The data support the hypothesis that obese pregnant women have a greater risk of iron deficiency and that hepcidin may be a regulatory factor. Further, we show that the placenta responds to decreased maternal iron status by increasing pTFR1 expression.

In conditioned taste aversion (CTA), a subject learns to associate a novel taste (conditioned stimulus, CS) with visceral malaise (unconditioned stimulus, US). Considerable evidence indicates that the noradrenergic system in the amygdala plays an important role in memory consolidation for emotionally arousing experiences. The specific aim of the present set of experiments was to determine the involvement of noradrenergic activity in the basolateral amygdala (BLA) during the US presentation and consolidation of CTA as well as during the consolidation of a nonaversive/incidental gustatory memory. Selective bilateral microinfusions of the beta-adrenergic antagonist propranolol administered into the BLA immediately before intraperitoneal (i.p.) lithium chloride (LiCl) injections disrupted CTA memory. Additionally, propranolol infused into the BLA immediately after a pre-exposure to the saccharin (CS) significantly attenuated latent inhibition. The present findings indicating that alterations in noradrenergic function in the BLA affect taste memory formation, provide additional evidence that the BLA plays a critical role in modulating the consolidation of memory and that the influence is mediated by interactions with other brain regions that support memory for different kinds of experiences.

Conditioned taste aversion (CTA) is a learning paradigm in which an animal avoids a taste (conditioned stimulus) previously associated with visceral toxic effects [or unconditioned stimulus (US)]. Although many studies have implicated glutamate-mediated neurotransmission in memory consolidation of different types of learning tasks, including CTA, the exact role of this neurotransmitter system in memory formation is not known. Thus, we set out to determine whether glutamate mediates signaling of the US in CTA. We present evidence obtained by in vivo microdialysis that the US (i.p. injection of lithium chloride) induced a dramatic increase in glutamate release in the amygdala and a modest but significant release in the insular cortex. Moreover, CTA can be elicited by intra-amygdalar microinjections of glutamate; consequently, when glutamate is administered just before the presentation of a weak US, a clear CTA is induced. In contrast, the injection of glutamate alone or glutamate 2 h after the suboptimal US did not have any effect on the acquisition of CTA. These results indicate that glutamate activation of the amygdala can partially substitute the US in CTA, thus providing a clear indication that the amygdala conveys visceral information for this kind of memory.A number of studies (1-5) have implicated glutamatemediated transmission in consolidation of memory for different types of training, such as inhibitory avoidance, Morris water maze, and conditioned taste aversion (CTA). CTA is a learning paradigm in which the novel taste of food or drink (conditioned stimulus, CS) is paired with visceral signals of poisoning (unconditioned stimulus, US). Consequently, the animals avoid consuming the food or drink previously associated with toxic effects. CTA has unique properties; it is established after a single trial, permits long delays between stimuli presentation, and lasts for very long periods of time, even weeks. This feature makes it possible to separate the acquisition process into phases-CS presentation and US presentation-which can be studied independently under different experimental treatments (6).CTA is established by the interaction of brainstem, limbic, and neocortical structures underlying different phases of the acquisition storage and retrieval of gustatory memory (7). Among the structures involved in the initial phases of taste memory formation are the gustatory neocortex and amygdala (8). Thus, damage to either the gustatory insular cortex (IC) or amygdala in adult rats leads to impaired acquisition of CTA (6,7,[9][10][11][12][13][14][15][16][17]. However, the functional roles of IC and amygdala seem to be different during the phases of taste memory formation. Functional blockade of IC before taste presentation, but not between taste presentation and lithium chloride (LiCl) injection, blocks CTA (16, 18), suggesting that the gustatory cortex is involved in taste processing and͞or memory but is not necessary for processing the visceral signals of poisoning. Conversely, amygdala functional inactivation...

The presence of transitory viremia without seroconversion indicates that the vertical transmission of HCV is not important. This could be related to the viral charge and ingestion of milk of HCV-RNA-positive mothers. However, to advise avoidance of maternal breast feeding, it would be necessary to conduct larger studies.

- The effects of acute alcohol intoxication (AAI) on the pituitary-gonadal axis hormones, and the possible contribution of pituitary-adrenal axis hormones, beta-endorphin and prolactin to alcohol-induced dysfunction of pituitary-gonadal axis hormones were studied in adult men and women. Blood samples were drawn from adults of both sexes who arrived at the emergency department with evident behavioural symptoms of drunkenness (AAI) or from adult volunteers with nil consumption of alcohol (controls). Our results demonstrated that AAI produces a high increase in plasma prolactin, corticotropin (adrenocorticotropic hormone, ACTH), and cortisol in adults of both sexes, a decrease in luteinizing hormone levels only in men, an increase in dehydroepiandrosterone-sulphate (DHEAS) and a contradictory behaviour of testosterone according to gender, with increased plasma testosterone in women and a decrease in men. ACTH and prolactin correlated positively with cortisol, DHEAS and testosterone in women, which suggests that prolactin and ACTH could contribute to stimulated adrenal androgen production. In contrast, the decrease in testosterone and increase in beta-endorphin in men suggests that AAI could have an inhibitory effect on testicular testosterone, perhaps mediated by beta-endorphin. Our results suggest that the effect of alcohol on pituitary-gonadal axis hormones in humans could depend on the gender and degree of sexual maturity of the individual.

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In conditioned taste aversion (CTA), a subject learns to associate a novel taste with visceral malaise. Brainstem, limbic and neocortical structures have been implicated in CTA memory formation. Nevertheless, the role of interactions between forebrain structures during these processes is still unknown. The present experiment was aimed at investigating the possible interaction between the basolateral nucleus of the amygdala (BLA) and the insular cortex (IC) during CTA memory formation. Injection of a low dose of lithium chloride (30 mg/kg, i.p.) 30 min after novel taste consumption (saccharin 0.1%) induces a weak CTA. Unilateral BLA injection of glutamate (2 microg in 0.5 microL) just before low lithium induces a stronger CTA. Unilateral injection of an N-methyl-d-aspartate (NMDA) receptor antagonist (AP5, 5 microg in 0.5 microL) in IC has no effect. However, AP5 treatment in IC at the same time or 1 h after the ipsilateral BLA injection reverses the glutamate-induced CTA enhancement. Injection of AP5 in IC 3 h after BLA injection does not interfere with the glutamate effect. Moreover, the CTA-enhancing effect of glutamate was also blocked by contralateral IC injection of AP5 at the same time. These results provide strong evidence that NMDA receptor activation in the IC is essential to enable CTA enhancement induced by glutamate infusion in the BLA during a limited time period that extends to 1 but not to 3 hours. These findings indicate that BLA-IC interactions regulate the strength of CTA. The bilateral nature of these amygdalo-cortical interactions is discussed.

The basal forebrain complex, which includes the nucleus basalis magnocellularis (NBM), provides widespread cholinergic and ␥-aminobutyric acid-containing projections throughout the brain, including the insular and pyriform cortices. A number of studies have implicated the cholinergic neurons in the mediation of learning and memory processes. However, the role of basal forebrain activity in information retrieval mechanisms is less known. The aim of the present study is to evaluate the effects of reversible inactivation of the NBM by tetrodotoxin (TTX, a voltagesensitive sodium channel blocker) during the acquisition and retrieval of conditioned taste aversion (CTA) and to measure acetylcholine (ACh) release during TTX inactivation in the insular cortex, by means of the microdialysis technique in free-moving rats. Bilateral infusion of TTX in the NBM was performed 30 min before the presentation of gustative stimuli, in either the CTA acquisition trial or retrieval trial. At the same time, levels of extracellular ACh release were measured in the insular cortex. The behavioral results showed significant impairment in CTA acquisition when the TTX was infused in the NBM, whereas retrieval was not affected when the treatment was given during the test trial. Biochemical results showed that TTX infusion into the NBM produced a marked decrease in cortical ACh release as compared with the controls during consumption of saccharin in the acquisition trial. Depleted ACh levels were found during the test trial in all groups except in the group that received TTX during acquisition. These results suggest a cholinergic-dependent process during acquisition, but not during memory retrieval, and that NBM-mediated cholinergic cortical release may play an important role in early stages of learning, but not during recall of aversive memories.The cerebral cortex has been considered as the ubiquitous place for the storage of long-term memory. In this regard, a great deal of investigation into brain health has focused on a particular central nervous system disorder, Alzheimer's disease. This disease results, at least in part, from a deficit in acetylcholine (ACh) neurotransmission caused by a degeneration of large basal forebrain (BF) cholinergic neurons and a deficit in choline acetyltransferase, the enzyme that synthesizes ACh (1).Accumulative evidence supports the role of cholinergic neurons in the BF in processes such as arousal, attention, learning, and memory. Behavioral deficits associated with lesions produced by injections of excitatory amino acid agonists into the nucleus basalis magnocellularis (NBM) have been demonstrated in a variety of tasks (2, 3). However, the behavioral deficits of these lesions might be caused not only by the resulting cholinergic deafferentation, because 30-35% of the population of BF projections neurons to the cortex are ␥-aminobutyric acid-containing neurons (4-6).In this regard, there are several experiments trying to study more directly the modulatory role of ACh in the activity of cortical ...