Comparative analysis of volatile metabolites, quality and sensory attributes of Actinidia chinensis fruit.

Volatile organic compounds, quality and sensory parameters of four yellow- ('Dorì', 'G3', 'Jintao' and 'Soreli') and two green-fleshed ('Hayward' and 'Summer') kiwifruit cultivars were assessed. Statistical analysis was performed on volatiles, quality and sensory data for the identification of biomarkers of different kiwifruit cultivars. Principal component analysis showed that for all six samples a very good discrimination based on the cultivar was achieved. In particular, 2-pentylfuran can be used to distinguish between the green- and yellow-fleshed kiwifruit cultivars, while seven volatiles, can be identified as biomarkers of 'Dorì'. These findings are in agreement with the sensory analysis, which revealed that 'Dorì', the richest cultivar in esters, showed very high values of both ripe fruit smell and sweet sensory traits. Altogether, these results could offer recommendations for future breeding efforts for the production of kiwifruit cultivars with improved nutritional and aroma quality.

Volatile metabolites, quality and sensory parameters of "Ferrovia" sweet cherry cold stored in air or packed in high CO2 modified atmospheres.

Volatile organic compounds, quality and sensory attributes of sweet cherry cv "Ferrovia", cold packaged in Air or in different modified atmospheres (Low-O2 = 1% O2/0.03% CO2; High-CO2 = 16% O2/20% CO2; Mix = 1% O2/20% CO2), were monitored until 21 days of conservation. Results showed that sweet cherry cv "Ferrovia" is sensitive to CO2 accumulation (over 20%) in low oxygen (about 1%) modified atmosphere, as showed by the increase in respiration rate, biosynthesis of fermentative volatile metabolites, and sensory perception of off-odours. However, High-CO2 treatment seemed to preserve quality and sensory traits, presumably due to the high initial concentration of O2 (16%) that could limit the synthesis of ethyl esters and γ-butyrolactone, keeping the accumulation of off-flavours below their sensory perception threshold. Finally, PLSR analysis allowed to select 1-pentanol as putative marker of sensory alteration and hexanal and 2-hexenal as possible predictors of freshness for "Ferrovia" sweet cherries.

Differential distribution, affinity and plasticity of dopamine D-1 and D-2 receptors in the target sites of the mesolimbic system in an animal model of ADHD.

The distribution of dopamine (DA) D-1 and D-2 receptors has been studied by autoradiography in the anterior forebrain of the pre-hypertensive spontaneously hypertensive rat (SHR) as an animal model of attention-deficit hyperactivity disorder (ADHD) in children. Juvenile male SHR and Wistar Kyoto (WKY) controls were given either vehicle or the DA re-uptake blocker methylphenidate (MP; 3 mg/kg, i.p.), daily during a 2-week period. A saturation analysis for the D-1 receptor subfamily was carried out with 0.1-5.0 nM of [3H]SCH23390 and two competition studies for the D-2 receptor subfamily with 4 nM of [3H]raclopride or 5 nM of [3H]quinpirole were carried out with unlabelled spiperone and 7-OH-DPAT as unlabelled displacers on cryostat coronal sections of the anterior forebrain. Quantitative receptor autoradiography and computer-assisted image analysis with reference to co-exposed 3H-microscale standards showed in vehicle-treated SHR higher density of DA D-1/D-5 receptor subtypes in the caudate-putamen (CPU), the nucleus accumbens (ACB) core and shell and the olfactory tubercle (OT), which was associated to a lower affinity. MP treatment normalised the DA D-1/D-5 receptors by decreasing the number of binding sites and increasing the affinity to control level. In addition, MP treatment 'down-regulated' DA D-2/D-4 subtypes in the CPU, ACB and OT, and 'up-regulated' mostly D-3 subtype in CPU, ACB, OT in both rat lines and in the globus pallidus, ventral pallidum and lateral septum in WKY rats only. In contrast, D-3 receptors were 'down-regulated' in the islands of Calleja in both rat lines. Moreover, regional cross-correlative analyses revealed a modulatory influence of DA receptors in the cross-talk within the anterior forebrain, which was altered in the SHR. Thus, the differential distribution and regulation of DA receptor subtypes following DA re-uptake blocker as well as the different regional cross-talk in the target sites of nigrostriatal and mesolimbic DA systems lend support to the DA hypothesis of ADHD in children.

L-threonine injection into PPC modifies food intake, lateral hypothalamic activity, and sympathetic discharge.

Food intake and the firing rate of lateral hypothalamic neurons and nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures, were monitored in male Sprague-Dawley rats fed a threonine-free diet. These variables were measured before and after a bilateral injection of L-threonine (2 nmol into each side) into the prepiriform cortex (PPC). The same variables were also monitored in 1) rats fed a threonine-free diet and injected with saline, 2) animals fed a standard diet and injected with L-threonine, and 3) rats fed a standard diet and injected with saline. The results showed that injection of L-threonine into PPC increases food intake and firing rate of lateral hypothalamic neurons, whereas it decreases the sympathetic discharge and body temperature in animals fed a threonine-free diet. No changes were found in the animals fed a standard diet. These findings suggest a correlation between 1) threonine level in the PPC and 2) lateral hypothalamic activity and sympathetic discharge to IBAT.

Acute lesions of the ventromedial hypothalamus reduce sympathetic activation and thermogenic changes induced by PGE1.

The aim of this experiment was to evaluate the effects of an intracerebroventricular (icv) injection of prostaglandin E1 (PGE1) on the sympathetic activation and the thermogenic changes in rats with acute lesions of the ventromedial hypothalamus (VMH). Four groups of six Sprague-Dawley male rats were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue (IBAT) and the colonic and IBAT temperatures were monitored both before and after one of the following treatments: 1) VMH lesion plus icv injection of PGE1 (500 ng); 2) VMH lesion plus icv injection of saline: 3) sham lesion plus icv injection of PGE1; and 4) sham lesion plus icv injection of saline. PGE1 induced an increase in the firing rate of IBAT nerves and the colonic and IBAT temperatures. These effects were reduced by VMH lesion. The findings indicate that acute lesions of the VMH reduce the effects of PGE1 and seem to suggest a possible role played by the VMH in the control of the sympathetic activation and the thermogenic changes during PGE1 hyperthermia.

Lysine acetylsalicylate modifies aphagia and thermogenic changes induced by lateral hypothalamic lesion.

These experiments test the effect of intraperitoneal injection of lysine acetylsalicylate on 1) food intake and 2) the sympathetic and thermogenic changes induced by lesion of the lateral hypothalamus (LH). Food intake, firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), and IBAT and colonic temperatures (TIBAT and TC) were monitored in male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after intraperitoneal injection of lysine acetylsalicylate. The same variables were also monitored in 1) lesioned rats with intraperitoneal administration of saline, 2) sham-lesioned animals with intraperitoneal injection of lysine acetylsalicylate, and 3) sham-lesioned rats with intraperitoneal injection of saline. The results show that lysine acetylsalicylate modifies the aphagia by increasing food intake and also reduces the enhancements in firing rate, TIBAT, and TC induced by LH lesion. These findings suggest that prostaglandin synthesis plays a key role in the control of eating behavior in LH-lesioned rats by acting on the sympathetic and thermogenic changes induced by LH lesion.

NMDA and non-NMDA sensitive [L-3H]glutamate receptor binding in the brain of the Naples high- and low-excitability rats: an autoradiographic study.

The Naples high-excitability (NHE) and low-excitability (NLE) rat lines, selectively bred for high and low activity in a Làt maze, respectively, are used as an animal model in the study of hippocampal functions. The aim of this study was to investigate the anatomical distribution of N-methyl-D-aspartate (NMDA) and non-NMDA sensitive [3H]glutamate receptor binding by quantitative autoradiography in the brain of the NHE and NLE rats with a randomly bred line (NRB) as controls. Twenty-micron-thick cryostat sagittal sections were incubated at 4 degrees C with 150 nM [L-3H]glutamate alone or in the presence of 100 microM NMDA or 2.5 microM quisqualate (QA). Non-specific binding was determined in the presence of 1 mM of non-labeled glutamate. The sections were exposed to tritium-sensitive films for 3 weeks at 4 degrees C. Quantitative analysis revealed: (1) higher levels of total binding in NHE than in NRB and NLE rats in all areas but the cerebellum; (2) fewer binding sites for both NMDA and QA receptors and larger binding sites for QA receptors in the hippocampus of NLE and NHE rats, respectively; (3) a positive correlation between total binding sites and activity level in a Làt maze in all areas, except the cerebellar molecular layer with NLE < NHE, which was due to differential contribution from NMDA and non-NMDA types. Thus, the brain of the NHE rats shows an imbalance between NMDA and non-NMDA sensitive [L-3H]glutamate receptors.

Immediate early genes and brain DNA remodeling in the Naples high- and low-excitability rat lines following exposure to a spatial novelty.

The aim of these studies was to map the neural consequences of exposure to a spatial novelty on the expression of immediate gene (IEG) and on unscheduled brain DNA synthesis (UBDS) in two genetic models of altered activity and hippocampal functions, i.e., the Naples High- (NHE) and Low-excitability (NLE) rats. Adult male rats of NLE and NHE lines, and of a random-bred stock (NRB) were tested in a Làt-maze, and corner crossings, rearings, and fecal boli were counted during two 10-min tests 24 h apart. For IEG expression, rats were exposed to a Làt-maze with nonexposed or repeatedly exposed rats used as controls, and were sacrificed at different time intervals thereafter. For UBDS, rats were sacrificed immediately after the first or the second exposure o a Làt-maze. IEG expression was measured by immunocytochemistry for the FOS and JUN proteins. NRB rats exposed for the first time to the maze showed extensive FOS and JUN positive cells in the reticular formation, the granular and pyramidal neurons of hippocampus, the amygdaloid nuclei, all layers of somatosensory cortex, and the granule cells of the cerebellar cortex. The positivity, stronger in rats exposed for the first time, was present between 2 and 6 h and was prevented by the NMDA receptor antagonist CPP (5 mg/kg). The positivity was very low in NHE rats, and it was stronger in NLE compared to NRB rats. UBDS was measured in ex vivo homogenates of brain areas by the incorporation into DNA of 3H-[methyl]-thymidine given intraventricularly 15 min before test trial 1 or 2 (pulse of 0.5 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric oxide and long-term habituation to novelty in the rat.

The role of nitric oxide in learning and memory processes has been tested in the albino rat by a histochemical and a behavioral study, following behavioral habituation to spatial novelty. Histochemically, the neural consequences of behavioral testing were mapped in the brain by staining for NADPH-d, known to be a NOS, whereas behaviorally the formation of LTH has been interfered with by posttrial NOS-inhibition. In the histochemical study, adult male Sprague-Dawley rats were tested in a Làt-maze and sacrificed at different time intervals thereafter. Handled unexposed rats served as controls. The brains were perfused with aldheide and processed for NADPH-d staining. In unexposed control rats the basal expression of NADPH-d was low and scattered. It pertained to few cells in the neostriatum, cerebral cortex, and CA1 hippocampal regions. In contrast, rats that had been exposed for the first time to the maze (spatial novelty) showed NADPH-d activity in the dorsal hippocampus (granule cells, few hilar neurons, and some CA1 pyramidal cells), the caudate-putamen complex, the cerebellum, and in all layers of somatosensory cortex. The positivity was not due to activity per se, since immediately after exposure it was not different from baseline. In contrast, it was present by 2 h and decreased significantly 24 h later. In addition, a strong neuronal discharge induced by the convulsant pentylentetrazol did not induce NADPH-d 2 h afterwards. The staining was prevented by pretreatment with the NMDA receptor antagonist CPP (5 mg/kg) or with the NOS inhibitor L-NOARG (10 mg/kg). In the behavioral study, rats were given an intraperitoneal injection of 1-10 mg/kg (L-NOARG) or vehicle immediately following exposure to a Làt-maze. The highest dose used (10 mg/kg) disrupted habituation of the vertical component only, known to be mainly of emotional meaning. Conversely, both doses disrupted emotional habituation based on defecation scores. The data indicate that the formation of LTH to novelty triggers a cascade of neurochemical events also involving NOS neurons. Further, the widespread induction of NADPH-d by exposure to novelty suggests that spatial and emotional information processing activate neural networks across different organizational levels of the CNS.

Postprandial thermogenesis and conditioned taste aversion or preference.

Postprandial thermogenesis is under the control of the autonomic nervous system and alimentary conditioned stimuli change sympathetic and parasympathetic activity. Here we studied the effect of conditioned taste aversion on postprandial thermogenesis in rats. Two groups of animals were used, rats of the first group were controls, these were placed on a standard diet and, for some days, on two other different diets: one thiamine-free and the other thiamine-rich. Each diet had a different taste. The treated animals belonged to the second group, these were fed with the same three diets but for different lengths of times: thiamine-free diet for the first 5 wk afterwards, with thiamine-rich diet for 3 wk, and finally with laboratory standard diet for a few days. After a preference test with the three familiar diets, oxygen consumption rate and brown adipose tissue temperature were evaluated three times in both groups after ingestion of a test meal, each time with one of the three different diets. The preference test was unvaried for the three different familiar foods in controls, while the treated animals showed a lower preference for thiamine-free food than for the other two. Treated rats had a significantly higher increase in O2 consumption rate than controls. In this group intake of thiamine-free food induced a significantly lower increase in O2 consumption than the other two. The increase in brown adipose tissue temperature was also higher in treated than in control animals but in treated rats this was lower after intake of thiamine-free food than after the intake of the other two.(ABSTRACT TRUNCATED AT 250 WORDS)

NMDA receptors modulate long-term habituation to spatial novelty: dose- and genotype-dependent differential effects of posttrial MK-801 and CPP in rats.

To investigate the role N-methyl-D-aspartate (NMDA) receptors play in behavioral plasticity, adult male rats of the Naples high-(NHE) and low-excitability (NLE) lines, and of a random-bred Sprague-Dawley strain (NRB) received, the noncompetitive (MK-801:0.01 or 2.5 mg/kg) or the competitive (CPP: 0.01 or 5 mg/kg) NMDA receptor antagonists, or vehicle IP soon after a 10-min test in a Làt-maze. Retention was tested 1 week later. Habituation of activity and defecation score was monitored by the between-test decrement (LTH) in the frequency of corner-crossings (HA) and rearings (VA), with prevailing cognitive and noncognitive meaning, respectively, and of fecal boli. (i) In the NLE-rats, low and high doses of MK-801 facilitate LTH of HA, and a high dose of CPP facilitates LTH of HA. (ii) In the NRB-rats, MK-801 facilitates LTH of HA at a low dose and inhibits LTH of VA at a high dose, whereas CPP inhibits LTH of HA at a high dose only. In contrast, (iii) in the NHE-rats, high doses of MK-801 impair LTH of HA, and low doses of CPP facilitate LTH of HA. In conclusion, the dose- and genotype-dependent differential effects of allosteric and isosteric receptor blockade support the hypothesized modulatory role of NMDA receptors in behavioral plasticity; and the dissociation between retention of cognitive and noncognitive behavioral components suggests that NMDA receptors are involved in their parallel processing.

Evidence for and against the Naples high- and low-excitability rats as genetic model to study hippocampal functions.

The Naples high- (NHE) and low-excitability (NLE) are two rat lines, selectively bred for high and low activity levels in a Làt-maze, respectively. Because the activity level in a novel environment depends mainly on the integrity of the hippocampal formation, and NLE and NHE rats differ with a similar background of emotionality, arterial blood pressure, and learning ability, they have been proposed as animal model to study hippocampal functions. Our aim is to prove evidence in favor and against this hypothesis. The evidence in favor indicates that NLE/NHE rats have a defective spatial processing, and pertains to (a) Differential activity in a spatial novelty situation (selection trait), proportional to the stimulus complexity rats are exposed to (NHE are hyper- and NLE-rats hypoactive); and (b) Impaired working memory in a six-arm non-reinforced tunnel maze in both lines compared to random-bred rats, that was reversed by the introduction of a reinforcer. In addition, multiple evidence of (i) lower intra- + infrapyramidal mossy fiber terminals in both NLE/NHE vs. controls; (ii) increased sensitivity of hippocampal elements to microinjections of vasopressin (but not oxytocin) and of "delta" (but not "mu") opioids; (iii) lower number of high-affinity glucocorticoid receptors; (iv) lower number of alpha- but not beta-adrenergic receptors in the hippocampus and hypothalamus of NHE rats only; and (v) the genotype-dependent behavior of a DNA fraction with fast turnover, suggest that both NHE/NLE are "disintegrated" at the hippocampal interface. Further, neurobehavioral covariations among individual differences reveal nonlinear, complex relationships, an evidence apparently against the hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Distributed changes in c-Fos and c-Jun immunoreactivity in the rat brain associated with arousal and habituation to novelty.

The effects of exposure to spatial novelty on expression of the immediate early gene (IEG) products c-Fos and c-Jun were mapped in the rat brain by immunohistochemistry. Adult male Sprague-Dawley rats were tested for 10 min in a Làt-maze, and corner-crossings, rearings, and fecal boli were recorded. Rats were sacrificed at different time intervals after exposure to the maze (0.5, 2, 6, or 24 h). Unexposed rats or rats repeatedly exposed for 3 days at 24 h interval served as controls. Nonperfused brains were processed for immunocytochemistry for c-Fos and c-Jun on adjacent slices using the avidin-biotin method and diaminobenzidine as chromogen. In unexposed control rats the constitutive expression of the two IEGs products was low and scattered. In contrast, rats that had been exposed for the first time to the maze (spatial novelty) showed an extensive c-Fos- and c-Jun-like immunoreactivity in the reticular formation, the caudate-putamen complex, the hippocampus (granular and pyramidal neurons), the cerebellum (granular neurons), and all layers of somatosensory cortex. The positivity was stronger in rats exposed for the first time to the box than in repeatedly exposed or unexposed control rats. A maximal IEG expression was found in animals with postexposure survival times of 2 and 6 h. IEG expression in repeatedly exposed rats was still above baseline expression of unexposed rats but still lower than that of rats having been exposed only once to the maze.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of diet-induced thermogenesis following lesions of paraventricular nucleus in rats.

The effects of electrolytic lesions in the hypothalamus paraventricular nucleus were studied in adult male and female Sprague-Dawley rats, fed different diets, consisting of either palatable human food plus chow (cafeteria diet) or chow alone. The results showed that both cafeteria diet and lesions induced an increase in energy intake and weight gain in rats of both sexes. Oxygen consumption rate and colonic temperature were significantly decreased by lesions, while cafeteria diet increased the same parameters only in intact animals. The lesion decreased weight, protein and DNA, and temperature of brown adipose tissue, while cafeteria diet increased the values considered in brown adipose tissue of sham-injured rats, but not in lesioned animals. The response to norepinephrine administration was significantly greater in intact rats and those fed cafeteria diet. The results suggest that the larger body weight gain observed in lesioned rats, particularly evident in rats fed cafeteria diet, is partly due to the disappearance of diet-induced thermogenesis that depends on the reduced mass and functional activity of brown adipose tissue.

Thermogenetic changes following frontal neocortex stimulation.

Heat production changes were recorded in anesthetized female Sprague-Dawley rats after stimulation of orbital frontal neocortex. The results obtained show that orbital frontal neocortex stimulation significantly increases oxygen consumption, and core and brown adipose tissue temperature. The increase was more substantial after stimulation of left than right cortex. Administration of the beta-blocker propranolol abolished the increase in O2 consumption, core and brown adipose tissue temperature following cortical stimulation. These results are in agreement with our previous research showing that functional ablation of cerebral cortex blocked the increase in thermogenesis following lateral hypothalamic lesion. These findings also show that the orbital frontal neocortex in rats is specifically involved in the control of thermogenesis.

Heat production and motor deficit in rats lesioned in globus pallidus, entopeduncular nucleus and lateral hypothalamus.

Oxygen consumption, colonic and interscapular brown adipose tissue temperature were evaluated in four groups of male and four groups of female rats both before and after lesions in different brain regions, and following beta-blocker propranolol administration. Recovery of body weight with varying difficulties in reaching food was also recorded in the injured animals. Groups consisted of rats with bilateral lesions in the entopeduncular nucleus (group EN), rats with bilateral lesions in the globus pallidus (group GP), rats with lateral hypothalamic lesions in the left side and entopeduncular lesion in the right side (group EN-LH), and rats with bilateral lesions in the lateral hypothalamus (group LH). Colonic and brown adipose tissue temperature and oxygen consumption were significantly increased after lesions in rats of groups EN, LH and EN-LH, but not in animals of the GP groups. Similarly, propranolol administration blocked the rise in heat production only in EN, LH and EN-LH animals. No differences were found between sexes. The survival rate was the same in all groups. GP rats recovered body weight earlier than animals injured in the other regions. The difficulty in reaching food was an important factor only in rats damaged in the EN. The results suggest that lateral hypothalamus and entopeduncular nucleus share a common regulatory function of the energy metabolism, while EN lesions induce a motor deficit in addition.

Cortical control of hypoxic suppression of thermogenesis induced by lateral hypothalamic lesion.

Acute hypoxic hypoxia is reported to suppress both diet- and cold-induced components of metabolism. In the present experiment the effects of hypoxic hypoxia on the oxygen consumption and on colonic and brown adipose tissue temperature were studied in rats with lesion of the lateral hypothalamus. The electroencephalographic activity, slow potential changes and cortical extracellular potassium concentration were also recorded. The results showed that acute hypoxic hypoxia blocked the thermogenesis induced by lateral hypothalamic lesion and the changes in temperatures were always preceded by modification of the cerebral cortex activity.

Cortical control of thermogenesis induced by lateral hypothalamic lesion and overeating.

Increased O2 consumption was found in rats after bilateral lesions of the lateral hypothalamus (LH) or during voluntary overeating. This phenomenon appears to be mediated by the sympathetic nervous system (SNS) in both conditions, since it is blocked by the beta-blocker propranolol administration. In the first experiment we showed that the brain cortex is involved in the thermogenesis induced by LH lesion and this effect is mediated by SNS, since bilateral functional decortication induced by cortical-spreading depression (CSD) impaired the increase of O2 consumption to the same extent as administration of propranolol. In the second experiment the role played by the cerebral cortex on thermogenesis in rats during voluntary overeating of "cafeteria" diet and in control rats was investigated. Cafeteria rats showed a significantly higher colonic temperature, brown adipose tissue temperature (Tbat), and rate of O2 consumption than control animals. CSD led to a significant decrease of Tbat and O2 consumption in cafeteria rats but not in controls. On the basis of the results obtained in the two experiments, the possibility that the cerebral cortex could be involved in the metabolic responses for reduction of body weight to the "set-point" is hypothesized.