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Gabapentin 300 mg precio ) at 4 mg/kg/infusion, but not 10 mg/kg/infusion; in the sham group, dosing was at 2 mg/kg/inf infusion. In the second phase, same two doses of the drug were administered. results reported as mean ± SD.
Results Treatment effects
The dose of drugs that significantly increased the dose of activity glutamatergic synapses was 1.7 times (P < 0.01) higher in the animals that had received 4 mg/kg/infusion than in the control animals.
Treatment effects for the changes in firing rate and density of NMDA-type currents in the rat CA3 area, but not for the changes in firing rate, density, and density of long-term potentiation in the same area are shown in Figure 1. The increase both basal firing rate and the amplitude were found in synaptosystem at the onset of drug administration. After 4 d of drug administration, the average firing rate became 2.5-fold that of the control animals (P < 0.01). The increase in firing rate occurred mostly at high frequency frequencies (10–15 Hz) of the firing amplitude. In addition, dendrite of the soma was increased in rats that received the drugs. decrease of somal dendrite density from the synaptosomal level (Figure 1C) occurred at the same time Gabapentin 270 pills 20 mg - 295.48$ point (P < 0.01) as the increase in firing amplitude (Figure 1).
FIGURE 1
Figure 1. (A–C) Basal firing rate increases and amplitude were found in the synaptosomal level and at somatal dendrites. (A,B) Average firing rate decreases and buy gabapentin online without dr approval increases were found in the same area rats that received 200 and 1000 mg/kg/infusion. (C,D) The changes in firing activity of NMDA neurons have been compared in the somatotopically connected CA1 area with the synaptosomes from same area. dendritic density (C) and the firing activity (D) were studied.
Discussion
N‐methyl‐d‐aspartate (NMDA) receptors have been reported to be critical for the formation of GABA A receptors, the receptors responsible for inhibition of excitatory synaptic transmission. The activity of this class receptors is modulated in many cellular and animal models of depression anxiety. The mechanisms by which this occurs have been studied in some detail [6], and the role of NMDA receptors in the mechanisms of cognitive and emotional processes have been shown [7].
Our objective is to explore the involvement of NMDA receptors in cognitive and emotional processes depression anxiety in rats. The main focus of our investigation was to determine the involvement of receptors in formation new glutamatergic synapses and in the regulation of their properties after exposure to a drug, i.e., in the formation of new synaptic connections. In this context, we have established a new method of investigation on glutamatergic synapse formation. A is formed by presynaptic release of a neurotransmission protein, e.g, glycine from presynaptic terminals of a neuron by synapse‐forming enzyme, such as adenylate cyclase. After the synthesis of this neurotransmission protein, it is stored for some time as GluN1.
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