A marked deficiency in circulating and renal IGF-I peptide does not inhibit compensatory renal enlargement in uninephrectomized mice.

Objective: Increase in kidney IGF-I levels due to its increased trapping from the circulation was hypothesized to be a key mediator of compensatory renal enlargement. We tested this hypothesis using genetically engineered mice with extremely low circulating IGF-I levels.

Design: Both IGF-I deficient (ID) and normal (N) mice underwent a uninephrectomy (UNx) and sacrificed 2 or 9days later.

Uremia attenuates growth hormone-stimulated insulin-like growth factor-1 expression, a process worsened by inflammation.

Growth hormone (GH) resistance is common in uremia and together with resistance to insulin-like growth factor-1 (IGF-1) contributes to uremic growth retardation and muscle wasting. Previously, we found decreased GH-stimulated janus-kinase 2-signal transducers and activators of transcription 5 (STAT5) phosphorylation and nuclear translocation in uremia; however, it is unclear whether there are more distal defects. Therefore, we tested whether the binding of phosphorylated STAT5b to DNA is intact in uremia.

Explicit disassociation of a conditioned stimulus and unconditioned stimulus during extinction training reduces both time to asymptotic extinction and spontaneous recovery of a conditioned taste aversion.

Conditioned taste aversions (CTAs) may be acquired when an animal consumes a novel taste (CS) and then experiences the symptoms of poisoning (US). This aversion may be extinguished by repeated exposure to the CS alone. However, following a latency period in which the CS is not presented, the CTA will spontaneously recover (SR).

Time-dependent retrograde amnesic effects of muscimol on conditioned taste aversion extinction.

We explored how stimulation of GABA(A) receptors at different times during conditioned taste aversion (CTA) acquisition or extinction influenced extinction. In Experiment 1, rats acquired a CTA to 0.3% saccharin-flavored water (SAC) when it followed an injection of lithium chloride (LiCl; 81.

Spontaneous recovery of a conditioned taste aversion differentially alters extinction-induced changes in c-Fos protein expression in rat amygdala and neocortex.

Conditioned taste aversions (CTAs) may be acquired when an animal consumes a novel taste (conditioned stimulus; CS) and then experiences the symptoms of poisoning (unconditioned stimulus; US). Animals will later avoid the taste that was previously associated with malaise. Extinction of a CTA is observed following repeated, non-reinforced exposures to the CS and represents itself as a resumption of eating/drinking the once-avoided tastant.

Acetaminophen self-administered in the drinking water increases the pain threshold of rats (Rattus norvegicus).

Previous studies have suggested that the addition of flavored acetaminophen suspension (for example, Children's Tylenol) in the drinking water of rats may not be effective in producing postoperative analgesia because of low levels of consumption. However, these investigations neither measured analgesia nor compared the consumption by rats that had undergone surgery with that by unmanipulated rats. The present study reports that although unmanipulated rats naive to the taste of flavored acetaminophen do indeed drink significantly less of this liquid than tap water, they drank sufficient amounts of the acetaminophen-containing solution to significantly raise pain thresholds, as measured by the hot-plate test.

A role for prefrontal cortex in the extinction of a conditioned taste aversion.

This study used immunohistochemical methods to determine if the medial prefrontal cortex (mPFC) is involved in the extinction of a conditioned taste aversion (CTA). As rats reached 90% reacceptance of a tastant (saccharin: SAC) that had previously been associated with lithium chloride-induced malaise, c-Fos protein expression increased dramatically as compared to animals with active CTAs, animals without CTAs (i.e.

Long-term age-dependent behavioral changes following a single episode of fetal N-methyl-D-Aspartate (NMDA) receptor blockade.

Background: Administration of the N-methyl-D-aspartate (NMDA) antagonist ketamine during the perinatal period can produce a variety of behavioral and neuroanatomical changes. Our laboratory has reported reliable changes in learning and memory following a single dose of ketamine administered late in gestation. However, the nature of the drug-induced changes depends on the point during embryonic development when ketamine is administered.