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D Jordan

Publications and source records attributed to D Jordan.

At least 109 records · Page 6Linked to original sources

Immunohistochemical distribution of somatostatin in the infant hypothalamus.

Somatostatin (SS)-containing neurons were mapped in the normal infant hypothalamus with immunohistochemistry, using the peroxidase anti-peroxidase technique. Neurons displaying SS immunoreactivity show a widespread distribution throughout the hypothalamic region. Principal SS-immunoreactive like (SS-IL) perikarya are located in the paraventricular, infundibular and posterior nuclei and in the preoptic region. High SS innervation is also found in the ventromedial and in the lateral mammillary nuclei, and in the median eminence. In general this distribution of SS-IL agrees well with that reported for rat. Compared to the immunohistochemical distribution of SS in human adult hypothalamus, this mapping in the infant hypothalamus is grossly similar. However some differences may be underlined: the presence of a moderately dense group of SS-IL perikarya in the tuberal and posterior nuclei, and a dense innervation of the ventromedial nucleus and in the median eminence. This first detailed distribution of SS immunoreactivity in infant hypothalamus can provide basic knowledge for further studies of infant neuropathology.

Humans↗

Comparison of disposition values obtained by two assay methods for quinidine gluconate in patients with ventricular tachycardia.

Eight patients with previously untreated ventricular tachycardia, age 48.54 +/- 28.02 years (mean +/- SD), were enrolled in a protocol evaluating the disposition of quinidine gluconate as determined by two assay methods. Patients received two infusions of 5 mg/kg over 30 minutes separated by 20-30 (24.9 +/- 4.0) minutes of electrophysiologic testing. Blood samples were obtained at 0.17 hours and just prior to the second infusion, and then at 0.17, 0.25, 0.33, 1.0, 6.0, 12.0, and 24.0 hours after the second infusion. Paired serum samples were assayed for quinidine concentrations by fluorescence polarization immunoassay and high-performance liquid chromatography. The two assays compared well, with a linear regression equation of Y = 0.927X + 0.247 with a correlation coefficient of 0.985. With the exception of the beta elimination rate constant and beta distribution volume, t test comparison of disposition values demonstrated no significant difference. Differences in the estimates of the beta elimination rate constant reflected differences in the two methods and indicated that even though both assays were comparable, subtle differences in specificity could be reflected in significant differences in this variable.

Adult↗

Detection of a Thy-1 precursor in human T lymphoma cell lines.

In an attempt to gain insight into the biosynthesis and processing of human Thy-1, rabbit antisera (R alpha TP) were raised against a synthetic peptide (TP) of 13 amino acid residues of identical amino acid sequence to that of residues 110-122 of the putative Thy-1 precursor deduced from the cDNA sequencing. Immunoblotting assay showed that the IgG fraction of R alpha TP (R alpha TP-IgG) recognized the synthetic peptide without demonstrable cross-reactivity with isolated human brain Thy-1 and detergent-solubilized membrane proteins of human brain cells. Immunohistochemical studies showed that both R alpha TP-IgG and HB-2S-1 (a monoclonal antibody which reacts with both membrane-bound Thy-1 on viable cells and detergent-solubilized Thy-1) stained cells of two human T lymphoma cell lines (HUT-78 and HUT-102) but they did not stain cells of a human B lymphoma cell line (Raji). In contrast, in cell surface indirect immunofluorescence assay, HB-2S-1 reacted with HUT-78 and HUT-102 cells while R alpha TP-IgG did not. Taken together, these data indicate the existence of a precursor form of human Thy-1 which is processed prior to anchoring to the cell surface.

Antigens, Surface↗

Anatomical distribution of somatostatin immunoreactivity in the infant brainstem.

The distribution of somatostatin-immunoreactive structures in the infant brainstem was investigated using the peroxidase-antiperoxidase technique. A wide distribution of somatostatin-immunoreactive cell bodies and fibers was observed throughout the brainstem. Numerous somatostatin-immunoreactive cell bodies and fibers were present in several areas of the brainstem including the substantia grisea centralis and the reticular formation. Some immunoreactive cell bodies were seen in cranial nerve nuclei such as the nucleus praepositus, the nucleus nervi hypoglossi and the vestibular nuclei. Immunoreactive fibers were seen in the nucleus cuneatus, the locus coeruleus, the nucleus tractus solitarius, the nucleus ambiguus, the nucleus tractus spinalis nervi trigemini and the dorsal horn of the spinal cord. These data were in agreement with previous works on the human adult. However, a high density of somatostatin-immunoreactive cell bodies and fibers in the interpeduncular nucleus and in the nucleus centralis superior, and a dense network of somatostatin-immunoreactive fibers in the dorsal part of the nucleus inferior olivarius, were also observed. The role of somatostatin in some brainstem nuclei and its probable implication in some specific neuropathological diseases of the infant brainstem is discussed.

Brain Stem↗

Disposition of 3-hydroxyquinidine in patients receiving initial intravenous quinidine gluconate for electrophysiology testing of ventricular tachycardia.

The formation rate constant and elimination rate constant for 3-hydroxyquinidine were determined in eight patients with ventricular tachycardia. These two parameters (mean +/- SD) were found to be 0.784 +/- 0.202 and 0.042 +/- 0.058 h-1, respectively. Coefficients of determination for the computer-generated line of best fit for serum concentration-time data were 0.986 +/- 0.008. Patients received two infusions of quinidine gluconate 5 mg/kg over 30 minutes separated by a 20-30 minute electrophysiologic testing period. Unbound and total 3-hydroxyquinidine concentrations were also determined. Among the eight patients, 3-hydroxyquinidine was 61.9 percent bound. Studies in healthy volunteers had shown 50 percent binding. Linear regression of unbound and total 3-hydroxyquinidine was described by the equation Y = 0.3814X-1.448, r = 0.813. Although half-lives of 3.5-12.4 hours had been reported in healthy volunteers, prolonged half-lives were observed in all but two of our arrhythmia patients.

Adult↗

GnRH receptors in human granulosa cells: anatomical localization and characterization by autoradiographic study.

The presence of receptors for GnRH in human ovary has been investigated by quantitative autoradiography. Simultaneous visualization and characterization of specific receptors on frozen sections were obtained on six pairs of human ovaries. Among them only one exhibited a large preovulatory follicle. This dominant follicle exhibited a specific and high affinity binding capacity for 125I-GnRHa exclusively localized on the granulosa cell layer. Analysis of saturation curve indicates a Kd value of 0.22 nM and Bmax of 9.6 fmol/mg protein. In contrast LH-hCG binding sites were present in all antral follicles. These data demonstrate for the first time the presence of high affinity GnRH receptors in human granulosa cells at a late stage of follicular maturation.

Adult↗

[LHRH in the human hypothalamus. Immunohistochemical mapping in normal newborn infants or in sudden death infants].

The topographical distribution of neurons containing LHRH has been investigated in newborn hypothalamus using the peroxidase anti-peroxidase technique. In control subjects, LHRH immunoreactive (LHRH-IR) perikarya have been mainly observed essentially in the infundibular nucleus. The preoptic region displayed a moderate density of LHRH-IR cell bodies. High LHRH innervation was observed in the anterior hypothalamus in the lamina terminalis and in the mediobasal hypothalamus in the median eminence, and in the peri- and paraventricular regions. In sudden death infant syndrome, a comparable mapping was observed, except a low density in the mediobasal peri- and paraventricular areas.

Brain Mapping↗

[Immunohistochemical absence of adrenergic neurons in the dorsal part of the solitary tract nucleus in sudden infant death].

The immunohistochemical distribution of TH and PNMT containing neuronal elements was investigated utilizing peroxidase anti-peroxidase methods in newborn control and sudden infant death syndrome (SIDS) brainstems. The TH immunoreactive neurons, within the medulla oblongata, displayed a similar distribution in both control and SIDS tissue. However, PNMT immunoreactive neurons seen in the dorsal part of the nucleus of tractus solitarius in control tissue were not observed in SIDS tissue. This alteration of adrenergic neurons in the dorsal part of NTS (region reported to be implicated in the control of blood pressure and respiration) could explain the cardiorespiratory disorders in SIDS.

Epinephrine↗

Hypothalamic inhibition of neurones in the nucleus tractus solitarius of the cat is GABA mediated.

1. In pentobarbitone-anaesthetized cats extracellular activity of neurones in the vicinity of the nucleus tractus solitarius receiving inputs from the carotid sinus nerve (SN) and/or vagus nerve (VN) during stimulation of the hypothalamic defence area (HDA) and application of gamma-aminobutyric acid (GABA) and glycine and their antagonists have been studied. 2. A total of forty neurones have been tested, of which twenty-four only had an input from the SN, one only from the VN, twelve from both nerves and three had neither SN or VN inputs. 3. Short trains of stimuli to the HDA inhibited both the ongoing activity (if present) and evoked discharge in thirty-nine of the forty neurones tested. 4. In the forty cells tested ionophoretic application of GABA reduced (4) or totally inhibited (35) neuronal discharge whilst in the thirty-eight tested with glycine discharge was totally (25) or partially (12) suppressed. 5. Ionophoresis of bicuculline totally (14) or partially (6) antagonized the inhibitory actions of GABA in the twenty-five cells tested, and in eighteen of these the ongoing and/or evoked activity was simultaneously increased. In eighteen of the nineteen cells tested this level of bicuculline also antagonized the inhibitory actions of HDA stimuli whereas in none of the sixteen cells tested did it affect glycine-evoked inhibitions. 6. Ionophoretic application of strychnine antagonized the inhibitory effects of glycine in eight of nine cells tested but in these eight cells strychnine had no effect on ongoing or evoked discharges, GABA- or HDA-evoked inhibitions. 7. In a chloralose-anaesthetized cat five neurones receiving SN inputs (three also receiving VN inputs) were recorded. All could be inhibited by HDA stimuli and by application of GABA. In the three of four cells in which bicuculline antagonized GABA inhibitions, the effects of HDA stimuli were simultaneously antagonized whereas glycine-evoked inhibitions were unaffected. 8. In two neurones, in addition to inhibiting neuronal discharge HDA stimulation also evoked activity in the cells. In a further four neurones similar excitatory responses were uncovered when the HDA inhibitory effects were antagonized by bicuculline. 9. The importance of these observations in cardiovascular control and in the functioning of the baroreceptor reflex is discussed.

Action Potentials↗

Synaptic rhythm of caudal medullary expiratory neurones during stimulation of the hypothalamic defence area of the cat.

1. Intracellular recordings were made from caudal medullary expiratory neurones in anaesthetized, paralysed, artificially ventilated and vagotomized cats before during and after the tachypnoeic response evoked by stimulation of the perifornical region of the hypothalamus. 2. The tachypnoeic response was evoked in seven of ten cats tested, and was represented in the phrenic nerve by a rapid two- to threefold increase in the frequency of the respiratory rhythm. The shortened duration of inspiratory discharge in the phrenic nerve was accompanied by an increase in its rate of development. If initially present, post-inspiratory phrenic discharge was intensified and extended throughout the shortened expiratory interval. 3. Intracellular recordings were obtained from twenty-one expiratory neurones during intermittent hypothalamic stimulation with short trains of pulses. Eighteen neurones showed a regular, short-latency sequence of synaptic events which consisted of an initial depolarizing potential (presumed EPSP) and a following hyperpolarizing potential (Cl--mediated IPSP) of long duration (50-150 ms when measured in expiration). The IPSP was accompanied by a phasic cessation of phrenic nerve discharge of comparable duration which was succeeded by intensified discharge. In three neurones (one experiment) the IPSP response was absent. 4. Sixteen neurones showing the EPSP-IPSP sequence were held for sufficiently long to record changes in the respiratory-related membrane potential pattern accompanying stimulation. The reduced expiratory time accompanying the response resulted in a shortened expiratory burst. In four neurones showing evidence of IPSPs in early expiration (post-inspiratory IPSPs), stimulation resulted in a phasic weakening of this inhibition which resulted in a more rapid approach to threshold and a steady rather than delayed increase in discharge. A low level of post-inspiratory IPSPs extended throughout most of the shortened expiration, resulting in an alternating rhythm of inspiratory and post-inspiratory inhibition. In the twelve neurones lacking such post-inspiratory IPSPs stimulation had no obvious effect on the shape of the expiratory trajectory. 5. In neurones which received an IPSP from hypothalamic stimulation, the overall response was associated with reduced amplitude and increased rate of decline of inspiratory inhibition of expiratory neurones. Three neurones showed high-frequency (70-80 Hz) oscillation of the membrane potential during inspiration (Mitchell & Herbert, 1974b). Hypothalamic stimulation resulted in a transient suppression of this oscillation. 6. We conclude that the short-latency inhibitory component of the response to hypothalamic stimulation is widely distributed, including expiratory neurones, some fraction of the inspiratory population and the neurones responsible for inspiratory and post-inspiratory inhibition.

Animals↗

Characterization and distribution of receptors for gonadotropin-releasing hormone in the rat hippocampus.

Distribution and properties of receptors for gonadotropin-releasing hormone (GnRH) were analyzed in the brain of adult male rats. Binding of the iodinated GnRH agonist Des-Gly10-(D-Ala6)-GnRH ethylamide was studied in hippocampus and anterior pituitary using three convergent approaches: quantitative autoradiography on frozen tissue, binding to fresh slices, and binding to crude membrane preparations. In all cases, binding was specific, saturable, and time, pH, and temperature dependent. Quantitative autoradiography revealed that the density of binding sites was high in the stratum oriens and stratum radiatum of the CA1-CA4 regions of Ammon's horn. The pyramidal cell layer was faintly labelled. Binding was almost undetectable in the dentate gyrus. The highest density of sites (Bmax = 11.6 +/- 1.0 fmol/mg protein) was observed in the stratum radiatum of the CA3 region. Under the same conditions the value obtained for pituitary tissues was 20.7 +/- 2.8 fmol/mg protein. Analysis of saturation curves indicated only one class of high-affinity sites for the hippocampus (CA3; Kd = 0.28 +/- 0.03 nM) and for the pituitary (Kd = 0.29 +/- 0.08 nM). Both native GnRH and GnRH antagonist were potent competitors of binding. Fresh slices and membrane preparations from whole hippocampus confirmed these autoradiographic data and yielded affinity constants of 0.28 +/- 0.01 and 0.52 +/- 0.08 nM, respectively. In addition, a very high binding density was present in the amygdaloid complex, while binding was barely detectable in the hypothalamus. These results demonstrate that high densities of specific GnRH receptors are present in areas concerned with the regulation of behavioral functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiovascular and phrenic nerve responses to stimulation of the amygdala central nucleus in the anaesthetized rabbit.

1. The cardiovascular responses to electrical stimulation of the central nucleus of the amygdala (c.n.) have been studied in chloralose-anaesthetized rabbits. A pattern of response involving bradycardia, hypotension and hind-limb vasodilatation, accompanied by an increase in the rate of phrenic nerve discharge, was evoked only in response to stimulation within the medial portion of the c.n. 2. The cardiovascular responses were not secondary to the changes in respiratory activity since they were unaffected by altering central respiratory drive by either hypo- or hyperventilation of the animal. 3. The bradycardia was attenuated by the administration of atropine sulphate and abolished by the subsequent administration of propranolol, which when given alone attenuated the bradycardia. Atropine or propranolol given alone also attenuated the hypotension evoked by medial c.n. stimulation but the concurrent hind-limb vasodilatation was unaffected. 4. Atenolol, which unlike propranolol does not cross the blood-brain barrier, had little effect on the bradycardia in response to medial c.n. stimulation, but the subsequent administration of atropine abolished it. The hypotension in response to medial c.n. stimulation was also unaffected by atenolol. 5. The vasodilatation in response to medial c.n. stimulation was abolished by administration of guanethidine even after restoration of hind-limb perfusion pressure to control values by the infusion of angiotensin II into the hind-limb perfusion circuit. 6. Electrical stimulation of areas within 0.5 mm of the medial c.n. also resulted in bradycardia but then it was accompanied by hypertension and hind-limb vasoconstriction. Stimulation of areas 1.0 mm distant to the medial c.n. resulted in small and inconsistent cardiovascular responses. 7. These results show that hind-limb vasodilatation, mediated by withdrawal of sympathetic tone, occurs in response to stimulation within the medial c.n. of the rabbit and is in part responsible for the observed hypotension. It has also been confirmed that the bradycardia in response to medial c.n. stimulation is mediated by the vagus nerves.

Action Potentials↗

Effects of stimulation of nasal and superior laryngeal inputs on the hindlimb vasculature of anaesthetized cats.

1. In chloralose-anaesthetized artificially ventilated cats, either stimulation of the nasal mucosae with water or electrical stimulation of the superior laryngeal nerve (s.l.n.) resulted in apnoea, as measured from the phrenic nerve activity, and a rise in perfusion pressure of a hindlimb perfused at constant flow. In the absence of changes in venous pressure this vascular response would indicate vasoconstriction in the hindlimb. There was, however, no significant change in either heart rate or arterial blood pressure. 2. Simultaneous stimulation of the nasal mucosae and s.l.n. also resulted in apnoea but with a larger hindlimb vasoconstriction than was obtained with stimulation of only one input. This increased vasoconstriction was not significantly different from the one which in theory could be obtained by summing the two individual responses from stimulation of the nasal mucosae or s.l.n. 3. In cats anaesthetized with chloralose-urethane, stimulation of the nasal mucosae or s.l.n. also evoked an apnoea and hindlimb vasoconstriction. However, in these animals this was accompanied by a bradycardia and small fall in arterial blood pressure. 4. The present results show that whilst stimulation of two parts of the upper respiratory tract evokes qualitatively similar responses in the hindlimb vasculature, simultaneous activation of the two stimuli does not appear to result in facilitation of this hindlimb vasoconstrictor response, simply an addition of those obtained on separate stimulation. The bradycardia evoked in response to upper airway stimulation is dependent on the anaesthetic used and in the present experiments could only be obtained in animals anaesthetized with choralose-urethane.

Anesthesia, General↗

A convergent input from nasal receptors and the larynx to the rostral sensory trigeminal nuclei of the cat.

1. Extracellular recordings were made from ninety-one neurones in the vicinity of the rostral trigeminal nucleus in chloralose-anaesthetized cats. 2. Sixty-two neurones within this area were activated by electrical stimulation of the ipsilateral superior laryngeal nerve (s.l.n.). Only two of the twenty-one neurones tested had an additional input from the contralateral s.l.n. 3. Fifty of these sixty-two neurones were also activated synaptically by light mechanical stimulation of the ipsilateral nasal cavity and in the eight neurones tested electrical stimulation of the ipsilateral nostril evoked activity. All these neurones exhibited characteristics of postsynaptic responses to s.l.n. and nasal stimulation, showing a variable latency to onset to either stimulus, summation and facilitation of more than one stimulus. 4. None of those neurones receiving an s.l.n. input, or those with convergent inputs from the s.l.n. and nose, could be affected by mechanical stimulation of any part of the face. 5. The activity of a further twenty-nine neurones was also recorded within this same general region. Sixteen responded to movement of the whiskers, five to touching the skin of the lower jaw, two to touching the skin of the upper jaw, three to touch around the eyebrows and three to touching other parts of the face. None of these neurones were activated by s.l.n. stimulation. 6. The location of seventeen of these neurones showing a convergent s.l.n. and nasal input was determined histologically. They were closely grouped together in a region 3.5-4.5 mm rostral to obex in and around the main trigeminal sensory nucleus, dorsolateral to the retrofacial nucleus corresponding to the parvocellular division of the alaminar spinal trigeminal nucleus. 7. The lack of somatosensory input to those neurones receiving a convergent input from the nose and s.l.n. is discussed in relation to previous studies describing somatosensory-visceral convergence to neurones within trigeminal nuclei.

Anesthesia, General↗

Thyroid-hypophyso-hypothalamic axis of the genetically hypoprolactinemic rats (IPL nude rats).

In order to evaluate thyrotropin function in the genetically hypoprolactinemic rat, (IPL nude), we measured by radioimmunoassay TRH hypothalamic content, pituitary TSH content and serum TSH, T3, T4, both in IPL nude and control rats at various times over the 24-hour period. Compared to normal rats, the hypothalamic TRH content in the IPL nude rat showed similar variations during the day, whereas a slight increase was observed during the night characterized by a significant difference at 20.00 h. Pituitary weight and TSH content were doubled in IPL nude rats; however, when expressed as micrograms TSH/micrograms protein or DNA, a significant increase was found only at 17.00 and 20.00 h. Serum TSH and total serum T3, T4 depicted similar variations although they were minute but nonetheless significant modifications, i.e. an increase of TSH at 17.00 and 23.00 h and a decrease of T4 at 11.00 h. However, only FT4 concentrations (and not-FT3) were slightly but significantly decreased in IPL rats over the experimental times. In conclusion, the slight increase in hypothalamic TRH and pituitary TSH contents and the absence of main associated variations of serum TSH, T3 and T4 do not lend support to the hypothesis that TRH could be the cause of the hypoprolactinemia of these rats. On the contrary, the observed thyrotropin axis variations might be rather interpreted as the consequence of it.

Animals↗

Postnatal development of TRH and TSH rhythms in the rat.

We previously observed that under a 12-hour light/12-hour dark schedule (lights off at 19.00 h), adult male Sprague-Dawley rats showed a circadian rhythm for serum thyroid-stimulating hormone (TSH) with a zenith near midday. In the present work, the ontogenesis of serum TSH rhythm was determined as well as pituitary TSH variations. In addition, hypothalamic and blood TRH were measured in these rats aged 15, 25, 40 and 70 days when sacrificed. As from the first age studied (15 days), a hypothalamic thyrotropin-releasing hormone (TRH) circadian rhythm was present. The mesor and the amplitude of this hypothalamic TRH rhythm increased while the rats were growing up, in contrast with the decrease observed for these parameters as far as blood TRH circadian rhythm is concerned. The time of the acrophase moved from 17.32 h in the 15-day-old rats to 13.57 h in the 70-day-old rats, being constantly in phase opposition with the blood TRH acrophase. The low amplitude pituitary TSH circadian rhythm detected in the young rat disappeared in the adult while, in contrast, the serum TSH rhythm became consistent to reach the well-characterized circadian midday peak in the 70-day-old rats.

Aging↗

TRH and LH-RH distribution in discrete nuclei of the human hypothalamus: evidence for a left prominence of TRH.

Thyrotropin-releasing hormone (TRH) and luteinizing hormone-releasing hormone (LH-RH) have been measured by radioimmunoassay in individual human hypothalamic nuclei. A significant lateralization has been found for TRH in the ventromedial, dorsal and paraventricular nuclei, with higher concentration in the left side. In contrast LH-RH values did not differ between the left and the right side. This finding represents an additional example of cerebral specialization and the first report of lateralized peptide distribution in the human hypothalamus.

Adult↗