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On page 1 showing 1 ~ 4 papers out of 4 papers

Prenatal Ozone Exposure Induces Memory Deficiencies in Newborns Rats.

  • Verónica Custodio‎ et al.
  • Frontiers in molecular neuroscience‎
  • 2019‎

Air pollution is fully acknowledged to represent a major public health issue. Toxic environmental substances, such as ozone, interfere with prenatal development. Animals exposed to ozone (O3) in utero develop biochemical and morphological alterations. This gas has been proven to decrease cognitive capacity in different species. In the present study, we assessed the possible alterations in memory and spatial learning in the offspring of female rats who were exposed to 1.0 ppm of O3 embryonic development. Two instruments were used to evaluate possible alterations: the T-maze and a Skinner box. MAPK, ERK, p-ERK, and NR2B proteins, which are widely regarded as responsible for the learning process in the hippocampus and cortex, were also assessed by immunohistochemistry. We found that male rats exposed to O3 in utero displayed a significant delay to reach the correct response using the spatial learning test as compared to the control group. The female rats exposed to O3 showed a significant delay to reach the correct response as compared to the female control group in the Skinner box. We also found that while the male rats showed decrease in significant differences in the expression of NR2B, ERK and increase in MAPK. Females only showed increase in MAPK, p-ERK and decrease in ERK, when compared to their respective control group. It is possible that the deficits are associated to hormonal expression, inflammation and oxidative stress alterations. In summary, these results suggest that exposure to O3 can interfere with prenatal development, resulting in learning and memory deficiencies in rats.


Participation of the dentate-rubral pathway in the kindling model of epilepsy.

  • Miguel Hernández-Cerón‎ et al.
  • Journal of neuroscience research‎
  • 2017‎

Lesions of the cerebellar dentate nucleus (DN) reduce the after-discharge duration induced by repetitive kindling stimulation and decrease seizures to a lower rank according to Racine's scale. The DN sends cholinergic and glutamatergic fibers to the red nucleus (RN), which is composed of glutamatergic and GABAergic cells. To test the participation of these neurotransmitters in seizures, we compared the levels of glutamate and gamma-aminobutyric acid (GABA) at the RN in a control condition, a kindled stage, and a kindled stage followed by DN lesions. We found that the kindled stage was associated with significant reductions in glutamate and GABA in the RN and that the lesions of the DN in kindled rats reversed the severity of seizures and restored the GABA levels. GAD65 , a GABA-synthesizing enzyme, was increased in kindled rats and decreased after DN lesions. GAD65 commonly appears localized at nerve terminals and synapses, and it is only activated when GABA neurotransmission occurs. Thus, it is possible that the increased expression of GAD65 found in kindled rats could be due to an exacerbated demand for GABA due to kindled seizures. It is known that GABA maintains the inhibitory tone that counterbalances neuronal excitation. The decreased expression of GAD65 found after the DN lesions indicated that the GABA-synthesizing enzyme was no longer required once it eliminated the excitatory glutamate input to the RN. We thus conclude that DN lesions and their consequent biochemical changes are capable of decreasing the generalized seizures induced by kindling stimulation. © 2016 Wiley Periodicals, Inc.


Activity of nitric oxide synthase isoforms in acute brain oxidative damage induced by ozone exposure.

  • Juan Carlos Martínez-Lazcano‎ et al.
  • Nitric oxide : biology and chemistry‎
  • 2018‎

No abstract available


Inhibition of the NMDA Currents by Probenecid in Amygdaloid Kindling Epilepsy Model.

  • Edith González-Guevara‎ et al.
  • Molecular neurobiology‎
  • 2024‎

Epilepsy is characterized by a sustained depolarization and repeated discharge of neurons, attributed to overstimulation of N-methyl-D-aspartate receptors (NMDAr). Herein, we propose that probenecid (PROB), an inhibitor of the activity of some ATP binding-cassette transporters (ABC-transporters) can modify NMDAr activity and expression in amygdaloid kindled model. Some studies have suggested that NMDAr expression could be regulated by inhibiting the activity of P-glycoprotein (MDR1) and drug resistance protein-1 (MRP1). Besides, PROB was found to interact with other proteins with proven activity in the kindling model, such as TRPV2 channels, OAT1, and Panx1. Administering PROB at two doses (100 and 300 mg/kg/d) for 5 d decreased after-discharge duration and Racine behavioral scores. It also reduced the expression of NR2B and the activity of total NOS and the expression of nNOS with respect to the kindling group. In a second protocol, voltage-clamp measurements of NMDA-evoked currents were performed in CA1 hippocampal cells dissociated from control and kindled rats. PROB produced a dose-dependent reduction in NMDA-evoked currents. In neurons from kindled rats, a residual NMDA-evoked current was registered with respect to control animals, while a reduction in NMDA-evoked currents was observed in the presence of 20 mM PROB. Finally, we evaluated the expression of MRP1 and MDR1 in order to establish a relationship between the reduction of kindling parameters, the inhibition of NMDA-type currents, and the expression of these transporters. Based on our results, we conclude that at the concentrations used, PROB inhibits currents evoked by NMDA in dissociated neurons of control and kindled rats. In the kindling model, at the tested doses, PROB decreases the after-discharge duration and Racine behavioral score in the kindling model. We propose a mechanism that could be dependent on the expression of ABC-type transporters.


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