Biomedical subjects

Y Fathollahi

Publications and source records attributed to Y Fathollahi.

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

Eugenol depresses synaptic transmission but does not prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices.

Using field potential recording in the CA1 region of the rat hippocampal slices, the effects of eugenol on synaptic transmission and long-term potentiation (LTP) were investigated. Population spikes (PS) were recorded in the stratum pyramidal following stimulation of stratum fibers. To induce LTP, eight episodes of theta pattern primed-bursts (PBs) were delivered. Eugenol decreased the amplitude of PS in a concentration-dependent manner. The effect was fast and completely reversible. Eugenol had no effect on PBs-induced LTP of PS. It is concluded that while eugenol depresses synaptic transmission it does not affect the ability of CA1 synapses for tetanus-induced LTP and plasticity.

Action Potentials↗

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↗

PubMed2005

Responsiveness of vascular alpha1-adrenoceptors of diabetic rat knee joint to phenylephrine in acute inflammation.

In diabetic angiopathy, responsiveness of alphal-adrenoceptors in blood vessels increases. The aim of this study was to investigate the vasoconstrictor response of knee joint blood vessels to phenylephrine (a 1-adrenoceptor agonist) in diabetes and acute inflammation. Acute knee joint inflammation was induced by the intraarticular injection of a 3% kaolin/3% carrageenan suspension. Diabetes was induced by the intravenous injection of alloxan (70 mg/kg). Male albino rats weighing 70 to 90 g each were divided into the following 4 groups: untreated controls, diabetic, inflammatory, and diabetic inflammatory. The blood flow of the knee joint was measured using the laser Doppler flowmetry (LDF) technique. Vasoconstriction of the articular microvascular was measured in response to the topical application of different concentrations (10(-7) to 10(-3) mol) phenylephrine. The results of this study show that (a) increased knee joint diameter and circumference due to inflammation and the knee joint basal blood flow were significantly lower in diabetic than in control rats; (b) the responsiveness of alphal-adrenoceptors decreased in kaolin/carrageenan-induced acute inflammation; (c) carrageenan-induced acute inflammation did not decrease the responsiveness of alphal-adrenoceptors in diabetic rats. We conclude that diabetes inhibits the reductive effect of acute inflammation on the responsiveness of alpha1-adrenoceptors in rats.

Adrenergic alpha-Agonists↗

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↗

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

The role of N-methyl-D-aspartate receptors in synaptic plasticity of rat visual cortex in vitro: effect of sensory experience.

We examined the role of N-methyl-D-aspartate (NMDA) receptors in synaptic plasticity of visual cortex of light (LR) and dark (DR) reared adult rats in vitro. Layer IV stimulation resulted in field potentials in layer II/III, consisting of two excitatory postsynaptic potentials (EPSP) called EPSP1 and EPSP2. Tetanic stimulation induced long-term potentiation (LTP) in EPSP2 of both LR and DR visual cortices. NMDA receptor antagonist D, L-2-amino-5-phosphono-valeric acid (AP5) completely blocked the LTP of EPSP2 in DR visual cortex while it reduced slightly the extent of LTP of EPSP2 in LR ones. Another NMDA receptor antagonist ketamine blocked potentiation of EPSP1 as well as EPSP2 in both groups. Our findings demonstrate that dependency of LTP on NMDA receptors and/or sensitivity of these receptors to the antagonists are different in LR and DR animals.

2-Amino-5-phosphonovalerate↗

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

Anticonvulsant effect of bilateral injection of N6-cyclohexyladenosine into the CA1 region of the hippocampus in amygdala-kindled rats.

In this study the role of adenosine A(1) receptors of CA1 region of the hippocampus on amygdala-kindled seizures was investigated in rats. Results obtained showed that in kindled animals, bilateral injection of N(6)-cyclohexyladenosine (CHA), an adenosine A(1) receptor agonist, at doses of 0.1, 1 and 10 microM into the CA1 region of the hippocampus significantly decreased the afterdischarge duration and stage 5 seizure duration and increased the latency to stage 4 seizure, but there were no changes in seizure stage. Also, bilateral injection of 1,3-dimethyl-8-cyclopenthylxanthine (CPT), an adenosine A(1) receptor antagonist, at doses of 0.5 and 1 microM into the CA1 region of the hippocampus could not produce any changes in the seizure parameters. Intrahippocampal pretreatment of CPT (1 microM) before CHA (0.1 and 1 microM), reduced the effects of CHA on seizure parameters significantly. Thus, it may be suggested that CA1 region of the hippocampus plays an important role in spreading seizure spikes from the amygdala to other brain regions and activation of adenosine A(1) receptors in this region, participates in anticonvulsant effects of adenosine agonists.

Adenosine↗

PubMed2000

Do Ca2+ channels share NMDA receptors in plasticity of synaptic transmission in the rat visual cortex?

We examined the involvement of Ca2+ channels in LTP of responses in rat visual cortex slices. Stimulating layer IV, field potentials including EPSP1 and EPSP2 from layer II/III were recorded. L-type Ca2+ channel blocker nifedipine did not have a considerable effect on LTP of the responses. T-type Ca2+ channel blocker Ni2+ decreased potentiation of EPSP1 and almost blocked that of EPSP2. Effect of visual experience on the function of the channels is also considered. These results indicate that T-type Ca2+ channels play a real role in stable LTP of EPSP2. Also the function of the channels was almost the same in dark and light reared visual cortices.

Animals↗

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

Intraperitoneal and intraamygdala N(6)-cyclohexyladenosine suppress hippocampal kindled seizures in rats.

Effects of intraperitoneal and intraamygdala N(6)-cyclohexyladenosine (CHA), a selective adenosine A(1) receptor agonist, and 1,3-dimethyl-8-cyclopentylxanthine (CPT), a selective adenosine A(1) receptor antagonist, were examined in fully hippocampal kindled rats. Intraperitoneal administration of CHA (0. 25, 0.5 and 1 mg/kg) decreased hippocampal secondary afterdischarge duration (SAD) and amygdala afterdischarge duration (ADD). Only the 1 mg/kg dose induced a significant increase in latency to stage 4. Intraperitoneal administration of CPT (0.25, 0.5 and 1 mg/kg) induced a significant increase in stage 5 duration, hippocampal SAD and ADD. Pretreatment of animals with CPT (1 mg/kg), antagonized effects of CHA on seizure parameters. Intraamygdala microinfusion (1 microl over 2 min) of CHA (5 nM-1 mM) significantly reduced hippocampal SAD and amygdala ADD. These effects were antagonized by intraamygdala CPT (1 microM). Results obtained suggest that in hippocampal kindled rats, amygdala may be regarded as a relay point for AD propagation specially in recruit activity of the hippocampus.

Adenosine↗

PubMed2000

Effects of ketamine on synaptic transmission and long-term potentiation in layer II/III of rat visual cortex in vitro.

The effects of ketamine, which has NMDA receptor antagonist properties, on synaptic transmission and long-term potentiation in layer II/III of adult rat visual cortex were examined in vitro. Field potentials were recorded in layer II/III following layer IV stimulation. Primed-burst stimulation was used for induction of long-term potentiation. Stimulation of layer IV resulted in a two-component response in layer II/III, a population excitatory postsynaptic potential1 (EPSP1) and a population excitatory postsynaptic potential2 (EPSP2). DL-2-Amino-5-phosphono-valeric acid (AP5), a competitive NMDA receptor antagonist, reduced the amplitude of the population EPSP1 while ketamine increased the amplitude of the population EPSP2. The results showed that primed-burst stimulation induced long-term potentiation in layer II/III of the visual cortex in vitro. Preincubation for 30 min with AP5 (25-100 microM) reduced the extent of long-term potentiation of the population EPSP2 and blocked the induction of long-term potentiation of the population EPSP1. When ketamine (100-200 microM) was present for 30 min prior to tetanic stimulation, it blocked the induction of long-term potentiation of the population EPSP1 and reduced the extent of long-term potentiation of the population EPSP2. We conclude that ketamine can interfere with synaptic transmission in the visual cortex. Primed-burst stimulation is an effective protocol for neocortical potentiation. NMDA receptors are involved in the induction of long-term potentiation by primed-burst stimulation of the population EPSP1 and population EPSP2 in adult rat visual cortex in vitro.

2-Amino-5-phosphonovalerate↗

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↗

PubMed1999

Primed-bursts induced long-term potentiation in rat visual cortex: effects of dark-rearing.

Theta burst stimulation (TBS) and primed bursts (PBs) stimulation are among the effective tetanic stimulations for induction of long-term potentiation (LTP) in the hippocampus. Recent studies have indicated that TBS is effective in LTP induction of layer III synapses of neocortex, only if applied to layer IV. However, the possibility of neocortical LTP induction using PBs has not been investigated yet. Sensory deprivation greatly influences the development of neocortex. According to the effect of sensory deprivation on synaptic plasticity of developing neocortex, we studied the induction of LTP by PBs in visual cortical slices of control and dark-reared rats. The results showed that application of PBs to layer IV could effectively induce LTP of layer II/III field potentials. These potentials are consisted of two components: pEPSP1, (population excitatory postsynaptic potential 1) and pEPSP2. In control slices PBs led to selective potentiation of pEPSP2. Visual deprivation increased the incidence of LTP of pEPSP1 and decreased the amount of LTP of pEPSP2. These findings showed that PBs could be used as an effective tetanic stimulation to study the synaptic plasticity in neocortex. The effects of visual deprivation on PBs-induced LTP are consistent with its role in the development of excitatory system in neocortex.

Animals↗