Association of dietary patterns of pregnant women with pregnancy outcomes: A hospital-based study.

Diet is one of the main factors influencing pregnancy outcomes. Maternal and child health both seem to be related to dietary patterns. So far, no study on dietary pattern has been performed on pregnant women and its association with pregnancy outcomes in Rasht. Therefore, the present study aimed to investigate the association between dietary patterns and pregnancy outcomes in Rasht. In this cross-sectional study, 300 healthy pregnant women were included from three public hospitals in Rasht. Data on demographic, dietary intake, physical activity (PA), and anthropometric measurements of mothers were recorded. Outcomes of newborns were also gathered. Dietary patterns were identified using principal component analysis. General linear model was used for data analysis. Prior to pregnancy, only 40% of women had a normal body mass index (BMI). More than half of them (52.3%) had a gestational weight gain in excess of the guidelines. The dominant dietary patterns among pregnant women were traditional, Western, and healthy, respectively. High adherence to the Western pattern had a direct association with gestational weight gain (B = 1.48, p = .046) and inverse association with birth length (B = -0.71, p = .043). However, the results did not remain significant after adjusting for covariates. The present study indicated that several factors can affect the association of the Western diet with pregnancy outcomes. Therefore, making policies for interventional programs to improve maternal lifestyle factors along with their diet quality is recommended.

Activation of cannabinoid CB1 receptors in the central amygdala impairs inhibitory avoidance memory consolidation via NMDA receptors.

In the present study, we investigated the influence of bilateral intra-central amygdala (intra-CeA) microinjections of N-methyl-D-aspartate (NMDA) receptor agents on amnesia induced by a cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA). This study used a step-through inhibitory (passive) avoidance task to assess memory in adult male Wistar rats. The results showed that intra-CeA administration of ACPA (2 ng/rat) immediately after training decreased inhibitory avoidance (IA) memory consolidation as evidenced by a decrease in step-through latency on the test day, which was suggestive of drug-induced amnesia. Post-training intra-CeA microinjections of NMDA (0.0001, 0.001 and 0.01 µg/rat) did not affect IA memory consolidation. However co-administration of NMDA with ACPA (2 ng/rat) prevented the impairment of IA memory consolidation that was induced by ACPA. Although post-training intra-CeA administration of the NMDA receptor antagonist, D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 0.01, 0.05 and 0.1 µg/rat) alone had no effect, its co-administration with an ineffective dose of ACPA (1 ng/rat) impaired IA memory consolidation. Post-training intra-CeA microinjection of an ineffective dose of D-AP5 (0.01 µg/rat) prevented an NMDA response to the impaired effect of ACPA. These results suggest that amnesia induced by intra-CeA administration of ACPA is at least partly mediated through an NMDA receptor mechanism in the Ce-A.

ß1-noradrenergic system of the central amygdala is involved in state-dependent memory induced by a cannabinoid agonist, WIN55,212-2, in rat.

In the present study, we investigated effects of intra-central amygdala (intra-CeA) administrations of a ß1-receptor agonist and antagonist, isoprenaline (isoproterenol) and atenolol respectively, on state-dependent memory induced by a cannabioid agonist, WIN55,212-2. This study used a step-through inhibitory avoidance task to assess memory in male Wistar rats. The results showed that post-training intra-CeA administrations of different doses of WIN55,212-2 (0.01, 0.05, 0.1 and 0.25µg/rat) decreased memory as revealed by a decrease in memory retrieval on the test day. The decrease in retrieval induced by post-training WIN55,212-2 (0.25µg/rat) was reversed by pre-test administration of the same dose of the drug, which was suggestive of drug-induced state-dependent memory. Although pre-test intra-CeA administrations of isoprenaline (0.01, 0.025 and 0.05µg/rat) alone had no effect, its co-administrations at doses of 0.025 and 0.05µg/rat with an ineffective dose of WIN55,212-2 (0.1µg/rat) restored memory retrieval that impaired by post-training WIN55,212-2 (0.25µg/rat). The results also showed that pre-test intra-CeA administrations of atenolol (0.01, 0.05 and 0.1µg/rat) alone had no effect, but at dose of 0.1µg/rat disrupted state-dependent memory induced by WIN55,212-2. Moreover, the improving effect of isoprenaline (0.025µg/rat) on retrieval of state-dependent memory induced by WIN55,212-2 (0.1µg/rat) was prevented by intra-CeA co-injections of atenolol. Taken together, our results suggest that the CeA may be potentially critical for state-dependent memory induced by WIN55,212-2 and the ß1-noradrenergic receptor mechanism(s) interact with the cannabinergic system in the modulation of this kind of memory in the CeA.

Adrenoceptor mechanisms underlying imipramine-induced memory deficits in rats.

The post-training administration of tricyclic antidepressant imipramine impairs memory consolidation in the passive avoidance task. The present study investigated the effects of intrahippocampal (i.h.) injection of adrenoceptor agents on imipramine-induced (2-8 microg/rat) amnesia. The administration of the alpha1-adrenoceptor agonist phenylephrine (0.05 microg/rat) and the alpha1-adrenceptor antagonist prazosin (0.5 microg/rat) did not alter the effect of imipramine. The lower doses of phenylephrine (0.005 and 0.015 microg/rat) impaired, while the higher dose of the drug (0.025 and 0.05 microg/rat) improved retention. The effect of phenylephrine was not altered by prazosin (0.5 and 1 microg/rat) pretreatment, although prazosin alone decreased retention latencies. The alpha2-adrenoceptor antagonist yohimbine (0.5 and 1 microg/rat) decreased the response induced by imipramine. However, the alpha2-adrenoceptor agonist clonidine (0.08 microg/rat) did not alter the effect of the drug. Clonidine (0.15 and 0.3 microg/rat) by itself decreased, while yohimbine (1 and 2 microg/rat) increased retention latencies. Yohimbine pretreatment attenuated the effect of clonidine. It is concluded that alpha2-adrenoceptor mechanism(s) may be involved in imipramine-induced impairment of memory.