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P Fort

Publications and source records attributed to P Fort.

At least 55 records · Page 3Linked to original sources
PubMed1997

High-frequency oscillatory ventilation for adult respiratory distress syndrome--a pilot study.

OBJECTIVE: To evaluate the safety and effectiveness of high-frequency oscillatory ventilation using a protocol designed to recruit and maintain optimal lung volume in patients with severe adult respiratory distress syndrome (ARDS). SETTING: Surgical and medical intensive care units in a tertiary care, military teaching hospital. DESIGN: A prospective, clinical study. PATIENTS: Seventeen patients, 17 yrs to 83 yrs of age, with severe ARDS (Lung Injury Score of 3.81 +/- 0.23) failing inverse ratio mechanical conventional ventilation (PaO2/FiO2 ratio of 68.6 +/- 21.6, peak inspiratory pressure of 54.3 +/- 12.7 cm H2O, positive end-expiratory pressure of 18.2 +/- 6.9 cm H2O). INTERVENTIONS: High-frequency oscillatory ventilation was instituted after varying periods of conventional ventilation (5.12 +/- 4.3 days). We employed lung volume recruitment strategy that consisted of incremental increases in mean airway pressure to achieve a PaO2 of > or = 60 torr (> or = 8.0 kPa), with an FiO2 of < or = 0.6. MEASUREMENTS AND MAIN RESULTS: High-frequency oscillator ventilator settings (FiO2, mean airway pressure, pressure amplitude of oscillation [delta P] frequency) and hemodynamic parameters (cardiac output, oxygen delivery [DO2]), mean systemic and pulmonary arterial pressures, and the oxygenation index (oxygenation index = [FiO2 x mean airway pressure x 100]/PaO2) were monitored during the transition to high-frequency oscillatory ventilation and throughout the course of the high-frequency protocol. Thirteen patients demonstrated improved gas exchange and an overall improvement in PaO2/FiO2 ratio (p < .02). Reductions in the oxygenation index (p < .01) and FiO2 (p < .02) at 12, 24, and 48 hrs after starting high-frequency oscillatory ventilation were observed. No significant compromise in cardiac output or DO2 was observed, despite a significant increase in mean airway pressure (31.2 +/- 10.3 to 34.0 +/- 6.7 cm H2O, p < .05) on high-frequency oscillatory ventilation. The overall survival rate at 30 days was 47%. A greater number of pretreatment days on conventional ventilation (p < .009) and an entry oxygenation index of > 47 (sensitivity 100%, specificity 100%) were associated with mortality. CONCLUSIONS: High-frequency oscillatory ventilation is both safe and effective in adult patients with severe ARDS failing conventional ventilation. A lung volume recruitment strategy during high-frequency oscillatory ventilation produced improved gas exchange without a compromise in DO2. These results are encouraging and support the need for a prospective, randomized trial of algorithm-controlled conventional ventilation vs. high-frequency oscillatory ventilation for adults with severe ARDS.

Adolescent↗
PubMed1996

Effect of strychnine on rat locus coeruleus neurones during sleep and wakefulness.

The noradrenergic neurones of the locus coeruleus (LC) discharge tonically during wakefulness, decrease their activity during slow wave sleep and are virtually quiescent during paradoxical sleep. We recently demonstrated an inhibitory glycinergic input to the locus coeruleus and proposed that this could be responsible for inhibition of the LC during paradoxical sleep. To test this proposal, we developed a method combining polygraphic recordings, iontophoresis and single-unit extracellular recordings in the unanaesthetized head-restrained rat. Iontophoretically applied strychnine, a specific glycine antagonist, induced strong excitation of LC neurones during paradoxical sleep, but also during slow wave sleep and wakefulness. These results suggest that glycine tonically inhibits noradrenergic LC neurones throughout the entire sleep-waking cycle and not only during paradoxical sleep.

Anesthesia↗
PubMed1996

Origin of the glycinergic innervation of the rat trigeminal motor nucleus.

In order to determine the localization of the glycinergic neurones responsible for the hyperpolarization of the rat trigeminal motoneurones during paradoxical sleep, we developed a new double immunohistochemical method combining the b subunit of the cholera toxin (CTb), a very sensitive retrograde tracer, with glycine immunohistochemistry. After iontophoretic injections of CTb into the trigeminal motor nucleus (Mo5), a large number of double-labelled cells was observed bilaterally in the parvocellular reticular nucleus alpha, dorsolateral to the descending branch of the facial nerve. A moderate number of double-labelled neurones was found in the ipsilateral parvocellular reticular nucleus at the level of the facial nucleus, and bilaterally in the raphe magnus and the gigantocellular reticular alpha nuclei. These results suggest that the glycinergic neurones hyperpolarizing the trigeminal motoneurons during paradoxical sleep might be localized in the parvocellular reticular nucleus alpha.

Animals↗
PubMed1996

A delayed-early response nuclear gene encoding MRPL12, the mitochondrial homologue to the bacterial translational regulator L7/L12 protein.

We have characterized a new delayed-early response mRNA encoding a 21-kDa product (MRPL12) that accumulates during the G1 phase of growth-stimulated cells. MRPL12 is the mammalian homologue to chloroplastic and bacterial L12 ribosomal proteins. Immunofluorescence microscopy and cell fractionation indicate a predominant mitochondrial localization in various mammalian cell lines. The NH2-terminal 49 amino acids are necessary and sufficient to target the protein within the mitochondria and are probably cleaved off during import. MRPL12 proteins associated in vitro and cofractionate with ribosomal structures, as is the case for prokaryotic L12 proteins. Expression of a dominant inhibitory truncated protein leads to a severe reduction in cell growth by inhibiting mitochondrial ATP production. MRPL12 is the first mammalian mitochondrial ribosomal protein to be characterized.

3T3 Cells↗
PubMed1996

Lower brainstem catecholamine afferents to the rat dorsal raphe nucleus.

A large body of data suggests that the activation of alpha 1 receptors by a tonic noradrenergic input might be responsible for the tonic discharge of the serotonergic neurons of the dorsal raphe nucleus (DRN). To test this hypothesis, it was necessary to determine the origin of the noradrenergic and adrenergic innervation of these neurons. For this purpose, we combined small iontophoretic injections of the sensitive retrograde tracer cholera toxin b subunit (CTb) in the different subdivisions of the DRN with tyrosine hydroxylase immunohistochemistry. After CTb injections in the ventral or dorsal parts of the central DRN, a small number of double-labeled cells was observed in the locus coeruleus (A6 noradrenergic cell group), the A5 noradrenergic group, the dorsomedial medulla (C3 adrenergic cell group), and the lateral paragigantocellular nucleus (C1 adrenergic cell group). After CTb injections in the lateral wings or the dorsal part of the rostral DRN, a similar number of double-labeled cells was seen in C3. Slightly more double-labeled cells were seen in A6 and A5. In addition, a substantial to large number of double-labeled cells appeared in C1, the commissural part of the nucleus of the solitary tract (A2 noradrenergic cell group) and the caudoventrolateral medulla (A1 noradrenergic cell group). These results indicate that the noradrenergic and adrenergic inputs to the DRN arise from all the catecholaminergic cell groups of the lower brainstem except the A7 noradrenergic group. They further reveal the existence of a topographical organization of these afferents to the different subdivisions of the DRN.

Afferent Pathways↗
PubMed1996

Distribution of glycine-immunoreactive cell bodies and fibers in the rat brain.

To localize glycinergic cell bodies and fibers in the rat brain, we developed a sensitive immunohistochemical method combining the use of specific glycine antibodies (Campistron G. et al. (1986) Brain Res. 376, 400-405; Wenthold R. J. et al. (1987) Neuroscience 22, 897-912) with the streptavidin-horseradish peroxidase technique and 3,3'-diaminobenzidine.4HCl-nickel intensification. We confirmed the presence of numerous glycine-immunoreactive cell bodies and fibers in the cochlear nuclei, superior olivary complex, nucleus of the trapezoid body, cerebellar cortex, deep cerebellar nuclei and area postrema. For the first time in rats, we described a large to very large number of cell bodies in the medial vestibular ventral part, prepositus hypoglossal, gracile, raphe magnus and sensory trigeminal nuclei. A large number of cells was also observed in the oral and caudal pontine, parvocellular, parvocellular pars alpha, gigantocellular and gigantocellular pars alpha reticular nuclei. In addition, glycine-immunoreactive cells were seen in the ambiguous and subtrigeminal nuclei, the lateral habenula and the subfornical organ. We also provide the first evidence in rats for a very large number of fibers in the trigeminal, facial, ambiguous and hypoglossal motor nuclei, all nuclei of the medullary and pontine reticular formation, and the raphe and trigeminal sensory nuclei. We further revealed the presence of a substantial number of fibers in regions where glycine was not considered as a main inhibitory neurotransmitter, such as the pontine nuclei, the periaqueductal gray, the mesencephalic reticular formation, the anterior pretectal nucleus, the intralaminar thalamic nuclei, the zona incerta, the fields of Forel, the parvocellular parts of the paraventricular nucleus, the posterior hypothalamic areas, the anterior hypothalamic area, and the lateral and medial preoptic areas. These results indicate that, in contrast to previous statements, glycine may be an essential inhibitory neurotransmitter not only in the lower brainstem and spinal cord, but also in the upper brainstem and the forebrain.

Animals↗
PubMed1996

Rhythmic firing of medial septum non-cholinergic neurons.

The presence of theta rhythm (5-10 Hz) in the hippocampus has been shown to enable long-term potentiation, a synaptic mechanism which has been proposed to underlie learning and memory. Medial septum cholinergic and GABAergic neurons that project to the hippocampus have been hypothesized to play conjointly a major role in the genesis of this rhythm. Building upon previous studies that have established the electrophysiological criteria for distinguishing cholinergic and non-cholinergic neurons in this area, it is demonstrated here that medial septum non-cholinergic neurons, putatively GABAergic, have the ability to discharge in rhythmic clusters of action potentials occurring at frequencies ranging from 1 to 8 Hz. Within the clusters, the firing frequency of action potentials varied between 13 and 57 Hz in a voltage-dependent manner. In addition, small voltage-dependent subthreshold membrane potential oscillations (16-54 Hz) were observed between clusters. Both subthreshold oscillations and clusters were eliminated by tetrodotoxin at 1 microM. These results indicate that non-cholinergic medial septum neurons could convey to the hippocampus not only theta but also higher frequency rhythmicity in the beta-gamma range (20-60 Hz).

Animals↗
PubMed1996

Differential oscillatory properties of cholinergic and noncholinergic nucleus basalis neurons in guinea pig brain slice.

Evidence has suggested that the nucleus basalis magnocellularis has the potential to influence the functional state of the cerebral cortex through topographically organized, widespread projections of the cholinergic cells in that nucleus. It has also been shown that, in addition to the cholinergic neurons, other non-cholinergic magnocellular basal forebrain neurons, some of which have been identified as gamma-aminobutyric acid-ergic, project into the cerebral cortex and thus may also participate in the modulation of its activity. We have performed a comparative study of the intrinsic rhythmic properties of immunohistochemically and morphologically characterized choline acetyltransferase (ChAT)-positive and ChAT-negative cells of the nucleus basalis by means of intracellular recordings in guinea pig brain slices. Our results demonstrate that relatively large, multipolar cholinergic and non-cholinergic neurons each display differential voltage-dependent properties that allow them to discharge rhythmically in spike bursts and spike clusters, respectively, at low frequencies (< 10 Hz). Cholinergic cells display bursts of 2-4 action potentials (at approximately 200 Hz) riding on low-threshold spikes recurring at a low frequency (< 5 Hz) when depolarized from a membrane potential more negative than -55 mV and display low-frequency (< 10-15 Hz) tonic firing when depolarized from a more positive level. In contrast, non-cholinergic cells fire in a unique mode, displaying non-adapting clusters of spikes interspersed with rhythmic subthreshold membrane-potential oscillations when depolarized from levels less negative than -55 mV. The spike clusters repeat rhythmically at relatively low frequencies (2-10 Hz). The intracluster spiking frequency is relatively high and coincides approximately with that of the intervening membrane-potential oscillations (approximately 20-70 Hz). The cluster frequency of the non-cholinergic cells corresponds, in the same manner as the burst frequency of the cholinergic cells, to a delta (1-4 Hz) or theta (4-10 Hz) range of activity, whereas the intra-cluster and tonic spike frequencies of the non-cholinergic cells correspond to high beta to gamma ranges of electroencephalographic activity (19-30 Hz and 30-60 Hz, respectively). We propose that the different modes of oscillatory firing by the cholinergic and non-cholinergic basal forebrain cell populations could collectively contribute to the rhythmic modulation of slow and fast rhythms within the cerebral cortex.

Animals↗
PubMed1996

Incidence of transient congenital hypothyroidism due to maternal thyrotropin receptor-blocking antibodies in over one million babies.

To determine the incidence of transient congenital hypothyroidism due to TSH receptor-blocking antibodies, we screened dried blood specimens obtained from 788 neonates identified as having possible congenital hypothyroidism (from a total population of 1,614,166 babies) and 121 controls. A RRA was used. The potency of blood spot TSH binding inhibitory activity was compared with the severity of congenital hypothyroidism to assess the possible etiological relationship. Maternal serum was studied to confirm the presence of blocking antibodies by both RRA and bioassay. Blood spots obtained from 9 infants contained potent TSH receptor-blocking activity. Samples from 2 additional babies, studied because of clinical suspicion of the disease, were also positive. Long term outcome was known in 8 of the 11 babies, and all had transient disease. Neonates with TSH receptor-blocking activity greater than 132 U/L had a significantly lower T4 level (P < 0.05) and higher TSH (P < 0.005) than those in whom TSH binding-inhibitory activity was less than 132 U/L. All 9 mothers had autoimmune thyroid disease, and 3 had more than 1 affected child. Potent blocking activity was present in 7 maternal serum samples as long as 7 yr after the births of their affected babies. We conclude that measurement of TSH binding-inhibitory activity in dried neonatal blood specimens is a simple and effective method to predict the occurrence of transient congenital hypothyroidism. The incidence of this disorder in North America is 1 in 180,000 normal infants, or approximately 2% of babies with congenital hypothyroidism.

Acute Disease↗
PubMed1995

Origin of the dopaminergic innervation of the rat dorsal raphe nucleus.

The aim of the present study was to describe the distribution of dopamine (DA) fibres in the dorsal raphe nucleus (DRN) and to determine their neurones of origin. Using an anti-DA antibody, we observed a moderate density of DA varicose fibres over the DRN and a dense plexus of DA fibres in the ventrolateral central grey. With a sensitive retrograde tracing technique combining the use of cholera toxin subunit b with tyrosine hydroxylase immunohistochemistry, after tracer injections in the DRN, a few double-labelled cells were observed in the ventral tegmental area and the A10 dorsocaudal DA cell group, as already described. In addition, a moderate number of double-labelled cells was seen in the A11 hypothalamic DA cell group.

Animals↗
PubMed1995

Rhythmical bursts induced by NMDA in guinea-pig cholinergic nucleus basalis neurones in vitro.

1. Intracellular recordings were performed in neurones within the basal forebrain of guinea-pig brain slices. Following injection of biocytin (or biotinamide), a subset of recorded neurones which displayed distinct intrinsic membrane properties were confirmed as being cholinergic by immunohistochemical staining for choline acetyltransferase (ChAT). They were all located within the nucleus basalis magnocellularis. The response of the cholinergic cells to NMDA and to the agonists of the other glutamate receptors was tested by bath application of NMDA, t-ACPD, AMPA and kainate. 2. When depolarized from a hyperpolarized level, cholinergic basalis neurones display the intrinsic ability to discharge in rhythmic bursts that are generated by low-threshold Ca2+ spikes. In control solution, these rhythmic bursts were not sustained for more than 5-6 cycles. However, in the presence of NMDA when the membrane was held at a hyperpolarized level, low-threshold bursting activity was sustained for prolonged periods of time. This activity could be reversibly eliminated by D(-)-2-amino-5-phosphonopentanoic acid (D-AP5), showing that it depended upon specific activation of NMDA receptors. 3. NMDA-induced, voltage-dependent, rhythmic depolarizations persisted in the presence of tetrodotoxin (TTX), indicating that they did not depend upon a TTX-sensitive Na+ current and were generated postsynaptically. The rhythmic depolarizations were, however, eliminated by the partial replacement of Na+ with choline, demonstrating that they did depend upon Na+, the major carrier of the NMDA current. 4. In the presence of TTX, the NMDA-induced rhythmic depolarizations were also eliminated by removal of Ca2+ from or addition of Ni2+ to the bath, indicating that they also depended upon Ca2+, which is carried by both the NMDA current and the low-threshold Ca2+ current. The duration of the rhythmic depolarizations was increased in the presence of apamin, suggesting that the repolarization of the cells depended in part upon a Ca(2+)-activated K+ (SK) conductance, but that other mechanisms were additionally involved in the repolarization phase of the bursting. 5. In both the absence and presence of TTX, the NMDA-induced rhythmic activity persisted when Mg2+ was removed from the medium, indicating that the sustained rhythmic depolarizations did not hinge upon the Mg2+ block of the NMDA channels during hyperpolarization. The voltage dependence of the NMDA-induced rhythmic depolarizations in the absence of Mg2+ appeared to be determined by the properties of the low-threshold Ca2+ spike in the cholinergic basalis neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Noradrenergic modulation of cholinergic nucleus basalis neurons demonstrated by in vitro pharmacological and immunohistochemical evidence in the guinea-pig brain.

The effects of noradrenalin were tested upon electrophysiologically characterized cholinergic nucleus basalis neurons in guinea-pig brain slices. According to their previously established intrinsic membrane properties, the cholinergic cells were distinguished by the presence of low-threshold Ca2+ spikes and transient outward rectification that endowed them with the capacity to fire in low-threshold bursts in addition to a slow tonic discharge. A subset of the electrophysiologically identified cholinergic cells that responded to noradrenalin had been filled with biocytin (or biotinamide) and documented in previously published reports as choline acetyltransferase (ChAT)-immunoreactive. The noradrenalin-responsive, biocytin-filled/ChAT+cells were mapped in the present study and shown to be distributed within the substantia innominata amongst a large population of ChAT+ cells. Slices from another subset of noradrenalin-responsive, electrophysiologically identified cholinergic cells were stained for dopamine-beta-hydroxylase to visualize the innervation of the biocytin-filled neurons by noradrenergic fibres. These biocytin-filled neurons were surrounded by a moderate plexus of varicose noradrenergic fibres and were ostensibly contacted by a small to moderate number of noradrenergic boutons abutting their soma and dendrites. Applied in the bath, noradrenalin produced membrane depolarization and a prolonged tonic spike discharge. This excitatory action was associated with an increase in membrane input resistance, suggesting that it occurred through reduction of a K+ conductance. These effects persisted when synaptic transmission was eliminated (by tetrodotoxin or low Ca2+/high Mg2+) and were therefore clearly postsynaptic. The excitatory effect of noradrenalin was blocked by the alpha 1-adrenergic receptor antagonist prazosin and not by the alpha 2-antagonist yohimbine, and it was mimicked by the alpha 1-agonist L-phenylephrine but not by the alpha 2-agonists clonidine and UK14.304, indicating mediation by an alpha 1-adrenergic receptor. There was also evidence for a contribution by a beta-adrenergic receptor to the effect, since the beta-antagonist propranolol partially attenuated the effect of noradrenalin, and the beta-agonist isoproterenol produced, like noradrenalin, alone or when applied in the presence of the alpha 1-antagonist prazosin, membrane depolarization and an increase in tonic spike discharge. These results indicate that through a predominant action upon alpha 1-adrenergic receptors, but with the additional participation of beta-adrenergic receptors, noradrenalin depolarizes and excites cholinergic neurons. This action would tend to drive the cholinergic cells into a tonic mode of firing and to stimulate or increase the rate of repetitive spike discharge for prolonged periods.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗
PubMed1995

Growth-regulated expression of FKBP-59 immunophilin in normal and transformed fibroblastic cells.

Expression of many primary response cellular genes is observed during the early stages of transition from a resting G0 state to DNA synthesis. To identify gene products implicated in long-term response to growth factors, we have isolated genes sequentially activated several hours after serum stimulation of fibroblastic CCL39 cells. We report here the characterization of one of them as encoding the immunophilin of 56-59 kDa (FKBP-59), a component of the steroid receptor complex. FKBP-59 is encoded in several mammalian species by a unique gene located within the transition protein 2 gene locus. FKBP-59 mRNA is ubiquitously expressed at various levels in human organs. FKBP-59 gene activation in CCL39 fibroblasts requires protein synthesis during the first 2 h of stimulation, a period of time during which proto-oncogenes such as c-fos or c-jun are expressed. FKBP-59 mRNA degrades upon serum withdrawal and accumulates in proportion to the mitogenic strength of various purified growth factors. Its expression is reduced in CCL39 mutant-transformed cells or cells able to grow in low serum-containing medium, suggesting that FKBP-59 might participate in the negative feedback control to cell proliferation.

Alternative Splicing↗
PubMed1995

Cholinergic nucleus basalis neurons are excited by histamine in vitro.

Considerable evidence has shown that both cholinergic and histaminergic neurons in the brain may act to facilitate processes of cortical activation that occur during wakefulness. In the present study, the potential influence of histaminergic neurons upon cholinergic neurons of the basal forebrain was investigated in guinea-pig basal forebrain slices. We found that electrophysiologically identified and immunohistochemically verified cholinergic neurons of the nucleus basalis were depolarized and excited by histamine, as manifested by an increase in tonic firing. The depolarization was associated with an increase in membrane input resistance. The effect of histamine persisted in the presence of either tetrodotoxin or a high-magnesium/low-calcium solution, indicating that it is postsynaptic. By a process of elimination, the participation in this response of the three described histamine receptors was examined. Involvement of H3 receptors was excluded on the basis that the H3 agonist (R)-alpha-methyl-histamine had no direct effect, and the H3 antagonist, thioperamide, did not block the effect of histamine. In contrast, the presence of a small response to impromidine, a selective agonist of H2 receptors, and the partial block of the response to histamine by the H2 receptor antagonist, cimetidine, indicated the participation of H2 receptors. Finally, the complete elimination of histamine's effect occurred when low doses of the H1 antagonist, mepyramine, were added to the H2 antagonist, cimetidine, indicating the involvement and predominance of H1 receptors in the response. Our data thus suggest that histamine excites nucleus basalis cholinergic neurons by a concomitant activation of H1 and H2 receptors. Histaminergic tuberomammillary neurons may accordingly facilitate tonic firing of cholinergic neurons during wakefulness. Cholinergic basalis neurons could thus act in tandem with histaminergic neurons during periods of arousal to collectively promote widespread cortical activation.

Action Potentials↗
PubMed1994

Afferents to the nucleus reticularis parvicellularis of the cat medulla oblongata: a tract-tracing study with cholera toxin B subunit.

The aim of this study was to examine anatomical evidence in cats of whether the nucleus reticularis parvicellularis (Pc) is part of the circuit responsible for the inhibition of brainstem motoneurons during paradoxical sleep. For this purpose, we made iontophoretic injections of the retrograde and anterograde tracer cholera toxin B subunit (CTb) in the Pc. After CTb injections in the Pc, a large number of retrogradely labeled neurons were seen in the central nucleus of the amygdala, the lateral part of the bed nucleus of the stria terminalis, the posterior hypothalamic areas, the mesencephalic reticular formation, the nucleus locus subcoeruleus, the nucleus pontis caudalis, other portions of the Pc, the nucleus reticularis dorsalis, the trigeminal sensory complex, and the nucleus of the solitary tract. We further found that the Pc receives 1) serotoninergic afferents from the raphe dorsalis, magnus, and obscurus nuclei; 2) noradrenergic inputs from the dorsolateral pontine tegmentum; 3) cholinergic afferents from the lateral medullary reticular formation; 4) substance P-like afferents from the central nucleus of the amygdala, bed nucleus of the stria terminalis, periaqueductal gray, and nucleus of the solitary tract; and 5) methionine-enkephalin-like projections from the periaqueductal gray, the nucleus of the solitary tract, the lateral pontine and medullary reticular formation, and the spinal trigeminal nucleus. We further found that the Pc do not receive afferents from brainstem structures responsible for muscle atonia, such as the ventromedial medulla and the dorsomedial pontine tegmentum, and therefore may not be part of the circuit inhibiting the brainstem motoneurons during paradoxical sleep.

Animals↗
PubMed1993

Pharmacological and immunohistochemical evidence for serotonergic modulation of cholinergic nucleus basalis neurons.

Identified electrophysiologically by low threshold bursts and transient outward rectification, cholinergic nucleus basalis neurons were recorded and labelled intracellularly in guinea-pig basal forebrain slices. By means of a triple labelling immunofluorescent technique, serotonin-immunoreactive fibres were visualized in close proximity to the soma and dendrites of the biocytin-labelled, choline acetyl transferase (ChAT)-immunoreactive cells. By bath application, 5-hydroxytryptamine (5-HT) produced a direct hyperpolarization of the identified cells which was mimicked by 5-HT1A receptor agonists, suggesting that it may inhibit the tonic firing but also modulate the low threshold bursting of the cholinergic nucleus basalis neurons.

Animals↗
PubMed1993

Histaminergic system in the cat hypothalamus with reference to type B monoamine oxidase.

It is known that histamine (HA) and type B monoamine oxidase (MAO-B), an enzyme involved in its metabolism, are present in the posterior hypothalamus, but the sites where MAO-B intervenes in HA metabolism remain uncertain. The present study examined and compared the detailed distribution and morphology of neurons immunoreactive to HA (HA-ir) and MAO-B (MAO-B-ir) in the cat hypothalamus. HA-ir neurons were localized almost exclusively in the posterior hypothalamus with the largest group in the tuberomammillary nucleus and adjacent areas. MAO-B-ir staining was detected in the vast majority of HA-ir neurons, suggesting that the degradation of tele-methylhistamine (t-MHA), the direct metabolite of HA, may occur within these cells. Nevertheless, a few HA-ir cells showed no detectable or very weak MAO-B-ir labeling; a small group of neurons containing MAO-B alone was detected in the area dorsolateral to the caudal part of the arcuate nucleus. Numerous HA-ir axons and terminal-like structures were distributed unevenly in virtually all hypothalamic regions. One of their principal trajectories ascended through the ventrolateral part of the hypothalamus and rostrally formed an axon column, which ascended into the preoptic area and contributed fibers to the diagonal band of Broca and bed nucleus of the stria terminalis. Other HA-ir axons passed laterally, dorsal to the zona incerta or ventrally through a narrow zone dorsal to the optic tract. Numerous long HA-ir axons coursed dorsomedially from the ventrolateral posterior hypothalamus to the dorsal hypothalamic area. Many are oriented vertically to the thalamus in the midline. MAO-B-ir axons and fibers were detectable throughout the hypothalamus and overlapped the areas distributing HA-ir fibers. They were, however, weaker in staining intensity and apparently fewer than the HA-ir fibers. MAO-B-ir glial cells were numerous in all hypothalamic structures rich in HA-ir fibers. These results suggest that the metabolism of t-MHA may also occur within HA terminals and glial cells.

Animals↗