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  • Finally it is possible that

    2022-07-01

    Finally, it is possible that the increase in the number of EAAT-3-labelled cells in the DG at PD 60, when compared with the control and experimental animals at PD 14, is associated with natural changes in the number of neurons present during the postnatal development of the hippocampus (41, 42) and, to a lesser extent, to the changes induced by MSG evident in cells labeled for GAT-1. Moderate immunoreactivity to GAT-1 has been found around the stratum pyramidale and granular layer between PD 5 and PD 30 (14), and after PD 45, the subgranular region is the area most densely stained, in conjunction with the punctuate staining of the pyramidal and granular cell layers between the nonexpressing cell bodies. This temporal gradient of GAT-1 expression during development in untreated rats correlates well with our results.
    Acknowledgments This research was supported by grants COECYTJAL–University of Guadalajara (PS-2009-489 and 558) and CONACYT-SEP-CB 106179. We wish to thank Dr. Sonia Luquín de Anda for assistance with the fluorescence microscopy.
    Introduction Organophosphorus (OP) compounds refer to a large group of insecticides or nerve agents, which act by inhibiting the enzyme acetylcholinesterase (AChE), the enzyme responsible for the breakdown of acetylcholine. Subsequently, accumulation of 3576 (ACh) leads to hyperstimulation of muscarinic and nicotinic receptors and produces a series of centrally and peripherally pathological responses, including hypersecretions, fasciculation, tremor, convulsions, respiratory distress, and death (Shih et al., 2003). Poisoning with pesticides, especially OP insecticides, is a major public-health concern worldwide (Albuquerque et al., 2006, Buckley et al., 2004). OP insecticide parathion is converted to its bioactive metabolite paraoxon by oxidative desulforation in the liver. Paraoxon is used in civilian laboratories as a surrogate nerve agent (Deshpande et al., 2014). Although the primary known mechanism of OP action is disruption in acetylcholine neurotransmission, these compounds have also been reported to interfere with other neurotransmitter systems, including GABAergic and glutamatergic systems. Current standard treatments for reducing OP-induced toxicity include anticholinergic compounds to reduce the muscarinic syndrome, oximes to reactivate inhibited AChE, and anticonvulsants to control OP-induced seizures. However, such treatments failed to prevent long-term OP-induced seizures and subsequent brain damages (Guo et al., 2015, Shih et al., 2003). Therefore, research efforts are necessary in order to identify more efficient drugs to provide neuroprotection against OP-induced brain damages. Modulation of the glutamatergic system and reduction of glutamate excitotoxicity appear to be one of the therapeutic strategies to prevent neuronal death and consequent cognitive impairment caused by OP-induced seizure (Myhrer et al., 2005). Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system and essential for normal brain function including cognition, memory, and learning. However, the extracellular concentration of glutamate must remain below its excitotoxic levels to limit overstimulation of glutamate receptors and prevent neuronal damage or death (Danbolt, 2001). In addition to the amount of glutamate released, the concentration of glutamate in the synaptic cleft is determined by its clearance through high affinity sodium dependent glutamate transporters, also called excitatory amino acid transporters, EAATs. These transporters include five members: EAAT1 (glutamate-aspartate transporter, GLAST), EAAT2 (glutamate transporter-1, GLT-1), EAAT3 (excitatory amino acid carrier 1, EAAC1), EAAT4, and EAAT5. EAAT1 and EAAT2 are mainly expressed in astrocytes, whereas EAAT3 is expressed in neurons. EAAT4 and EAAT5 appear to be restricted to cerebellar Purkinje cells and the retina, respectively (Danbolt, 2001, Simantov et al., 1999, Zhou and Danbolt, 2013). These transporters are responsible for extracellular glutamate clearance by glutamatergic axon terminals and astrocytic processes (Danbolt, 2001). Astrocytic glutamate transporters, especially EAAT2, have the main role in clearing glutamate from the extracellular space (Danbolt, 2001, Rothstein et al., 1996).