Effect of inhibitory avoidance training on [3H]-glutamate binding in the hippocampus and parietal cortex of rats

Abstract

Glutamate receptors have been implicated in memory formation. The aim of the present study was to determine the effect of inhibitory avoidance training on specific [ 3 H]-glutamate binding to membranes obtained from the hippocampus or parietal cortex of rats. Adult male Wistar rats were trained (0.5-mA footshock) in a step-down inhibitory avoidance task and were sacrificed 0, 5, 15 or 60 min after training. Hippocampus and parietal cortex were dissected and membranes were prepared and incubated with 350 nM [ 3 H]-glutamate (N = 4-6 per group). Inhibitory avoidance training induced a 29% increase in glutamate binding in hippocampal membranes obtained from rats sacrificed at 5 min (P<0.01), but not at 0, 15, or 60 min after training, and did not affect glutamate binding in membranes obtained from the parietal cortex. These results are consistent with previous evidence for the involvement of glutamatergic synaptic modification in the hippocampus in the early steps of memory formation. It has been postulated that long-term potentiation (LTP) of glutamatergic synapses is a cellular mechanism underlying learning and memory. Glutamate receptors are involved in both the induction and the expression of LTP. LTP induction depends on activation of the N-methyl-D-aspartate (NMDA) type of glutamate receptor channel and the metabotropic glutamate receptor (mGluR), whereas its maintenance and expression depend on a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor channels (1).As with LTP, glutamate receptors play a role in both the formation and the expression of memory for the step-down inhibitory avoidance task. Memory formation for this task depends on glutamate receptor activation in several brain areas. Among other structures, the hippocampus is particularly important in the early phase of memory formation, while the posterior parietal cortex plays a late role in consolidation (4). Posttraining infusion of the NMDA receptor antagonist aminophosphonopentanoic acid impairs retention of inhibitory avoidance in rats when given into the hippocampus immediately after training (2,3), or when given into the posterior parietal cortex 180 min after training (4). Intrahippocampal infusion of the mGluR antagonist methyl-carboxyphenyl glycine immediately after training (5) or of the AMPA receptor antagonist cyanonitroquinoxaline-dione (CNQX) up to 3 h after

Posterior parietal cortex and long-term memory: some data from laboratory animals

“…Some of this work has involved classic animal (Compton et al, 1994; Rogers and Kesner, 2007; Berryhill et al, 2007; Keene and Bucci, 2008) or human (Berryhill et al, 2010a,b; Drowos et al, 2010) lesion studies, and typical post-training microinjection and assay techniques (Zanatta et al, 1996; Ardenghi et al, 1997; Izquierdo et al, 1997; Barros et al, 1998; Schröder et al, 2000; Luft et al, 2004; Bonini et al, 2005; Alonso et al, 2005) or post-training lesion studies (Rossato et al, 2004). …”

“…Thus, some of the molecular components of the role of the PPC in memory encoding or consolidation have been identified by pharmacological means; i.e., by the microinfusion of a variety of drugs into this structure bilaterally at various times in the post-training period (Ardenghi et al, 1997; Izquierdo et al, 1997; Barros et al, 1998; Schröder et al, 2000; Luft et al, 2004; Alonso et al, 2005; Bonini et al, 2005); others by measuring biochemical changes in this structure at those times (Alonso et al, 2005; Izquierdo et al, 2007). They were found to participate, as said, beginning 60–90 min post-training, i.e., 60–90 min after the participation of the hippocampus and the basolateral amygdala in consolidation, and 30 or so min after that of the entorhinal cortex (Izquierdo and Medina, 1997; Izquierdo et al, 2006).…”

Propylthiouracil-induced hypothyroidism during lactation alters leucine and mannose metabolism in rat cerebellar slices

“…21 High-mannose oligosaccharides are considered essential components influencing neuroplasticity. 22,23 Although the relevance of thyroid hormones for normal brain physiology is well documented ( protein and neurotransmitter synthesis, energetic metabolism), 24,25 studies regarding the effects of hypothyroidism on brain metabolism are still limited.…”