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F E Bloom

Publications and source records attributed to F E Bloom.

At least 109 records · Page 6Linked to original sources
PubMed1994

Intrasubject reliability and validity of somatosensory source localization using a large array biomagnetometer.

Neuromagnetic fields were evoked by tactile stimuli and detected with a multi-channel biomagnetometer through 72 independent repetitive measurements on a single subject. Each measurement consisted of a somatosensory evoked response (N = 256 stimuli) using a single probe placement. These fields were then analyzed for source localization using an equivalent current dipole model and demonstrated highly reliable localizations. The 3 major neuromagnetic somatosensory response components peaking at 35, 65 and 110 msec all localized to the same area of cortex. The relative contributions of intrinsic brain activity, habituation, probe placement, and choice of fiduciary points for headframe determination were quantified. Intrinsic factors were found to constitute the major source of inter-measurement error. Sources localized by magnetic source imaging (MSI) appeared valid relative to neuroanatomical estimation of the central fissure on MRI. Non-invasive presurgical biomagnetic localization of somatosensory cortex produces reliable and valid functional localizations which can be of potential value in risk assessment and may provide a useful guide for invasive functional mapping.

Adult↗
PubMed1994

Alteration of intracerebral cytokine production in mice infected with herpes simplex virus types 1 and 2.

Previously we reported that a lethal strain of herpes simplex virus type 2 (HSV-2) infects the brain following ocular inoculation of mice. We now demonstrate that HSV-2 mediates an unusual intracellular sequestering of class II major histocompatibility complex (MHC) antigens. With use of an RNase protection assay, we observed a selective inhibition of IFN-gamma and IL-6 gene transcription in brains of mice infected with HSV-2. It is likely that the inhibition of cytokine gene expression was mediated through a failure to activate CD4+ lymphocytes. These data suggest that the infecting herpesvirus can influence the profile of intracerebrally produced cytokines, which in turn may determine the outcome of the infection.

Animals↗
PubMed1994

P300 from an auditory oddball task: inter-laboratory consistency.

Event-related potentials (ERPs) were recorded from normal subjects for the purpose of evaluating measurement consistency among six laboratories located in different cities within the United States. At each laboratory location 15 male subjects were tested using a simple auditory stimulus discrimination task and identical electrophysiological equipment and recording methods. Assessment of the N1, P2, N2, and P3(00) potentials from both the target and standard stimuli resulted in no reliable differences among laboratories for component amplitudes, latencies, and scalp distributions. Quantitative evaluation of overall waveform and specific component morphology yielded good to excellent agreement across laboratories. The findings suggest that large-scale inter-laboratory human electrophysiological studies are feasible and may prove of value when using ERPs to evaluate cognitive function in humans.

Adult↗
PubMed1994

Meta-analysis of P300 amplitude from males at risk for alcoholism.

The P3(00) event-related brain potential (ERP) is used to study the development of alcoholism by comparing males who have a positive family history of alcoholism with control Ss who have no such familial history. Meta-analysis indicated that overall, smaller P3 amplitudes were obtained from males with family histories of alcoholism compared to controls. Moderator analysis indicated that paradigms using difficult visual tasks yielded the most reliable effects. Furthermore, no differences in outcomes were obtained among studies that recruited positive family history Ss exclusively from among individuals whose father had received treatment for alcoholism as compared with other studies. These findings are discussed in the context of using ERPs as an evaluative tool in the study of psychopathology.

Adolescent↗
PubMed1994

Neurological abnormalities associated with feline immunodeficiency virus infection.

Specific pathogen-free cats were infected with the Maryland strain of FIV (FIV-MD) for the purpose of assessing the effects of FIV infection on the central nervous system (CNS). Two separate studies were performed, involving a total of 13 infected cats and six age-matched, sham-inoculated controls. All animals infected with FIV-MD seroconverted by 8 weeks post-infection and virus was recovered from peripheral blood mononuclear cells of all infected cats. All of the infected animals had lower absolute CD4+ cells counts and decreased CD4+/CD8+ ratios. Virus was recovered from the cerebrospinal fluid (CSF) of certain infected individuals, and antiviral antibody and pleocytosis were evident in the CSF of the majority of infected cats. Additionally, virus was recovered from tissue explants from the cerebellum, midbrain and brainstem of one sacrificed FIV+ cat. Specific neurological changes included anisocoria, delayed righting reflex and delayed pupillary reflex, as well as delayed visual and auditory evoked potentials, and marked alterations in sleep patterns similar to those reported for human immunodeficiency virus (HIV)-positive individuals. Histological evaluation revealed the presence of perivascular cuffing and glial nodules in FIV-infected cats. These results indicate that FIV causes an acute neurological disease that closely resembles the early neurological effects of HIV infection in humans and should serve well as an animal model for lentivirus-induced CNS disease.

Acute Disease↗
PubMed1994

IL-1 beta potentiates the acetylcholine-induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala.

In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1 beta immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1 beta (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1 beta, atropine (10 microM) or mecamylamine (10 microM). IL-6, like IL-1 beta, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-alpha nor interferon-gamma had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1 beta and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendoc ine and immune systems. Understanding the mode of interaction between IL-1 beta and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.

Acetylcholine↗
PubMed1994

IL-2 induces vasopressin release from the hypothalamus and the amygdala: role of nitric oxide-mediated signaling.

The neuropeptide arginine vasopressin (AVP) can replace the cytokine interleukin 2 (IL-2) as a T-cell mitogen for the induction of interferon gamma (IFN gamma) expression in splenic cultures. IL-2-like and IL-2 receptor immunoreactivity have been reported in different brain regions, under normal and pathophysiological conditions. Regulatory functions for IL-2 in the CNS have been suggested. In addition to the spleen, AVP might also mediate some IL-2 effects centrally. In the present study, we evaluated the effect of IL-2 on the in vitro release of AVP from the hypothalamus and amygdala. In addition, we used these release systems to study the possible involvement of NO-mediated signaling in AVP release, based on the reported detection of nitric oxide synthase (NOS) in the hypothalamus and amygdala. IL-2 rapidly stimulates AVP release in both regions, in a calcium- and dose-dependent manner. In addition, nitroprusside also induces AVP release. Norepinephrine also induces AVP release from both the hypothalamus, as well as the amygdala. The norepinephrine-induced AVP release is antagonized by phentolamine, but not by propranolol, suggesting an alpha-adrenergic receptor-mediated AVP response in both brain regions. The IL-2- and acetylcholine-induced AVP release is antagonized by Ng-methyl-L-arginine, indicating a role for NO in this AVP release. Ng-methyl-L-arginine does not affect the norepinephrine-induced AVP release. A stimulatory effect of IL-2 on hypothalamic CRF release and plasma ACTH has already been reported. Our results suggest that in addition to CRF, AVP may also mediate the IL-2 stimulation of ACTH secretion. These data further suggest that in addition to the hypothalamus, the amygdala may also play a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-2 with AVP could clarify the pathophysiologic or toxic effects of high brain levels of IL-2.

Acetylcholine↗
PubMed1994

Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress.

Acute exposure to stress leads to activation of the pituitary-adrenal axis (PA-axis) while repeated exposure to a homotypic stressor generally results in habituation of this response. Previous studies suggested that such habituation is largely due to changes in afferents of the PA-axis. To examine where within these afferents habituation occurs, we studied the effect of acute and repeated exposure to 2 hr restraint stress on expression of c-fos mRNA, as a marker of altered neuronal activity, in brain regions previously shown to influence the activity of the PA-axis. Acute restraint stress increased expression of c-fos mRNA in cortex, hippocampus, hypothalamus, septum, and brainstem. In contrast, the effect of restraint stress on c-fos expression in the aforementioned brain regions was much smaller in animals restrained once daily for 4 d, and nonexistent in animals restrained once daily for 9 d. A similar pattern of induction and habituation of jun-B, but not zif-268, c-jun, or jun-D mRNA expression, was observed in the cortex of animals exposed to acute versus repeated restraint stress. The habituation of c-fos responses was stressor specific: exposure of restraint-adapted animals to a novel (20 min swim) stress produced an increase in levels of c-fos mRNA in every examined brain region comparable to that seen in animals exposed to this stressor for the first time. Adrenalectomy did not alter the pattern of c-fos expression induced by acute and repeated restraint stress. Therefore, activation and habituation of these c-fos responses are independent of changes in circulating levels of corticosterone.

Adrenalectomy↗
PubMed1994

1G5: a calmodulin-binding, vesicle-associated, protein kinase-like protein enriched in forebrain neurites.

We have characterized cDNA clones of 1G5, an mRNA highly enriched in the mammalian forebrain that encodes a 504-residue protein found in association with perikaryal membranes and neurites. The protein, which accumulates predominantly postnatally, is associated with vesicles in both axons and dendrites. The sequence of the 1G5 protein highly resembles those of protein kinases with serine/threonine specificity; however, although most residues universally conserved among protein kinases are present, a few signature residues are absent from the 1G5 protein. Furthermore, although recombinant 1G5 protein binds calmodulin in the presence of calcium, it lacks kinase activity with a sample substrate.

Amino Acid Sequence↗
PubMed1994

Aggregation of vasopressin mRNA in a subset of axonal swellings of the median eminence and posterior pituitary: light and electron microscopic evidence.

The mRNA encoding vasopressin has recently been documented within the magnocellular hypothalamo-neurohypophyseal projections of the rat such as the median eminence (ME) and the posterior pituitary (PP), suggesting the possibility of its axonal transport. To address the origin of this mRNA and to investigate the functional significance of this unexpected axonal transport of mRNA, we have examined its subcellular localization within both magnocellular perikarya and their axonal projections. For this purpose, we have used nonradioactive in situ hybridization techniques in order to localize the vasopressin mRNA with precision at the ultrastructural level in magnocellular perikarya, dendrites, and axons from control, salt-loaded, and lactating rats. This approach permitted us to demonstrate directly the axonal localization of vasopressin mRNA. Moreover, we were able to obtain novel information concerning vasopressin mRNA compartmentation within both perikarya and axons. At both light and electron microscopic levels, we observed vasopressin mRNA-containing cells in the hypothalamic magnocellular cell body groups, but not in the ME or in the PP. When vasopressin mRNA was detected in medium-size dendrites, it was always associated with the rough endoplasmic reticulum (RER). Within the labeled magnocellular perikarya, the abundant vasopressin mRNA was mainly associated with discrete areas of the RER. However, vasopressin mRNA was never detected in the Golgi apparatus or in association with neurosecretory granules, in perikarya or axons. These data suggest that vasopressin mRNA translation is restricted to certain segments within the RER, and that axonal transport of vasopressin mRNA does not involve the classical neurosecretory pathway, via the Golgi apparatus and the neurosecretory granules, as has been proposed. Within the magnocellular neuron axons, vasopressin mRNA could be detected only in a subset of axonal swellings, all of which were confined to the internal layer of the ME and the PP. The mRNA-containing swellings were numerous in 7 d salt-loaded animals, less abundant in lactating animals, and almost undetectable in control animals. In all groups of animals, no vasopressin mRNA was detectable in any other region of the magnocellular neuron axons, including undilated axonal segments or varicose swellings. These results strongly suggest that, under physiological activation such as chronic salt loading, axonal vasopressin mRNA is increased and becomes aggregated in a selected subset of swellings of the ME and the PP. Furthermore, these data indicate that along the magnocellular neuron axons, the swellings may differ in their biochemical and functional features. Further analysis focused on the mRNA-accumulating swellings may illuminate the function of RNA within the axonal compartment.

Animals↗
PubMed1993

Human immunodeficiency virus infection of human brain capillary endothelial cells occurs via a CD4/galactosylceramide-independent mechanism.

Neuropathologic studies of AIDS patients have shown that brain capillary endothelial cells are a cellular target for human immunodeficiency virus (HIV) in vivo. We have established in vitro cultures of primary human brain capillary endothelial (HBCE) cells. Using this model system, we have shown a significant HIV infection of HBCE cells that is productive yet noncytopathic. The infection is mediated by a cellular interaction with gp120 that does not involve CD4 or galactosylceramide. HIV infection of HBCE cells may contribute to AIDS-associated neuropathology by disturbing the physiology of the endothelium and directly or indirectly facilitating dissemination of virus to the central nervous system.

CD4 Antigens↗
PubMed1993

Modulation of early sensory processing in human auditory cortex during auditory selective attention.

Neuromagnetic fields were recorded from human subjects as they listened selectively to sequences of rapidly presented tones in one ear while ignoring tones of a different pitch in the opposite ear. Tones in the attended ear evoked larger magnetic brain responses than did unattended tones in the latency ranges 20-50 msec and 80-130 msec poststimulus. Source localization techniques in conjunction with magnetic resonance imaging placed the neural generators of these early attention-sensitive brain responses in auditory cortex on the supratemporal plane. These data demonstrate that focused auditory attention in humans can selectively modulate sensory processing in auditory cortex beginning as early as 20 msec poststimulus, thereby providing strong evidence for an "early selection" mechanism of auditory attention that can regulate auditory input at or before the initial stages of cortical analysis.

Acoustic Stimulation↗
PubMed1993

Presumptive Renshaw cells contain decreased calbindin during recovery from sciatic nerve lesions.

A subpopulation of calbindin-immunoreactive neurons in lamina VII of the spinal cord has been identified by its location as Renshaw cells, the anatomical substrate for recurrent inhibition. The expression of calbindin (28 kDa) in these calbindin-containing rat ventral horn interneurons was studied with immunocytochemistry after sciatic nerve injuries. One week after axotomy calbindin immunoreactivity was strongly reduced on the lesioned side between levels L4 and L6, while calbindin-containing neurons and fibers were still numerous contralaterally and cranially to the lesioned levels. With the progression of regeneration, calbindin-immunoreactive neurons reappeared, reaching a normal distribution 6-8 weeks after the crush. Similar changes could be mimicked by the intramuscular administration of botulinum toxin. These results suggest that calbindin expression in putative Renshaw cells of the spinal cord might be functionally responsive and that maintenance of calbindin expression may depend on the integrity of motoneurons and neuromuscular transmission.

Animals↗
PubMed1993

Noninvasive somatosensory homunculus mapping in humans by using a large-array biomagnetometer.

To validate the feasibility of precise noninvasive functional mapping in humans, a large-array biomagnetometer was used to map the somatosensory cortical locations corresponding to numerous distinct tactile sites on the fingers, hand, arm, and face in different subjects. Source localizations were calculated by using a single equivalent current dipole (ECD) model. Dipole localizations were transposed upon the corresponding subject's magnetic resonance image (MRI) to resolve the anatomic locus of the individual dipoles within a given subject. Biomagnetic measurements demonstrated that (i) there were distinct separations between the ECD locations representing discrete sites on the face and hand; (ii) the ECD localizations from facial sites clustered in a region inferior to ECD localizations from hand and digit sites; and (iii) there was clear spatial resolution of ECD locations representing closely spaced tactile sites on the hand and face. The ability of magnetoencephalography (MEG) to provide high-resolution spatial maps of the somatosensory system noninvasively in humans should make MEG a useful tool to define the normal or pathological organization of the human somatosensory system and should provide an approach to the rapid detection of neuroplasticity.

Adult↗
PubMed1993

Interference with major histocompatibility complex class II-restricted antigen presentation in the brain by herpes simplex virus type 1: a possible mechanism of evasion of the immune response.

Host survival of herpes simplex virus type 1 (HSV-1) infection depends on the establishment of latent infections in both peripheral and central nervous systems. Strains of HSV-1 that are successful in escaping the immune response produce a lethal infection. We now report a possible mechanism of immune response evasion used by HSV-1. After intraocular inoculation of mice, HSV-1 strain F established a latent infection in the brain, whereas strain KOS did not. The immune response to HSV-1 infection (strains KOS and F) in the brain was characterized by induction of major histocompatibility complex class II expression and recruitment of CD4+ and CD8+ cells to highly restricted sites of intracerebral viral infection. Major histocompatibility complex class II antigen expression was primarily intracellular in strain KOS infection centers and at the cell surface in strain F infection centers. We propose that major histocompatibility complex class II-restricted viral-antigen presentation to T cells is interrupted during strain KOS infections, thereby allowing KOS infection to evade T-cell-mediated events that would normally protect the host from a lethal infection. Immunocompromised mice (athymic or irradiate mice) could not survive strain F infections; however, latent F infections were established in irradiated mice reconstituted with naive lymph node and spleen cells. These data suggest that class II-restricted presentation of viral antigens is required for the control of HSV-1 infections in the nervous system.

Animals↗
PubMed1993

Reduction of exogenous vasopressin RNA poly(A) tail length increases its effectiveness in transiently correcting diabetes insipidus in the Brattleboro rat.

Magnocellular hypothalamic neurons in Brattleboro rats can accumulate, transport, and translate exogenous [Arg8]vasopressin (AVP) mRNA after injection in the hypothalamo-hypophysial tract in amounts sufficient to reverse transiently the animals' characteristic diabetes insipidus. In the present study, different preparations of hypothalamic RNA extracted from normal rats or synthetic AVP RNA were injected into the lateral hypothalamus of Brattleboro rats. Poly(A)- RNA and poly(A)+ RNA from which tails were removed by RNase H digestion were much more effective than poly(A)+ RNA in expressing AVP in the magnocellular hypothalamic neurons and in raising urine osmolarity. Synthetic AVP RNA lacking a poly(A) tail also produced a very potent dose-dependent diabetes insipidus reversal. Our results suggest that a short or absent poly(A) tail may facilitate the accumulation, transport, or expression of exogenous AVP mRNA by magnocellular neurons.

Animals↗