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V Arango

Publications and source records attributed to V Arango.

At least 55 records · Page 3Linked to original sources
PubMed1993

Computerized three-dimensional reconstruction reveals cerebrovascular regulatory subregions in rat brain stem.

Three-dimensional wireframe reconstructions were used to examine the relationship between the anatomical localization of electrode sites and the cerebrovascular response which was elicited by electrical stimulation of the dorsal raphe nucleus (DRN). Reconstructions of the rat brain and DRN were done from atlas plates and from Nissl-stained coronal sections (100-micron increments). Data points were entered and three-dimensional reconstructions were performed using commercially available software and a personal computer. Display of the entire brain yielded views which obscured visualization of the DRN. The data file was edited to reduce the number of contours without affecting the display resolution of the DRN. Selective display of the DRN and electronic rotation from the coronal to a sagittal view revealed a functional organization of the cerebral blood flow responses which was not apparent in two-dimensional coronal sections.

Animals↗
PubMed1993

Electroconvulsive shock increases tyrosine hydroxylase and neuropeptide Y gene expression in the locus coeruleus.

Electroconvulsive seizures (ECS) increase tyrosine hydroxylase (TH) activity in the locus coeruleus (LC) but not in the substantia nigra (SN). To determine whether new enzyme synthesis contributes to the increase in TH activity, we carried out in situ hybridization histochemistry to determine the effect of ECS on TH mRNA levels in the LC and SN. The effect of ECS on neuropeptide Y (NPY) mRNA levels in the LC was also studied because NPY coexists with norepinephrine in the LC neurons and has been implicated in depressive disorders. A significant increase was observed in TH mRNA and NPY mRNA levels in LC neurons in the ECS group. There was no difference between TH or NPY mRNA levels in the left and right LC. No change was observed in TH mRNA expression in the SN compacta or SN reticulata. We conclude that the regionally selective increase in TH activity after ECS is at least partly due to increased gene expression and that NPY gene expression is regulated in a similar fashion following ECS.

Animals↗
PubMed1992

Regulation of cortical blood flow by the dorsal raphe nucleus: topographic organization of cerebrovascular regulatory regions.

We examined in rat: (1) the time-course and magnitude of change in cortical blood flow (CoBF) following electrical stimulation of the dorsal raphe nucleus (DRN) and (2) whether DRN lesions affect resting CoBF or the cerebrovascular response to CO2. Animals were anesthetized (chloralose), paralyzed, and artificially ventilated. The effect of stimulus frequency (1-200 Hz) and intensity (10-100 microA) on arterial pressure, heart rate, and CoBF was examined; lesions were made electrolytically. CoBF was measured using a laser-Doppler flowmeter with the probe placed extradurally over the parietal sensorimotor cortex. The DRN was computer reconstructed in three dimensions from Nissl stained coronal sections for localization of electrode placements. Brief stimuli (8 s; n = 6) elicited frequency and intensity-dependent increases in arterial pressure, heart rate, and CoBF. Sustained intermittent trains of stimuli of rostral DRN (200 Hz; 1 s on/1 s off; 70 microA) elicited a decrease (85 +/- 12% of baseline; n = 9) in CoBF (p less than 0.05) while stimulation in caudal DRN resulted in increased CBF (126 +/- 13% of baseline; n = 9). Phenylephrine infusion (0.1-1 microgram; i.v.; n = 8) increased arterial pressure and CoBF less than that elicited by brief DRN stimulation (p less than 0.05). DRN lesions did not affect resting CoBF (140 +/- 25 perfusion units (PU) before; 127 +/- 16 PU after DRN lesion; p greater than 0.05, n = 5) or mean arterial pressure (127 +/- 13 before; 120 +/- 11 after); nor did it affect the cerebrovascular response to change in arterial PCO2. Sustained intermittent stimulation of the DRN can evoke either increases or decreases in CoBF depending on the anatomical sublocalization. The DRN does not tonically maintain resting CoBF, nor participate in the cerebrovascular response to change in PCO2.

Animals↗
PubMed1992

Alterations in monoamine receptors in the brain of suicide victims.

Suicide has been linked to alterations in the serotonergic and noradrenergic systems. Using in vitro quantitative receptor autoradiography, we compared the binding of 125I-lysergic acid diethylamide (5-hydroxytryptamine-2 sites) and 125I-pindolol (beta-adrenergic sites) with slide-mounted sections from the prefrontal and the temporal cortex of a group of suicide victims, matched to control specimens on postmortem interval, age, sex, and race. A specific laminar distribution of 5-hydroxytryptamine-2 binding was found in both groups, with layers III and IV having the highest level of binding, but beta-adrenergic binding did not differ across cortical layers. Binding to both 125I-lysergic acid diethylamide and 125I-pindolol was increased in the prefrontal cortex of the suicide victims, whereas only beta-adrenergic binding was increased in the temporal cortex of the suicide group.

Adolescent↗
PubMed1992

Integration of neurobiology and psychopathology in a unified model of suicidal behavior.

Suicidal behavior is the result of a combination of factors that span the domains of psychopathology, genetics, early life experience, family interactions, social stress, physical illness, and neurobiology. To develop predictive and explanatory models of suicidal behavior it is necessary to consider all of these domains. A stress-diathesis model is proposed that classifies risk factors for suicidal behavior into those that are trait-dependent and those that are state-dependent. The timing of suicidal behavior is determined by state-dependent factors. The relationship of psychopathologic factors such as severity of depression or anxiety to suicide will be discussed. Biologic changes that correlate with suicide may be either state- or trait-dependent. Particular emphasis will be given to changes in the serotonin system and how these may represent a constitutional risk factor as opposed to a state-dependent risk factor for suicidal behavior.

Brain↗
PubMed1990

Demonstration of high- and low-affinity beta-adrenergic receptors in slide-mounted sections of rat and human brain.

Studies using isolated cell membranes have shown that beta-adrenergic receptors exist in two interconvertible conformations, one with high affinity for agonists and the other with low affinity. Guanine nucleotides and sodium shift high-affinity receptor sites into low-affinity sites. We sought to demonstrate affinity states of the beta-adrenergic receptor in slide-mounted sections of rat and human postmortem brain, and to determine using quantitative receptor autoradiography the regional distribution in the brain of high-affinity receptors relative to the total population of beta-adrenergic receptors. The beta-adrenergic agonist isoproterenol inhibited the binding of 125I-iodopindolol to slide-mounted sections of rat forebrain and human premotor cortex in a biphasic manner. Approximately 80% of the beta-receptor sites in both rat and human brain showed high-affinity for isoproterenol (7-14 nM). Treatment with 0.1 mM non-hydrolyzable guanine nucleotide 5'-guanylylimidodiphosphate and 25 mM NaCl abolished high-affinity binding in rat brain sections and reduced it in human brain sections. These findings were confirmed by membrane studies using similar tissue samples. For autoradiographic studies, 17 nM isoproterenol displaced 71% of the high-affinity sites without affecting low-affinity beta-adrenergic receptors. Digital subtraction was used to selectively visualize beta-receptors in the high-affinity conformation. The proportion of beta-adrenergic receptors in the high-affinity conformation differed significantly across rat brain regions and across human cortical layers. We conclude that beta-adrenergic affinity states, presumably reflecting the interaction of the receptor with a G-protein, occur in slide-mounted sections of rat brain and persist in human postmortem material.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Autoradiographic demonstration of increased serotonin 5-HT2 and beta-adrenergic receptor binding sites in the brain of suicide victims.

Suicidal behavior has been linked to a deficiency in serotonin neurotransmission, but it is not known which brain regions are involved. We determined the pattern of alteration in serotonin 5-HT2 (5-HT2) receptor binding sites in suicide victims in prefrontal cortex compared with temporal cortex using a matched-pairs design to study 11 suicide victims and 11 matched controls, by both membrane binding and quantitative receptor autoradiography. Since a relationship between the serotonergic and noradrenergic systems has been proposed, we also examined beta-adrenergic receptor binding sites. Binding to 5-HT2 and beta-adrenergic sites in slide-mounted sections correlated strongly with binding site number in membrane preparations. A specific laminar distribution of 5-HT2 binding sites was found in both the control and suicide groups, whereas beta-adrenergic binding sites did not differ across cortical layers. A significant increase was found in suicide victims across all cortical layers in both receptor subpopulations in the prefrontal cortex, but only beta-adrenergic sites were increased in the temporal cortex. We conclude that suicide is associated with a localized increase in 5-HT2 binding sites.

Adolescent↗
PubMed1990

Serotonin and suicidal behavior.

Studies of the brain of suicide victims indicate there is a decrease in brain stem levels of 5-HT and/or 5-HIAA. There also appears to be a region-specific increase in 5-HT2 receptors, which are post synaptic and may therefore be increased in number secondary to decreased serotonin levels. Lack of information about how 5-HT2 and other serotonin receptor populations are regulated hamper our ability to explain the mechanisms underlying these findings. If the initial reports of a decrease in the number of imipramine binding sites prove to be correct then this finding would be further evidence for an effect involving the serotonin neurons, seen in this case at the level of the terminals. The relationship between suicide attempters and completers remains to be worked out. However, studies of suicide attempters, particularly those making more lethal attempts, appear to confirm the findings made in the brain of suicide completers. Neuroendocrine and CSF studies indicate the presence of serotonin subresponsivity and lower levels of CSF 5-HIAA. Thus, the overall direction of change is towards a weaker serotonin signal which rather than being due to a primary receptor defect (a possibility that cannot be ruled out but for which there is no current evidence), appears to be due to reduced levels of serotonin release. The causes of this effect represent a research challenge. It is clear that reduced levels of serotonin alone cannot explain the timing and type of suicidal behavior. Future studies must address the role of other neurotransmitters which may explain why some aggression is directed outward (towards other people) and in other cases the aggression is directed toward the self (suicidal behavior). Defining the role of serotonin and other involved transmitter systems is a necessary step before a comprehensive pharmacological treatment plan can be designed and tested.

Brain↗
PubMed1989

Evidence for the 5-HT hypothesis of suicide. A review of post-mortem studies.

Although suicide was traditionally considered an extreme response to stress, with the most frequent stress being depressive illness, severity of depression does not distinguish those who commit suicide from non-suicide attempters. A biological role involving the serotonergic system, possibly associated with a genetic risk factor, has been postulated. Low levels of 5-HT and 5-HIAA have been found in post-mortem examinations of brain-stem tissues of suicide victims (levels in cortical tissue were generally normal). An increased number of 5-HT2 receptors was found in the pre-frontal cortex of suicide victims, such upregulation having been demonstrated in induced 5-HT deficiency states; 5-HT1A receptors were also increased. Receptor populations may be altered by chronic psychotropic medication; e.g. 5-HT2 downregulation occurs following administration of antidepressants. There is some indication that the adrenergic system may be involved as well, but this will require further study. Antidepressant drugs may be effective in preventing suicide in patients with non-depressive syndromes who exhibit suicidal behaviour.

Brain↗
PubMed1989

Neurochemical studies of violent and nonviolent suicide.

Considerable data have been reported indicating that there is a relationship between suicide or more serious suicide attempts and alterations in indices of serotonin (5-HT) function in patients. The fact that these data are based on studies of both suicide completers as well as more serious suicide attempters and involve a range of experimental techniques spanning biochemical assays of postmortem brain tissue as well as neuroendocrine challenge tests and platelet studies strengthens this finding. However, whether altered serotonin indices are specifically associated with violent compared to nonviolent suicide remains less clear. The relationship may be with some other aspect of suicidal behavior such as the overall lethality of the suicide method, impulsivity, or degree of planning. Suicide method appears to be related to modeling effects or to the relative availability of different methods of suicide, which argues against a predominant role for biological factors in selecting suicide methods. The relative importance of biological vs. modeling and sociological factors in determining suicide method will require more comprehensive studies in which the contribution of all of these factors is assessed simultaneously in the same patient population.

Brain Chemistry↗
PubMed1988

Catecholaminergic neurons in the ventrolateral medulla and nucleus of the solitary tract in the human.

Catecholaminergic neurons in the ventrolateral medulla (VLM) and nucleus of the solitary tract (NTS) are important because of their presumed roles in autonomic regulation, including the tonic and reflex control of arterial pressure, neuroendocrine functions, and the chemosensitivity associated with the ventral medullary surface. However, little is known about the connections of these neurons in the human brain. As a first step in analyzing the functional biochemical anatomy of catecholamine neurons in the human, we used antisera against tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) to localize medullary catecholamine-containing neurons and processes in the VLM and the NTS. Cells staining for TH were located throughout the VLM. Most cells staining for TH and PNMT, which are therefore adrenergic, occurred in an area of the VLM probably corresponding to the rostroventrolateral reticular nucleus. Axons of TH-immunoreactive neurons in the VLM projected (1) dorsally, in a series of parallel transtegmental trajectories, toward the dorsomedial reticular formation, the NTS, and vagal motor nucleus, (2) longitudinally, through the central tegmental field, as fascicles running parallel to the neuraxis, (3) ventrolaterally toward the ventral surface (VS) of the rostral VLM where they appeared to terminate, and (4) medially into the raphe, where they arborized. Similar systems of fibers were labeled for PNMT; the longitudinal bundles of PNMT-labeled axons were limited to the principal tegmental bundle and concentrated dorsally. Fibers containing PNMT were also identified in the medullary raphe, on the medullary ventral surface, and contacting intraparenchymal blood vessels. In the NTS, neurons exhibited immunoreactivity to both TH and PNMT: Four principal subgroups of TH-immunoreactive neurons were seen: a ventral, an intermediate, a medial, and a dorsal group. Perikarya containing PNMT were restricted to the dorsolateral aspect of the NTS. Processes containing TH and PNMT immunoreactivity were identified in the medial and dorsolateral NTS; others appeared to project between the NTS and the VLM and within the solitary tract. The presence of catecholaminergic fibers of the VLM interconnecting with the NTS, raphe, intraparenchymal microvessels, VS, and possibly the spinal cord suggests that the autonomic and chemoreceptor functions attributed to these neurons also may apply to the human.

Adult↗
PubMed1988

Quantitative distribution of muscarinic receptors and choline acetyltransferase in rat medulla: examination of transmitter-receptor mismatch.

Recent reports have identified discrepancies between the anatomical distribution of transmitters and their receptors, a phenomenon known as transmitter-receptor mismatch. However, quantitative determinations of transmitter activity and receptor density in individual brain regions have not been conducted in parallel. We therefore sought to determine quantitatively the relationship between muscarinic acetylcholine receptor density and the density of cholinergic innervation as reflected by activity of the biosynthetic enzyme for acetylcholine, choline acetyltransferase (ChAT). To assure sampling of equivalent regions using the two methods, an 'electronic micropunch' technique was developed to allow measurement of [3H]quinuclidinyl benzilate ([3H]QNB) binding within the corresponding cylinders of tissue obtained by the micropunch cannula. Nineteen regions of the rat medulla (1 mm diameter, 1 mm height) were studied. The micropunch region containing the gracile nucleus, the area postrema and the choroid plexus of the fourth ventricle contained the highest ChAT activity, but exhibited little [3H]QNB binding to muscarinic receptors. However, among the remaining 18 regions a strong correlation was obtained between uncorrected muscarinic receptor density and ChAT activity within each micropunched region (r = 0.89, n = 18). Correction for autoradiographic efficiency weakened the overall relationship between receptor density and ChAT activity (r = 0.58, n = 18). This was due to a relatively high density of receptors associated with fiber tract regions containing low ChAT activity. The presence of receptors within white matter is ordinarily obscured by high tritium quenching. This is consistent with the hypothesis that a portion of muscarinic receptors are located extrasynaptically and may be present within axons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A high density of muscarinic receptors in the rostral ventrolateral medulla of the rat is revealed by correction for autoradiographic efficiency.

Previous reports of a low density of muscarinic receptors in the vicinity of the rostral ventrolateral reticular nucleus (RVL) conflict with the presence of a muscarinic cholinergic mechanism regulating arterial pressure, and may reflect low autoradiographic efficiency due to quenching of tritium emissions by white matter. Regional autoradiographic efficiency was determined using brains uniformly labeled with O-[3H]methylglucose. Within the RVL, autoradiographic efficiency was only 50 +/- 2% relative to gray matter. The uncorrected density of muscarinic receptors (M2) labeled by [3H]quinuclidinyl benzilate in the RVL appeared to be low relative to cranial nerve nuclei, but the corrected muscarinic receptor density approximated that within the nucleus tractus solitarii. We conclude that a high density of M2 muscarinic acetylcholine receptors is present in the RVL.

Animals↗
PubMed1988

CNS adrenergic receptors and beta blockade.

The changes in noradrenergic and adrenergic activity that regulate beta-adrenergic receptors in the CNS have been assessed by lesion studies as well as by pharmacologic enhancement and inhibition of transmission. Beta-adrenergic receptor subtypes are differentially distributed throughout the CNS and are probably differentially regulated. An effect of normal aging on beta receptors has been found in studies of both animal and human brain tissue. Preliminary studies relating to neuropsychiatric disorders in humans and animal studies on the action of antidepressants suggest that CNS beta receptors may play a critical role in affective disorders and their treatment. This may explain why beta-blocker medication is associated with side effects such as depression and lethargy, which are generally reversible when selective hydrophilic beta blockers are used or when the therapy is withdrawn.

Adrenergic beta-Antagonists↗
PubMed1985

Loss and displacement of ganglion cells after optic nerve regeneration in adult Rana pipiens.

After studying pathway selection in the brain of Rana pipiens during unilateral optic nerve regeneration, several frogs were allowed to survive for lengthy periods for use in the present investigation. Retina flat-mounts were prepared from both eyes at 42-50 weeks postoperation. In some cases, HRP was infiltrated into both optic nerves prior to sacrifice to assist in identifying retinal ganglion cells. All specimens showed reduced cell-densities in the ganglion cell layer of the eye that had sustained the nerve regeneration. In addition, many ganglion cells were displaced, abnormally, into the inner plexiform layer, and the normally-situated cells formed irregular bands and islands in some parts of the retina. Cell-counts showed an apparently time-related change in neuron number ranging from a loss of 41% compared with the unaffected eye at 42 weeks, to losses as great as 71% at 50 weeks. The probable number of displaced amacrine cells in the ganglion cell layer, assumed to be unaffected by the experiment, was estimated at a maximum of 16%. Possible factors underlying the loss and displacement of ganglion cells are discussed.

Animals↗
PubMed1983

The anti-retinotopic organization of the frog's optic nerve.

In Rana pipiens, axons marked by the intraretinal application of horseradish peroxidase (HRP) were traced within the optic nerve and tract. Axons arising from dorsal regions of the peripheral retina collect at the dorsal end of the elongate optic disc and form a compact group on the dorsal side of the nerve. Correspondingly, ventral axons locate on the ventral side of the nerve. However, nasal and temporal peripheral axons share passage on both the nasal and temporal sides of the nerve, segregating only upon reaching the brain. The ultimate sorting of nasal and temporal axons in the brain, following their intermingling in the optic nerve, supports the operation of a chemoaffinity mechanism, rather than passive mechanical guidance.

Afferent Pathways↗