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Introduction Epilepsy is a common neurological disorder that affects millions of people worldwide. While there are many treatment options available, including drug and non-drug therapies, there is still a need for effective treatments that can help manage seizures.The present study aimed to investigate the intensity-dependent effects of mild electric foot stimulation on seizure intensity following pentylenetetrazol (PTZ)chemical kindling in rats. Methods: Kindled seizures were induced in rats by repeated injections of PTZ. Twenty-seven male rats were randomly divided into three groups: kindling group, kindling group + 0.1 mA electrical stimulation, and kindling group + 0.01 mA electrical stimulation. Electrical stimulation was induced using an electric box equipped with steel rods following acquisition of kindled seizures. The intensity of the mild electric foot stimulation was either 0.1 or 0.01 mA depending on the tested group. Results: The study found that while mild electric foot stimulation with intensity of 0. 1 mA had proconvulsive effects on PTZ-induced kindled rats, and decreased the latency to the onset of stage 5 seizure (p<0.05), stimulation with intensity of 0.01 mA did not have significant effects on seizure parameters. Conclusion: Obtained results suggested that mild electric foot stimulation may have anticonvulsant effects, but only at certain intensity. This finding has important implications for future research into the use of mild electric foot stimulation as a treatment for epilepsy. [ABSTRACT FROM AUTHOR]

The role of opioid receptor and voltage dependent calcium channels on the kindling induced by the convulsant pentylenetetrazole (PTZ) were investigated in the rats. Experiment involved 24 rats which were divided into four groups. Kindling was established with PTZ in subconvulsive dose (37.5 mg/kg i.p.) every 48 h and effects were observed within 20 min using five-point scoring system. All animals were kindled to three consecutive-stage five seizures and their stability was tested. Saline, verapamil (calcium channel blocker), naloxone (opioid antagonist) or both of them were then administrated 20 min before PTZ application. Convulsant parameters were significantly (P<0.05) reduced by verapamil. Naloxone had no significant effect on the seizure expression of fully kindled animals, whereas simultaneous application of naloxone and verapamil had profound inhibitory effect on all seizure parameters. The results of the present study suggest that naloxane increased the inhibitory effect of verapamil on the seizure induced by PTZ kindling [ABSTRACT FROM AUTHOR]

Background: Nutrition assessment is a routine method for determining the nutritional needs of individuals, especially for vulnerable groups (women, infants, and children). One of the important criteria for assessment of nutritional status is determining the concentration of a nutrient after its intake. Materials and Methods: In this cross-sectional study, 80 lactating mothers were selected from private and public hospitals in Tabriz. Data gathered through the questionnaire included general information concerning lactating mothers and also their nutritional diet. Since vitamin A and beta-carotene were measured through Karr-Price method, vitamin A and betacarotene concentrations were measured at 620 nm wavelength. Results: There was a significant positive correlation between retinol intake and colostrum retinol of lactating mothers (p=0.01) (r = 0.28). Also, retinol intake showed a positive and significant correlation with total vitamin A (retinol equivalent) in colostrum (p=0.002) (r= 0.33). Conclusion: Daily retinol and beta-carotene intake affect retinol of colostrum which its proper concentration in mother's milk can play an important role in better function of this vitamin for both mother and child. [ABSTRACT FROM AUTHOR]

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.

To elucidate chronic actions of brain-derived neurotrophic factor (BDNF) on GABAergic synapses, we examined effects of a long-term application of BDNF for 10-15 days on autapses (synapses) of solitary GABAergic neurons cultured from rat visual cortex. Solitary neuron preparations were used to exclude a possible contamination of BDNF actions on excitatory neurons in dissociated neuron culture or slice preparations. Neurons were confirmed to be GABAergic pharmacologically with bicuculline, a selective antagonist for GABAA receptors and immunocytochemically with antibody against glutamic acid decarboxylase 65, a GABA synthesizing enzyme. To evaluate GABAergic synaptic function, evoked and/or miniature inhibitory postsynaptic currents (IPSCs) were recorded in the whole-cell voltage-clamp mode. The treatment with BDNF at a concentration of 100 ng/ml enhanced the amplitude of evoked IPSCs and the frequency of miniature IPSCs. In contrast, BDNF did not have a detectable effect on the amplitude of miniature IPSCs and the paired pulse ratio of IPSCs evoked by two, successive activations. To evaluate morphological changes, neurons were immunocytochemically stained with antibodies against microtubule-associated protein 2, to visualize somatodendritic region and synapsin I, to visualize presynaptic sites. The quantitative analysis indicated that BDNF increased the area of soma, the numbers of primary dendrites and dendritic branching points, the total length of dendrites and the number of synaptic sites. Such an action of BDNF was seen in both subgroups of GABAergic neurons, parvalbumin-positive and -negative neurons. To visualize functionally active presynaptic sites, neurons were stained with a styryl dye, FM1-43. BDNF increased the number of stained sites that was correlated with the frequency of miniature IPSCs. These results suggest that the chronic treatment with BDNF promotes dendritic and synaptic development of GABAergic neurons in visual cortex., (Copyright 2004 IBRO)

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.

Possible anticonvulsant effects of 2-chloroadenosine injected focally into the perirhinal cortex of amygdala kindled rats were investigated over a 2 h period. Animals were microinfused (1 microl) with 2-chloroadenosine (2-CLA; 5, 10, 15, 25 and 100 nM) or artificial cerebrospinal fluid applied through a cannula located in the perirhinal cortex. At the doses employed, 2-CLA significantly reduced afterdischarge duration and stage 5 seizure duration. The latency to stage 4 seizure was increased only at the highest dose of 2-CLA (100 nM), while even at this dose no significant change in seizure stage could be seen. The maximum effect of 2-CLA was obtained 30 min after microinfusion of the drug. Pre-treatment (intraperirhinal cortex) of animals with the nonselective adenosine antagonist, caffeine (50 microM; 1 microl), blocked the anticonvulsant activity of 2-CLA. These results suggest that adenosine receptors located in the perirhinal cortex may play an important role in the suppression of seizure activity elicited from the amygdala.