PubMed Health⌕ Search

Biomedical subjects

S J Jabbur

Publications and source records attributed to S J Jabbur.

At least 37 records · Page 2Linked to original sources
PubMed1997

Hyperalgesia induced by low doses of thymulin injections: possible involvement of prostaglandin E2.

Thymulin injection into rats (20-150 ng) i.p. caused a significant reduction in both mechanical (paw pressure test) and thermal (hot plate and tail flick tests) nociceptive thresholds. Thymulin injection also doubled IL-1beta level in the liver of these animals. Induced hyperalgesia was reversed completely by alpha-MSH related tripeptide, Lys-D-Pro-Val in low doses, which is known to antagonize IL-1beta and PGE2 induced hyperalgesia, but was only partly reversed by IL-1beta related tripeptide, Lys-D-Pro-Thr at high doses, which is known to antagonize IL-1beta induced hyperalgesia only. We conclude from these results that thymulin causes hyperalgesia and that this effect is at least in part mediated via PGE2 and its effectiveness at low concentration implies a physiological role for this thymic hormone.

Animals↗
PubMed1997

Involvement of interleukin-1 beta, nerve growth factor and prostaglandin E2 in endotoxin-induced localized inflammatory hyperalgesia.

1. Intraplantar endotoxin (ET) injection (1.25 micrograms) into the hind paw of rats resulted in a localized inflammatory hyperalgesia, as assessed by paw pressure (PP), paw immersion (PI), tail flick (TF) and hot plate (HP) tests. 2. ET injection resulted in a significant elevation in the levels of interleukin-1 beta (IL-1 beta) and nerve growth factor (NGF) in the injected foot as compared with the non-injected foot. This increase was attenuated by intraperitoneal injections of dexamethasone (200 and 400 micrograms kg-1) and to a lesser extent by indomethacin (2 and 8 mg kg-1). 3. The tripeptide Lys-D-Pro-Val, which is known to antagonize IL-1 beta and prostaglandin E2 (PGE2) reversed mechanical hyperalgesia, as assessed by the PP test, and reduced significantly thermal hyperalgesia, as assessed by the HP and TF tests. 4. IL-1ra reversed both mechanical (PP) and thermal (PI) nociceptive thresholds tested on the injected leg and significantly reduced thermal hyperalgesia, as assessed by the HP and TF tests. 5. A sheep, anti-mouse NGF antiserum reversed mechanical hyperalgesia (PP test) but had little or no effect on thermal hyperalgesia (PI, HP and TF tests). 6. Our results indicate the importance of IL-1 beta, NGF and prostaglandin E2 (PGE2) in the development of ET induced hyperalgesia and the possible existence of different mechanisms underlying thermal and mechanical as well as central and peripheral hyperalgesia.

Animals↗
PubMed1997

Effects of various analgesic and anti-inflammatory drugs on endotoxin-induced hyperalgesia in rats and mice.

A new model of endotoxin (ET)-induced hyperalgesia has been used to test the effects of four classes of drugs in rats and mice. Hyperalgesia was assessed by paw pressure (PP), hot plate (HP) and tail flick (TF) tests. Each drug was injected intraperitoneally 24 and 12 h before ET injection and just before each pain test at 3, 6, 9 and 24 h after ET injection. At the dosages used, acetaminophen and dexamethasone were the most effective in reducing PP hyperalgesia and least effective on TF hyperalgesia, while indometacin and morphine produced their main effect on TF hyperalgesia. The four drugs were about equally effective in reversing HP hyperalgesia. We conclude that ET hyperalgesia is mediated by both prostaglandin-sensitive and prostaglandin-independent mechanisms.

Acetaminophen↗
PubMed1996

Thymulin reduces hyperalgesia induced by peripheral endotoxin injection in rats and mice.

In a new model of peripheral localized inflammation, induced by intraplantar endotoxin (1.25 micrograms) injection in the hind paw of rats and mice, thymulin, a hormone of the thymus gland involved in immunomodulation, reduced inflammatory pain. High doses of thymulin reduced significantly, and in a dose-dependent manner, mechanical hyperalgesia as assessed by the paw pressure test and thermal hyperalgesia as assessed by the hot plate test and tail immersion test.

Animals↗
PubMed1996

Endotoxin-induced local inflammation and hyperalgesia in rats and mice: a new model for inflammatory pain.

Lipopolysaccharide, also known as endotoxin (ET), is a major constituent of the outer membrane of the cell wall of most gram negative bacteria. ET is known to cause a number of pathophysiological changes associated with illness including inflammatory pain. The aim of this study is to characterize the peripheral hyperalgesia induced by ET in rats and mice. Different groups of rats and mice received different doses of ET ranging from 0.6 microgram to 40 micrograms dissolved in 50 microliters saline and injected in the plantar area of the left hind legs. All animals were subjected to tail immersion (TF), hot plate (HP) and paw pressure (PP) tests, 2-3 days prior to ET injection and during the following 1-2 days. ET injections produced a dose-dependent decrease in the latencies of the HP and PP tests of the injected leg reaching a maximum decrease of 50-60% of the control with 20-40 micrograms ET at 9 h (rats) and 24 h (mice) after the injection. Almost complete recovery was observed after 24 h in rats and 48 h in mice. TF latencies showed a less but a significant decrease while PP of the opposite leg and all tests in saline-injected animals did not elicit significant variations and served as additional controls. Our results indicate that the use of ET-produced hyperalgesia is a valid model for local and reversible inflammatory pain, with minimal distress to the animal. This model can also be used to study the efficacy of various anti-inflammatory and analgesic drugs and the molecular mechanisms of inflammation induced by bacterial invasion.

Animals↗
PubMed1996

Effects of cerebral cortical and striatal lesions on autotomy following peripheral neurectomy in rats.

Peripheral nerve lesions have been reported to produce deafferentation pain and persistent changes at various levels of the central nervous system. Using autotomy in rats following leg denervation, as a model for deafferentation pain, we studied the effect of various cerebral lesions on this abnormal behavior. Under deep anesthesia, rats were subjected either to massive hemidecortication or to subtotal hemispherectomy (involving parts of basal ganglia and limbic areas), which was followed 1 week later by a denervation of the ipsilateral or contralateral leg. Hemidecortication significantly delayed autotomy from 7.8 +/- 2.8 to 25.6 +/- 2.1 days without reducing its incidence, whereas hemispherectomy abolished the incidence of autotomy in the contralaterally denervated leg and delayed its onset from 7.8 +/- 2.8 to 34 +/- 6.1 days and decreased its incidence (from 100% to 60%) in the ipsilaterally denervated leg. Chemical lesions of the neostriatum produced similar effects on autotomy to those produced by hemispherectomy. Hemispherectomized and striatum-lesioned rats that failed to elicit autotomy in the contralaterally denervated leg were subjected after 7 weeks to denervation of the ipsilateral leg. Sixty to seventy percent of these rats showed autotomy and in half of them the attack was directed simultaneously to both legs. These results suggest an involvement of the cerebral cortex and a stronger contribution of subcortical structures (like striatum and limbic system) in the processing of nociceptive information.

Animals↗
PubMed1993

Explosive autotomy induced by simultaneous dorsal column lesion and limb denervation: a possible model for acute deafferentation pain.

We report on a new "explosive" form of self-mutilation behavior (autotomy) characterized by rapid onset (1-2 days), short duration (1-2 days), and unpredictable progression. The possible neural mechanism(s) underlying this novel behavior were examined in rats by combining at varying time intervals one leg denervation with a lesion to the dorsal columns (DC lesion) or to a dorsolateral funiculus (DLF lesion). DC lesion, followed immediately by leg denervation, resulted in explosive autotomy in 62% of the rats and regular autotomy in 25% of the rats. Regular autotomy was characterized by slow onset (2-3 weeks), prolonged duration (2-3 weeks), and stereotyped progression from distal to proximal parts of the leg. DC lesion, followed 1 week later by leg denervation, resulted in regular autotomy in 71% of the rats which was not different from autotomy resulting from denervation alone. DC lesion preceded 1 week earlier by leg denervation resulted in slightly accelerated regular autotomy in 77% of the rats. Simultaneous DC lesion and leg denervation immediately preceded by application of a local anesthetic (4% procaine) for 30 or 60 min to the exposed lumbar spinal cord resulted in regular autotomy in all rats. All rats in a sham group, in which the procaine was replaced by normal saline, exhibited explosive autotomy. DLF lesion, followed immediately by leg denervation, resulted in accelerated regular autotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1993

The role of previous nociceptive input in development of autotomy following cordotomy.

Intractable pains have been described after surgical or accidental lesions in the peripheral or central nervous system. The possible contribution of antecedent injury to the appearance of these pains was examined in an animal model for chronic pain which involved observing self-mutilation or autotomy behavior in rats. Various combinations of previous injury, selective spinal cut, and peripheral denervation were carried out on rats. Injuries ranged from mild to moderate and were produced by nociceptive stimuli from formaldehyde injection, induced local arthritis, or hot water application. Selective spinal cuts included either a dorsal column (DC), a dorsal quadrant which included a DC and a dorsolateral funiculus, an anterolateral column (ALC), or a hemisection. In rats without prior exposure to injury the various types of spinal cuts were not associated with any autotomy. In rats with prior exposure to formaldehyde injection, autotomy was associated only with spinal cuts that involved the ALC. In an otherwise similar group of rats but with prior induction of local arthritis, a stronger association of ALC lesion and autotomy was observed. In an earlier study, rats with ALC lesion prior to denervation showed reduced autotomy. In this study, we demonstrated that in rats with previous exposure to heat injury, an ALC lesion was strongly associated with autotomy. Autotomy was absent, however, in rats with heat injury only. These findings strongly suggest that pain resulting from previous exposure to injury produces a memory trace in the central nervous system which can account for the phantom pains encountered in various clinical conditions.

Animals↗
PubMed1990

Effects of lesions in the anterolateral columns and dorsolateral funiculi on self-mutilation behavior in rats.

The possible role of the anterolateral columns (ALCs) and dorsolateral funiculi (DLF) in pain mechanisms was examined from the effects of lesions in these tracts (alone or combined) on tests for chronic deafferentation pain (autotomy) in rats. Spinal lesions alone (i.e., without denervation) in either ALC or DLF or combined DLF-ALC did not lead to any form of self-mutilation behavior. Cervical surgery, without spinal lesion, followed by limb denervation (sham) resulted in similar autotomy characteristics to those observed following limb denervation alone (control). Both results were considered as one set of controls. ALC lesions simultaneous with, or 1-2 weeks prior to limb denervation (ipsilaterally or contralaterally) produced significant delay in onset of autotomy and decrease in percentage of rats showing this behavior. DLF lesions followed by limb denervation produced significant acceleration of onset of autotomy and increase in percentage of rats showing this behavior. Combined DLF-ALC lesions with limb denervation produced intermediate effects between those observed following either ALC or DLF lesions alone. These results give further support to the concept that autotomy is related to rostral transmission of nociceptive information and that a spino-bulbo-spinal inhibitory loop involving the DLF and ALC is triggered by chronic deafferentation pain.

Animals↗
PubMed1989

Dorsal column input to cochlear neurons in decerebrate-decerebellate cats.

In decerebrate-decerebellate cats with cervical spinal cuts sparing only the dorsal columns (DCs), activation of one DC modulates sound-evoked discharges of neurons in both dorsal cochlear nuclei. In a sample of 50 neurons, 34% were excited or facilitated, 12% were inhibited and 54% were not affected by DC stimulation. This modulation appears to be mediated through direct projections from the dorsal column nuclei to the dorsal cochlear nuclei.

Acoustic Stimulation↗
PubMed1989

Characteristics and displaceability of neurotensin binding sites in the rat cerebral cortex and corpus striatum.

1. Neurotensin binding to synaptosomes isolated from the rat cerebral cortex and corpus striatum reached saturation after 4 min of incubation. 2. The rates of binding were found to be higher in the corpus striatum than in the cerebral cortex. 3. Concentration study revealed the presence of two different and independent classes of neurotensin binding sites with a negative cooperative interaction within each class of binding sites. 4. At saturation levels, the low affinity binding component was found to have a flat regional difference, while the high affinity binding component showed regional differences in terms of maximal binding capacity, suggesting a higher number of high affinity binding sites in the striatum than in the cortex. 5. In the competition related experiments, dopamine was found to displace around 70% of neurotensin binding sites in the corpus striatum and the cerebral cortex. 5. Substance P displaced around 50% of [3H]neurotensin in the cerebral cortex. Whereas, 50% and 70% displacement were observed in the striatum at high and low affinity binding sites, respectively. 6. These results show the overlap in the binding sites of neurotensin, dopamine and substance P.

Animals↗
PubMed1989

Neurochemical transmission in the dorsal column nuclei.

The transmitter chemistry of the dorsal column nuclei is reviewed, with special emphasis on the monosynaptic component of the dorsal column-medial lemniscal pathway. It is maintained that in this anatomically addressed system concerned mainly with fast, secure sensory transmission, amino acids represent the predominant mechanism used for chemical relay of primary afferent impulses. The major excitatory primary afferent transmitter is most likely glutamic acid, whereas gamma-aminobutyric acid (GABA) fulfills adequately the role of transmitter of recurrent, postsynaptic and presynaptic inhibition. Recent immunohistochemical and physiological evidence indicates that 5-hydroxytryptamine, originating mainly from neurons of the raphé nuclei, plays a modulatory role in dorsal column transmission of innocuous sensory information. The basic synaptic elements involved in transmission across this relay, along with their corresponding chemical identities, are presented in the form of a speculative model.

Afferent Pathways↗
PubMed1988

Dopaminergic and adrenergic binding affinities in rabbit retinal synaptosomes.

1. Dopamine binding to amacrine membrane vesicles isolated as synaptosomal fractions P1 and P2 from rabbit retinas showed saturation within less than a minute. 2. Dopamine binding to retinal synaptosomal membranes (RSM) in P1 and P2 is a two-component system: the first saturated at 1.00 microM 14C-dopamine in P1 and 1.25 microM in P2, and the second saturated at 2.00 microM in both pellets. 3. The affinity of RSM receptors to dopamine in P1 was equal to that in P2 (Km = 2.00 microM), whereas the calculated Vmax of dopamine binding was increased in P2 (1.25 pmol/micrograms protein) as compared to P1 (0.625 pmol/micrograms protein). 4. Dopamine binding to the beta-adrenergic sites showed a lower affinity (Km = 10 microM) in P2 relative to P1 (Km = 4.0 microM), whereas Vmax in P2 (5.0 pmol/micrograms protein) was 4-fold higher than P1 (1.25 pmol/micrograms protein). 5. The P1 and P2 fractions of rabbit RSM contain dopaminergic and beta-adrenergic binding sites with higher concentration of dopaminergic receptors and lower concentration of beta-adrenergic receptors in P2 relative to P1.

Animals↗
PubMed1987

Effect of vagal nerve stimulation on L-leucine absorption in the cat jejunum.

The effects of vagal nerve stimulation in the neck and in the lower thorax were studied on L-leucine absorption in/the cat jejunum. Four series of in vivo experiments were performed in 26 cats using single pass perfusion technique with samples collected every 10 min and examined for their phenol red and radioactive L-leucine concentrations. The first two series acted as controls for the time it took to reach steady-state absorption and for the effects on L-leucine absorption of mechanical handling of the vagus nerve. In the third series, vagal stimulation in the neck (with a 20-second train of shocks at 7 Hz repeated every 10 min for either 16 or 4 stimulus sessions) resulted in a 3-fold increase in L-leucine absorption which was maintained throughout the stimulation period (up to 160 min). L-Leucine absorption started increasing within 10 min and peaked around 30-40 min after the initiation of stimulation and returned to control levels within 40 min after cessation of stimulation. In the fourth series, similar increases and returns to control L-leucine absorption levels were noted following vagal stimulation in the lower thorax (with a 20-min train of shocks at 7 Hz given for 3 sessions). The findings suggest a definite role of the vagus nerve in the control of leucine transport across the small intestine.

Animals↗
PubMed1986

Prolonged discharge of wide-dynamic-range spinal neurons evoked by formaldehyde injected in their cutaneous receptive fields.

In decerebrate, unanesthetized cats, subcutaneous injection of formaldehyde solutions (0.05 ml, 2.5%) in the receptive fields of spinal wide-dynamic-range neurons elicited an immediate and continuous discharge or burst activity in the neurons that lasted 10 to 55 min. This discharge was reduced by conditioning stimulation of the medial raphe nucleus and was completely abolished by morphine (3 mg/kg, i.v.). Low-threshold cutaneous mechanoreceptive neurons in the dorsal horn and dorsal column nuclei did not show a sustained response.

Animals↗
PubMed1986

Gastric pH changes following intramedullary electrical stimulation in anesthetized and decerebrate cats.

In anesthetized and decerebrate cats, a pH-sensitive glass electrode inserted into the gastric antral region through a fistula recorded immediate pH changes. In the anesthetized cats (pentobarbital sodium, 35-40 mg/kg, i.p.), electrical stimulation within the medulla oblongata with a coaxial electrode (train of pulses at 300-500 Hz for 10-30 sec; individual pulse width 0.1-0.5 msec and amplitude not exceeding 0.5 mA) induced an increase in gastric acid secretion equivalent to a delta pH of 1.26 +/- 0.1 units. In the decerebrate (following induction with ether), the same type of stimulation elicited a more intense gastric acid secretion equivalent to a delta pH of 5.18 +/- 0.09 units which is significantly different (P less than 0.001) from that recorded in the anesthetized cats. Reversible blockage of the vagus nerves eliminated these responses during the block. Our results indicate that electrical stimulation in the posterior region of the medulla oblongata evokes an immediate and significant increase in gastric acid secretion, which is mediated through the vagus nerve, and is most evident in decerebrate unanesthetized cats.

Animals↗