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… Show more
“…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).…”
The posterior parietal cortex (PPC) was long viewed as just involved in the perception of spatial relationships between the body and its surroundings and of movements related to them. In recent years the PPC has been shown to participate in many other cognitive processes, among which working memory and the consolidation and retrieval of episodic memory. The neurotransmitter and other molecular processes involved have been determined to a degree in rodents. More research will no doubt determine the extent to which these findings can be extrapolated to primates, including humans. In these there appears to be a paradox: imaging studies strongly suggest an important participation of the PPC in episodic memory, whereas lesion studies are much less suggestive, let alone conclusive. The data on the participation of the PPC in episodic memory so far do not permit any conclusion as to what aspect of consolidation and retrieval it handles in addition to those dealt with by the hippocampus and basolateral amygdala, if any.
“…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).…”
The posterior parietal cortex (PPC) was long viewed as just involved in the perception of spatial relationships between the body and its surroundings and of movements related to them. In recent years the PPC has been shown to participate in many other cognitive processes, among which working memory and the consolidation and retrieval of episodic memory. The neurotransmitter and other molecular processes involved have been determined to a degree in rodents. More research will no doubt determine the extent to which these findings can be extrapolated to primates, including humans. In these there appears to be a paradox: imaging studies strongly suggest an important participation of the PPC in episodic memory, whereas lesion studies are much less suggestive, let alone conclusive. The data on the participation of the PPC in episodic memory so far do not permit any conclusion as to what aspect of consolidation and retrieval it handles in addition to those dealt with by the hippocampus and basolateral amygdala, if any.
“…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.…”
Thyroid hormone deficiency during perinatal development results in significant alterations in neurological functions. The relationship between such events and brain metabolism is not completely understood. The aim of this study was to investigate the effects of hypothyroidism on leucine, mannose, glucose and lactate metabolism in rat cerebellar slices. Experimental hypothyroidism was induced by exposing mothers and pups to propylthiouracil (PTU) until weaning - postnatal day 21. Metabolic analyses were performed in postnatal day 10 (PND10) and 21 (PND21) animals. A matching group of animals received the same oral treatment also after weaning until adulthood PND60 with T3 supplement during lactation (P1-P21). In PND21 animals, PTU treatment significantly increased the rate of leucine oxidation to CO2, although glucose and lactate oxidations were not affected. PTU treatment also increased the oxidation of leucine to CO2 at PND60 (adult animals). PND10 hypothyroidism animals showed a decrease in conversion of mannose to glycolipids and glycoprotein compared with the control group. However, PTU treatment increased the conversion of mannose to glycolipids and glycoprotein in PND21 animals. The replacement of T3 normalized mannose and leucine metabolism in adult rats. These results indicate that deficits in thyroid hormones during lactation could delay or alter brain development and metabolism.
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