hypothalamic growth hormone-releasing factor.

Hypothalamic growth hormone-releasing factors (GRFs) have been purified recently from human pancreatic (hp) tumours and from rat hypothalamus (rh). GRF peptides have strong homology with peptides of the glucagon, vasoactive intestinal polypeptide and PHI-27 family. Aside from their potent actions on release of somatotropin, no other biological actions of GRFs have been reported. GRF has been localized in neurones bordering the ventromedial hypothalamic nucleus, a region associated frequently with experimental analysis of feeding behaviour. We now report that intracerebroventricularly (i.c.v.)-administered rhGRF and hpGRF(1-40) in doses of 0.2, 2.0 and 20.0 pmol, produced an increase in food intake in hungry rats. This effect seemed to be specific to GRF as i.c.v. injections of a structurally related but physiologically inactive peptide in the same doses had no effect on feeding. In addition, peripheral injections of rhGRF or growth hormone had no effect on food intake, suggesting that the present effects may be mediated centrally. Injections (i.c.v.) of rhGRF (0.2, 2.0 and 20.0 pmol) had no effect on general activity, suggesting that GRF does not produce nonspecific arousal.

Animals↗
PubMedDate not supplied

Osmotic stress mimics effects of vasopressin on learned behaviour.

It has been suggested that arginine vasopressin (AVP) is involved in the retention of learned responses, in addition to its classical physiological functions of water retention and modulation of blood pressure. AVP administered subcutaneously (s.c.), intraventricularly or intracerebrally can prolong extinction of active avoidance behaviour and can enhance retention in inhibitory (passive) avoidance. These effects have been interpreted as a direct action of AVP on the central nervous system to facilitate memory consolidation. AVP also has facilitatory effects on cognitive function in humans, and marked deficits in AVP function have been associated with certain types of psychopathology. Alternative hypotheses for the behavioural actions of AVP have involved motivational constructs such as arousal, and our recent work has focused on the role of arousal resulting from the activation of peripheral visceral signals in the behavioural effects of peripherally administered AVP. The development of a specific antagonist for AVP, 1-deaminopenicillamine-2-O-methyl tyrosine arginine vasopressin (dPTyr(Me)AVP), which can reverse the behavioural effects of exogenously administered AVP, has provided a powerful tool for examining the role of AVP in the behavioural responses produced by physiological challenges known to release vasopressin. However, the relationship between the behavioural effects of exogenously administered AVP and the behavioural function of endogenously released AVP has not been evaluated. We report here that a potent peripheral osmotic stimulus, the intraperitoneal (i.p.) injection of hypertonic saline, at doses known to release AVP both centrally and peripherally, will produce behavioural effects similar to those of exogenously administered AVP. Furthermore, the prolongation of active avoidance induced by this osmotic stimulus is reversed by pretreatment with dPTyr(Me)AVP, suggesting that endogenously released AVP may also produce behavioural effects.

Animals↗
PubMedDate not supplied

Calbindin immunoreactivity alternates with cytochrome c-oxidase-rich zones in some layers of the primate visual cortex.

Calcium ions have a pivotal role in many neuronal activities, but little is known about their involvement in the cortical processing of visual information. Using immunohistochemical methods, we have now detected a calcium-binding protein, calbindin-D-28K, which may confer on certain compartments of cortical area 17 the ability to modulate Ca2+ metabolism. Thus, calbindin occurs in the primate striate cortex in a pattern almost complementary to that displaying strong cytochrome c-oxidase activity. From this and other observations, we deduce that the distribution of calbindin-immunoreactive sites corresponds mainly to extra-geniculocortical connections of the primary visual cortex. This implies that the geniculocortical and extra-geniculocortical compartments of area 17 differ in an intracellular system for Ca2+ homeostasis.

Animals↗
PubMedDate not supplied

Longitudinal analysis of behavioral, neurophysiological, viral and immunological effects of SIV infection in rhesus monkeys.

A model is proposed in which a neurovirulent, microglial-passaged, simian immunodeficiency virus (SIV) is used to produce central nervous system (CNS) pathology and behavioral deficits in rhesus monkeys reminiscent of those seen in humans infected with human immunodeficiency virus (HIV). The time course of disease progression was characterized by using functional measures of cognition and motor skill, as well as neurophysiologic monitoring. Concomitant assessment of immunological and virological parameters illustrated correspondence between impaired behavioral performance and viral pathogenesis. Convergent results were obtained from neuropathological findings indicative of significant CNS disease. In ongoing studies, this SIV model is being used to explore the behavioral sequelae of immunodeficiency virus infection, the viral and host factors leading to neurologic dysfunction, and to begin testing potential therapeutic agents.

Animals↗
PubMedDate not supplied

IL-1-alpha and TNF-alpha differentially regulate CD4 and Mac-1 expression in mouse microglia.

The regulatory effects of the proinflammatory cytokines, interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) were investigated on CD4 and Mac-1 expression in mouse microglial cultures. The identity of the microglia in cultures was confirmed by multiple indices including morphology, uptake of acetylated low-density lipoprotein and lectin RCA 120 staining. Microglia growing on a monolayer of astrocytes (astrocyte-supported microglia) were both CD4- and Mac-1 positive (out of 94.5 % Mac-1-positive cells, 85.3% were also CD4 positive). When astrocyte-supported microglia were replated directly onto culture dishes (plate-supported microglia), the percentage of CD4- and Mac-1-positive cells decreased to 12-29 and 20-25% respectively. The addition of IL-1alpha or TNF-alpha to plate-supported microglia led to an upregulation of Mac-1 expression in a time- and dose-dependent manner with different EC50s (0.5 ng/ml for IL-1alpha and 2 ng/ml for TNF-alpha) but exhibited similar time-to-peak responses (over 12 h). The addition of IL-1alpha, but not TNF-alpha, also led to an increase in CD4 expression on plate-supported microglia with a similar dose response and time course. IL-1alpha treatment gave rise to an increase in the level of CD4 mRNA as assessed by RT-PCR. The possibility that cell proliferation was responsible for the observed effects on microglia was excluded by an analysis of 3H-thymidine incorporation. Our results suggest that cultured mouse microglia express CD4 molecules which can be upregulated by IL-1alpha while Mac-1 can be upregulated by both IL-1alpha and TNF-alpha.

Animals↗
PubMedDate not supplied

Locating the central sulcus: comparison of MR anatomic and magnetoencephalographic functional methods.

PURPOSE: To compare MR anatomic and magnetoencephalographic (MEG) functional methods in locating the central sulcus. METHODS: Eleven healthy subjects and five patients with focal cerebral lesions were studied. The central sulcus was located anatomically with MR by two independent observers using axial vertex and sagittal (midline and lateral) images. Locations via the MEG functional method were based on detecting the somatosensory-evoked magnetic fields elicited by painless tactile stimuli. RESULTS: The axial method yielded the most consistent interrater results, with complete agreement in 76% of sections in both control subjects and patients. The intermethod discordance of the sagittal midline and lateral methods was 32% in control subjects and 33% in patients. The concordance of MR and MEG methods ranged from 55% to 84% in control subjects and 65% to 67% in patients. CONCLUSION: MR anatomic techniques can usually identify the central sulcus, but in the presence of anatomic distortion, the MEG functional method adds significant information.

Adult↗