Biomedical subjects

S Semnanian

Publications and source records attributed to S Semnanian.

At least 19 recordsLinked to original sources

PubMed2005

Microinjection of ritanserin into the dorsal hippocampal CA1 and dentate gyrus decrease nociceptive behavior in adult male rat.

Prenatal 5HT depletion causes a significant decrease in the level of nociceptive sensitivity during the second phase of the formalin test behavioral response. These experiments were designed to test whether blocking 5HT2A/2c receptors in the CA1 region of the hippocampus and dentate gyrus would decrease nociceptive behaviors induced by a peripheral noxious stimulus formalin as an animal model of unremitting human being. The 5HT2A/2c receptor antagonist ritanserin (2, 4 and 8 microg/0.5 microl) was injected into the CA1 area and dentate gyrus of behaving rats 5 min before subcutaneous injection of formalin irritant. Nociceptive behaviors in both phases of the formalin test were significantly decreased by ritanserin (4 and 8 microg/0.5 microl) and ritanserin had no effect at 2 microg/0.5 microl. These results support the hypothesis that the hippocampal formation may modify the processing of incoming nociceptive information and that 5HT2A/2c receptor-sensitive mechanisms in the hippocampus may play a role in nociception and/or the expression of related behaviors.

Animals↗

PubMed2005

Epileptogenic insult causes a shift in the form of long-term potentiation expression.

The relationship between epilepsy, modeled here by pentylenetetrazol kindling, and learning deficits, modeled here by long-term potentiation (LTP), was studied. The field excitatory postsynaptic potentials and population spikes (PS) were recorded from strata radiatum and pyramidale, respectively, in urethane-anesthetized rat dorsal hippocampus CA1 area upon stimulation of Schaffer collaterals. To induce LTP, a 100 Hz primed-burst stimulation protocol was used. Experiments were carried out at approximately 30 days after the last pentylenetetrazol dose. The effects of voltage dependent calcium channel blocker verapamil and N-methyl-D-aspartate receptor antagonist MK-801 on LTP expression were examined. Tetanic stimulation elicited both field excitatory postsynaptic potential LTP and PS LTP in control animals, and LTP-induction of the PS in control animals was attenuated by MK-801, but not by verapamil. By contrast, kindled rats showed LTP of the PS only. MK-801 reduced the extent of potentiation of PS amplitude and verapamil inhibited the PS amplitude potentiation, completely. The results suggest that seizure induction modifies mechanisms underlying LTP induction and causes a shift in the form of LTP expression. The pentylenetetrazol-kindling-induced increase in PS LTP is sensitive to verapamil and not to MK-801 and therefore primarily dependent on activation of voltage dependent calcium channels rather N-methyl-D-aspartate receptors. Kindling may lead to a shift in synaptic plasticity thresholds much like the shift that occurs during aging, and such alterations may contribute to deficits in learning and memory.

Animals↗

PubMed2003

Long-term potentiation as an electrophysiological assay for morphine dependence and withdrawal in rats: an in vitro study.

Using a long-term potentiation (LTP) method, we attempted to establish an electrophysiological assay for morphine dependence and withdrawal in rats in vitro. The field excitatory postsynaptic potential (fEPSP) and orthodromic population spikes (OPS) were recorded from stratums radiatum and pyramidale, respectively, of area CA1 following stimulation of Schaffer collaterals in control and morphine-dependent slices. To induce LTP, a 100 Hz primed-burst stimulation protocol was used. Although morphine exposure had excitatory effects on control slices, namely, an increase in the amplitude of primary population spikes (PSs) and appearance of extra PSs, slices taken from dependent rats demonstrated tolerance to morphine. LTP of the fEPSP was not changed in slices from dependent animals although dependent slices did show an enhanced OPS LTP compared to control ones, which was attenuated by morphine exposure. In the presence of morphine, naloxone caused a withdrawal phenomenon; apparent as a robust enhanced OPS LTP in dependent slices. So we propose morphine-naloxone withdrawn slices as a suitable in vitro withdrawal-like model. Such an in vitro preparation could provide a convenient practical experimental tool for examination of the probable molecular and cellular mechanisms involved in withdrawal states.

Animals↗

PubMed2003

Synthesis and evaluation of pharmacological activities of 3, 5-dialkyl 1, 4-dihydro-2,6-dimethyl-4-nitroimidazole-3, 5-pyridine dicarboxylates.

New analogues of nifedipine, in which the 2-nitrophenyl group at position 4 is replaced by a 1-methyl-5-nitro-2-imidazolyl substituent, were synthesized. The symmetrical dialkyl 1, 4-dihydro-2, 6-dimethyl-4-(1-methyl-5-nitro-2-imidazolyl)-3, 5-pyridinedicarboxylates were prepared by a classical Hantzsch condensation. The asymmetrical analogues were synthesized using a procedure reported by Iwanami that involved the condensation of alkylacetoacetate with methyl-, ethyl- or isopropyl3-aminocrotonate and 1-methyl-5-nitroimidazole-2-carboxaldehyde. Calcium channel antagonist activities were determined in vitro using a guinea pig ileum longitudinal smooth muscle (GPILSM)assay. Many compounds exhibited superior, or equipotent, calcium antagonist activity (IC(50) = 10(-10) to 10(-13) M range) relative to the reference drug nifedipine (IC(50) = 1.09 +/- 0.12 x 10(-11) M). Antinociceptive effects of some compounds were evaluated by the mouse tail-flick assay in vivo. Results demonstrate that some of the compounds were active as an antinociceptive.

Analgesics↗

PubMed2002

The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study.

Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200 mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either theta-pattern primed bursts (PBs), perfusion with low Mg(2+) or with high Ca(2+), indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed.

Animals↗

PubMed2001

Differential effects of pentylenetetrazol-kindling on long-term potentiation of population excitatory postsynaptic potentials and population spikes in the CA1 region of rat hippocampus.

The effects of pentylenetetrazol-kindling on synaptic transmission and the effectiveness of θ pattern primed-bursts (PBs) for the induction of long-term potentiation (LTP) of population excitatory postsynaptic potentials and population spikes were investigated in hippocampal CA1 of pentylenetetrazol-kindled rats. Experiments were carried out in the control and kindled animals at two post-kindling periods, i.e., 48-144 h (early phase) and 30-33 days (long lasting phase). Field potentials (population excitatory postsynaptic potentials, pEPSPs; and population spikes, PSs) were recorded at the stratum radiatum and the stratum pyramidale following stimulation of the stratum fibers, respectively. PBs were delivered to stratum fibers and PB potentiation was assessed. The results showed that 48-144 h after kindling there was no significant difference for pEPSP slope and PS amplitude between two groups. But at 30-33 days after kindling, the pEPSP slope in the stratum radiatum of kindled animals decreased, whereas the amplitude of PSs increased compared to those of controls. Shortly after kindling, control animals had normal LTP of pEPSP slope and PS amplitude in response to PBs, but kindled rats lack LTP of pEPSP slope and PBs induced LTP of PS amplitude in most of kindled animals. In 30-33 days after kindling, PB potentiation was not observed in the stratum radiatum of kindled animals but PBs induced LTP of PS amplitude, which was significantly greater than that of control animals. The effect is compatible with the hypothesis, which postulates kindling-associated functional deficit in hippocampus, especially CA1, as an explanation for the behavioral deficits seen with the kindling model of epilepsy.

Action Potentials↗

PubMed2001

Caffeine increases paragigantocellularis neuronal firing rate and induces withdrawal signs in morphine-dependent rats.

Using single unit recording in nucleus paragigantocellularis neurons located in the rostral ventrolateral medulla, and measuring the precipitated withdrawal syndrome, we investigated whether chronic morphine administration would produce adaptive changes in the adenosine system. Caffeine (50 mg/kg, i.p.) induced withdrawal signs (head shakes, tooth chattering, ejaculation, chewing, and irritability) in morphine-dependent rats 10-18 min after the injection. Only the tooth chattering and diarrhea were expressed following a direct paragigantocellularis injection of caffeine (200 microM, 0.5 microl). The spontaneous activity of paragigantocellularis neurons was significantly decreased by microinjection of both adenosine (10 nM) and an adenosine A1 receptor-selective agonist, cyclohexyladenosine (200 microM), into the paragigantocellularis nucleus of both control and morphine-dependent rats, but the decrease in firing rate of paragigantocellularis neurons of morphine-dependent rats was greater than that of control ones. There was also a significant enhancement of spontaneous activity of paragigantocellularis neurons 8-15 min after caffeine administration (50 mg/kg, i.p.) and 10-18 min after the injection of an adenosine A1 receptor-selective antagonist 8-phenyltheophylline (10 mg/kg, i.p.) in both control and morphine-dependent rats. However, the effect of the antagonists was greater in morphine-dependent rats than in control ones. These data suggest that there is an increase in the sensitivity of nucleus paragigantocellularis neurons to adenosine receptor ligands in morphine-dependent rats that may be associated with the ability of caffeine to produce withdrawal signs.

Adenosine↗

PubMed2001

Occurrence of morphine tolerance and dependence in the nucleus paragigantocellularis neurons.

The occurrence of morphine tolerance and dependence in the nucleus paragigantocellularis neurons was investigated. The spontaneous activity was recorded from the nucleus paragigantocellularis neurons of urethane-anesthetized rats, using single unit recording. Morphine microinjected (20 mg/ml, 120-200 nl) into the nucleus paragigantocellularis of control rats had both excitatory and inhibitory effects. These effects were reversed by microinjection of naloxone, revealing the possible involvement of mu receptors. Morphine microinjected into morphine-dependent rats failed to change the spontaneous activity of the nucleus paragigantocellularis neurons that accounts for the occurrence of tolerance to morphine in these neurons. Microinjection of naloxone (25 mg/ml, 120-200 nl) in control rats had no effect on the spontaneous firing rate of the nucleus paragigantocellularis neurons but in morphine-dependent rats, either alone or after morphine microinjection, naloxone increased neuronal activity significantly, indicating the occurrence of dependence on morphine in the nucleus paragigantocellularis neurons. These data show that the nucleus paragigantocellularis neurons may play a role in physical dependence on morphine. This conclusion is consistent with the finding, that activation of the nucleus paragigantocellularis by electrical stimulation in morphine-naive rats can elicit behaviors similar to those observed during naloxone-precipitated morphine withdrawal.

Action Potentials↗

PubMed2001

Anti-inflammatory and antipyretic effects of Trigonella foenum-graecum leaves extract in the rat.

Anti-inflammatory and antipyretic effects of the Trigonella foenum-graecum (TFG) leaves extract, an Iranian medicinal plant, were examined. For anti-inflammatory activity, the formalin-induced edema model was used. Hyperthermia was induced by intraperitoneal injection of 20% (w/v) aqueous suspension of brewer's yeast. Sodium salicylate (SS) was used as a positive control. Both TFG and SS significantly reduced formalin-induced edema in single dose (TFG 1000 and 2000 mg/kg, SS 300 mg/kg) and chronic administration (TFG 1000 mg/kg and SS 300 mg/kg). TFG and SS also significantly reduced hyperthermia induced by brewer's yeast in 1 and 2 h after their administration. The results indicate that the TFG leaves extract possess anti-inflammatory as well as antipyretic properties in both i.p. and p.o. administration. Phytochemical studies indicate that alkaloids, cardiac glycosides, and phenols are the major component in the extract. Although existence of three anti-inflammatory, analgesic and antipyretic effects in this extract suggest a NSAID-like mechanism for it, but the presence of alkaloids, the absence of other effective compounds such as flavonoids, saponins, steroids, etc., and also its analgesic effect on tail-flick test that usually is not produced by NSAIDs, suggest another mechanism for the extract. So the possibility of alkaloids as effective compounds, in this extract, increases.

Analgesics, Non-Narcotic↗

PubMed2000

Systemic naloxone enhances cerebral blood flow in anesthetized morphine-dependent rats.

Laser-Doppler flowmetry was used to study cerebral cortical blood flow responses to morphine and naloxone in morphine-naive and -dependent rats. The experiments were performed in spontaneously breathing anesthetized rats. Morphine (10 mg/kg, i.p.) administration reduced regional cerebral blood flow in control, sham-operated and morphine-dependent rats, but the depressant effect of morphine in morphine-dependent animals was less than that in control and sham-operated groups. While naloxone (0.5 mg/kg, s.c.) had no considerable effect on regional cerebral blood flow in control and sham-operated groups, it increased regional blood flow in morphine dependent ones. The depressant effect of morphine in all groups and the enhancing effect of naloxone in morphine-dependent animals were not seen after local application of lidocaine at the recording site. This study may provide a framework to study the cellular and molecular mechanisms responsible for coupling neuronal electrical activity with regional alterations in blood flow during precipitation of morphine withdrawal.

Anesthesia↗

PubMed2000

Primed-burst potentiation occludes the potentiation phenomenon and enhances the epileptiform activity induced by transient pentylenetetrazol in the CA1 region of rat hippocampal slices.

The effects of pentylenetetrazol (PTZ) following induction of long-term potentiation (LTP) on population spikes in CA1 of hippocampal slices were investigated. Population spikes were evoked by activation of Schaffer collaterals with a range of stimulation intensities. LTP was induced using θ-pattern primed burst tetanic stimulation. Changes in the population spike amplitude and number of population spikes were used as indices to quantify the effects of PTZ exposure in the control (non-tetanized) and LTP (tetanized) conditions. The amplitude of population spike was measured 20 min before, during 20 min chemical application (3 mM), and also after 30 or 60 min washout period. In non-tetanized slices, the population spike input-output curve was significantly increased 20 min after PTZ application and persisted at least for 60 min. Multiple population spikes or after potentials also appeared, but did not persist. When PTZ was applied on tetanized slices, 60 min after LTP induction, the amplitude increase produced by PTZ was smaller than the increase seen in the control condition. Also LTP induction preceding PTZ exposure increased the number of population spikes evoked by stimulation of Schaffer collaterals. It is concluded that a transient PTZ application produces a long-lasting increase in population spike amplitude. Primed burst LTP occludes PTZ-induced potentiation while also increasing the epileptogenic effect of PTZ.

Action Potentials↗

PubMed2000

Effects of adrenoceptor agents on apomorphine-induced licking behavior in rats.

In the present study, intraperitoneal (IP) administration of the dopaminergic receptor agonist apomorphine (0.1, 0.25, and 0.5 mg/kg) induced a dose-dependent licking in rats. The intraperitoneal injection of the alpha1'''adrenoceptor agonist phenylephrine (1-8 mg/kg) but not the alpha2-adrenoceptor agonist clonidine (0.025-0.05 mg/kg) decreased licking induced by apomorphine. The alpha-adrenoceptor antagonists prazosin, phenoxybenzamine, and yohimbine also reduced the apomorphine response significantly. The response induced by phenylephrine was decreased by a dose of prazosin. The beta1-adrenenocepor agonist dobutamine and beta2-adrenenocepor agonist salbutamol did not alter the apomorphine response. However, beta2-adrenenocepor antagonists atenolol and propranolol reduced the apomorphine effect. It may be concluded that alpha1- and possibly beta1-adrenoceptor mechanisms may be involved in modulation of licking behavior.

Adrenergic Agents↗

PubMed2000

Differential effect of dark rearing on long-term potentiation induced by layer IV and white matter stimulation in rat visual cortex.

In the earlier work, we showed that primed-burst stimulation (PBs) is an effective protocol to induce long-term potentiation (LTP) in layer II/III of adult rat visual cortex in vitro. In the present study, we investigated effects of dark rearing on potentiation of layer II/III responses to stimulation of layer IV or the underlying white matter in the visual cortex in vitro. Long-term potentiation was induced by PBs applied to white matter or layer IV of the cortex in light and dark reared rats. Regardless of the stimulation site, layer II/III field potentials consisted of two components. In general, the latency of responses in dark reared rats was shorter than that in light reared ones. Whereas PBs of layer IV produced LTP of two components in both the groups, that of white matter induced an appreciable potentiation of the second component in both groups and the first component only in dark reared rats. These results indicate that PBs of either white matter or layer IV can gain access to the modifiable synapses that are related to the second component of layer II/III responses in light and dark reared visual cortex, but accessibility of the modifiable synapses that are related to first component depends on the tetanization site. The dark rearing enhances accessibility of the modifiable synapses that are related to the first component following PBs of the white matter. It is suggested that the immaturity of inhibitory circuits and/or better function of excitatory ones in the visual cortex of dark reared rats may contribute to the enhanced accessibility of the first component.

Animals↗

PubMed2000

Antinociceptive and anti-inflammatory effects of Elaeagnus angustifolia fruit extract.

In this study, probable antinociceptive and anti-inflammatory effects of Elaeagnus angustifolia fruit components, were evaluated. For evaluation of antinociceptive effects, the chronic (formalin test) and acute (tail-flick) pain models of rats were used. For the anti-inflammatory effects, the paw inflammation model was used through subcutaneous injection of 5% formalin to the paw of male rats. Water extracts of the fruit and its components in the single dose were assessed through comparison with the antinociceptive and anti-inflammatory effects of sodium salicylate (SS) as a positive control. Administration of 300 mg/kg of SS (i.p.) had no effect on tail flick latency, while 1000 mg/kg of total (i.p. and p.o.) and endocarp (i.p.) extract, increased this latency (P<0.01, P<0.001, respectively), which was not reversed by naloxone (2 mg/kg). In the formalin test, SS (300 mg/kg, i.p.) and the extract (1000 mg/kg, p.o. ) alleviated the animals nociception in the second phase, while in the first phase they were not effective. The total and endocarp extracts (1000 mg/kg, i.p.) showed a significant effect on both phases (P<0.01, P<0.001, respectively) which was also not reversed by naloxone (2 mg/kg, i.p.). In the acute anti-inflammatory test, the total extract and the aqueous extract of individual fruit components showed a significant effect (P<0.001). This anti-inflammatory effect was not significant compared with the anti-inflammatory effect of SS. Because of the extract effect on the tail-flick latency and both phases of the formalin test, the site of its analgesic action is probably central, and the mechanism of antinociceptive action of the extract are not related to the opioid system. Our phytochemical studies indicated that aqueous extract of E. angustifolia fruit contains flavonoids, terpenoids and cardiac glycosides.

Analgesics↗

PubMed1999

Influence of different adrenoceptor agonists and antagonists on physostigmine-induced yawning in rats.

In the present study, effects of adrenoceptor agonists and antagonists on physostigmine-induced yawning was investigated. Intraperitoneal (i.p.) injection of different doses of physostigmine (0.03, 0.05, 0.1, and 0.2 mg/kg) induced yawning in rats. The maximum response was obtained by 0.2 mg/kg of the drug. The alpha1-adrenoceptor agonist, phenylephrine, and the alpha2-adrenoceptor agonist, clonidine, decreased yawning induced by physostigmine. Prazosin and higher doses of phenoxybenzamine reduced the inhibitory effect of phenylephrine. Higher doses of yohimbine also reduced the clonidine response. The adrenoceptor antagonists, prazosin, phenoxybenzamine, and propranolol, did not significantly alter the physostigmine response. However, yohimbine, or lower doses of prazosin, decreased the physostigmine response. It may be concluded that alpha1- and alpha2-adrenoceptor stimulation decreases the physostigmine-induced yawning behavior in rats.

Adrenergic Agonists↗

PubMed1998

Morphine tolerance and dependence in the nucleus paragigantocellularis: single unit recording study in vivo.

In this study, a single unit activity was recorded in the nucleus paragigantocellularis (PGi), located in the rostral ventrolateral medulla of anesthetized, morphine-dependent rats. The spontaneous activity of PGi neurons was significantly decreased by administration of morphine (10 mg/kg; i.p.) in sham-operated, control and morphine-dependent rats. However, in PGi neurons of morphine-dependent rats, the firing rate decreased significantly less than those of sham-operated and control ones. There was also significant enhancement of spontaneous activity of PGi neurons for 30 min following administration of naloxone (2 mg/kg; s.c.) in morphine-dependent rats as an opiate withdrawal-induced activation of PGi neurons. The results indicated the occurrence of morphine tolerance and dependence in the PGi and/or elsewhere which appeared in PGi unit activity. The findings are consistent with the hypothesis that during morphine withdrawal, there is an increase in unit activity of the PGi afferents to the nucleus locus coeruleus (LC) or an increased release of excitatory transmitter from their nerve terminals in the LC.

Action Potentials↗

PubMed1998

Involvement of NMDA receptors and voltage-dependent calcium channels on augmentation of long-term potentiation in hippocampal CA1 area of morphine dependent rats.

The involvement of NMDA receptors and voltage-dependent calcium channels on augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral-CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-bursts tetanic stimulation. The amplitude of population spike was measured as an index of increase in postsynaptic excitability. d, l-AP5 and nifedipine were used as NMDA receptor antagonist and voltage-dependent calcium channel blocker, respectively. The amount of LTP of orthodromic population spike amplitude was higher in slices from dependent rats. Perfusion of slices from control or dependent rats with ACSF containing either D,L-AP5 (25 microM) or nifedipine (10 microM) and delivering tetanic stimulation, showed that D,L-AP5 completely blocked LTP of OPS in slices from both control and dependent rats, while nifedipine attenuated the amount of LTP of OPS in dependent slices and had no effect on control ones. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine dependent rats is primarily induced by the NMDA receptors activity and the voltage-dependent calcium channels may also be partially involved in the phenomenon.

2-Amino-5-phosphonovalerate↗

PubMed1998

Neurite outgrowth of dorsal root ganglia is delayed and arrested by aspirin.

In this study, the effect of increasing doses of aspirin on the neurite outgrowth of Dorsal Root Ganglia (DRG) was investigated. DRG were cultured in complete medium (DMEM + 10% FCS +100 ng/ml NGF + collagen Type1 in substratum in 96 multiwell plate) in the presence of concentration of 1.25, 2.5, 5 and 10 mM aspirin. The neurite outgrowth of DRG was followed in comparison with controls that lack aspirin. 10 mM aspirin treated DRG showed delayed neurite outgrowth and after 7 days it reached the same DRG neurite outgrowth control wells after 18 hrs. This growth has delayed approximately one week and showed no further development and in such stage the cells became apoptos. However at concentrations of 1.25, 2.5, 5 mM of aspirin, outgrowth was observed after 18-24 hrs. Although the rate of growth was lower than control, it was not significant. In the other experiment, when DRG cultured for one week in complete medium then treated with aspirin, at 10 mM, DRG neurite outgrowth was stopped, while it was continued in the control. It seem that the aspirin affected DRG became apoptosis.

Animals↗