Differential changes in taste perception induced by benzoic acid prickling.

Benzoic acid (Bz) is a prickling compound used to preserve foods. However, its effects on taste are unknown. This work examines Bz-taste interaction using psychophysical methods [magnitude estimation (ME) and paired comparison (PC)] to measure taste intensity in aqueous solutions of pure tastants (T) and their respective mixtures with 10 mM Bz (Mix). Prototypical tastants induced basic taste qualities (mM): sucrose [90-1440, sweetness (Sw)], citric acid [1-64, sourness (So)], NaCl [15-960, saltiness (Sa)], quinine [0.01-0.64, bitterness (Bitt)], KCl (12.5-400, Sa and Bitt). MEs were analysed using Steven's and Beidler's equations. Bz increased Sw (all concentrations) and ionic tastes (low concentrations) and Bz effects were reduced by concentration increase according with quality and tastant Bz reduced Bitt(Quinine) (high concentrations). Bz reduced taste slopes (percentage decrease): Sw 45% (P<.02), So 34% (P<.01), Sa 35% or 41% (NaCl or KCl, P<.03), Bitt 33% or 60% (quinine P<.01 or KCl P<.04). Bz reduced K(diss) (affinity(-1)) (percentage reduction): Sw 79% (P<.0002), So 40% (P<.03), Sa(NaCl) 63% (P<.005), Sa(KCl) 48% (P<.04), Bitt(KCl) 64% (P<.04). Bz reduced ME(max) (percentage reduction): Sw 31% (P<.004), Bitt(Quinine) 29% (P<.03). PCs confirmed taste increases by Bz (percentage of 'Mix(intensity)>T(intensity)' answers/total answers): Sw 79-69% (90-1440 mM sucrose), So 75% (1 mM citric acid) and 71% (2 mM citric acid), Sa 75-71% (15-120 mM NaCl). Negative concentration dependence of taste increases by Bz suggests different levels of interaction. Biophysical and neurophysiological changes are discussed in relation with Bz properties and mechanism of interaction with taste.

A kinetic study on benzoic acid pungency and sensory attributes of benzoic acid.

Aqueous solutions of benzoic acid (BA) were evaluated by two methods: (i) sensory profile: a descriptive test of sensory attributes combined with semiquantitative analysis; and (ii) pungency intensity measures as a function of time: a computerized recording using specific software. Kinetic parameters evaluated were maximal intensity (I(MAX)), total time of pungency (Ttot), rates of increase (V1) and decrease (V2), half-life (T1/2), area under curve (AUC) and time to maximal intensity (T(IMAX)). Results were analyzed by ANOVA, LSD test, iterative calculations and adjustment to equations according to mathematical models, regression analysis, principal component analysis (PCA) and clusters analysis. Pungency was the main sensory attribute of BA (3-36 mM) in the tongue and epiglottis. The seven kinetic parameters showed concentration-dependency (P < 0.001) and were described by different functions: (i) lineal: I(MAX) = 2.24 +/- 0.14C - 3.06 +/- 2.58, R2 = 0.98; T(IMAX) = 0.19 +/- 0.02C + 6.87 +/- 0.47, R2 = 0.92; V1 = 0.68 +/- 0.03C + 0.10 +/- 0.69, R2 = 0.99; AUC = 49.10 +/- 3.17C - 230.78 +/- 59.66, R2 = 0.98; (ii) potency: T1/2 = 6.62 +/- 0.61C(0.39+/-0.03), R2 = 0.97; V2 = 1.07 +/- 0.11C(0.53+/-0.04), R2 = 0.98; Ttot = 8.08 +/- 1.01C(0.43+/-0.04), R2 = 0.96. PCA revealed high correlation between (i) T(IMAX) and Ttot; (ii) T1/2 and V2; and (iii) I(MAX) and V1. Stimuli grouped across three main clusters: (i) 3 and 6 mM; (ii) 9, 12 and 18 mM; and (iii) 24 and 36 mM. Maximal pungency intensity best correlated with both concentration and persistence among kinetic parameters. Prototypical prickling of BA was observed at 12 and 18 mM.

Effect of ovarian hormones on the hypothalamic excitatory amino acids system during sexual maturation in female rats.

The present experiments were designed to study in female rats during sexual maturation: (1) the hypothalamic release of aspartate (Asp), glutamate (Glu) and glycine (Gly) which are the excitatory amino acids (EAAs) involved in NMDA neurotransmission and of taurine (Tau), a putative inhibitory amino acid of GnRH secretion; (2) the relationships between the effect of estrogen-progesterone (EP) on the release of these EAAs and the secretion of gonadotropins, and (3) the effect of hypothalamic NMDA receptor stimulation on EAAs release by the hypothalamus as well as the effect of EP on this release. The release of EAAs by the anterior preoptic and medial-basal hypothalamic areas (APOA-MBH) is significantly higher in peripubertal than in prepubertal rats (p < 0.01). EP treatment in prepubertal rats (16 days of age) decreased LH and FSH plasmatic levels and also the in vitro release of Asp, Glu, Gly and Tau. Contrary to the observations in prepubertal rats, in 30-day-old peripubertal rats the ovarian hormones significantly (p < 0.01) increased the levels of LH and FSH as well as the release to the medium of these amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of the in vitro treatment with gangliosides on the release of endogenous amino acids from rat hypoxic atria.

1. In the rat isolated atria the in vitro exposure to 60 min of hypoxia in the absence of glucose followed by 30 min of reoxygenation increased the release of the amino acids glutamate (Glu) and taurine (Tau). The efflux of the remaining amino acids assayed (aspartate, glycine and alanine) did not change throughout the period studied. 2. The increase in Tau release started 45 min after the onset of the hypoxic period whereas that of Glu started during the reoxygenation phase. These increases were not observed when glucose was present during the hypoxic period. 3. The in vitro pretreatment for 2 h with 50 microM bovine brain gangliosides (BBG) prevented the increases in the release of Tau and Glu induced by the hypoxia reoxygenation. 4. These results constitute a further example where BBG appears to exert a protective role in cardiac tissues submitted to injuries.

A possible inhibitory action of baclofen on hippocampus GABAergic neurones.

1. The function of the gamma-aminobutyric acid (GABA)ergic system in certain areas of the rat brain was investigated after baclofen treatment (30 mg/kg for 4 days). 2. Two h after the last dose of baclofen GAD activity was reduced in the hippocampus without changes in GABA levels. 24 h after baclofen, GAD activity was increased and the GABA content was decreased. 3. 48 h after the last dose both parameters returned to control values. 4. These results were not observed in any of the other areas investigated: frontal cerebral cortex, corpus striatum, olfactory bulbs, and medio basal hypothalamus. 5. In conclusion, the present study shows that baclofen 30 mg/kg for 4 days, induces an inhibitory action on hippocampus GABAergic neurones, which begins to disappear after 24 h free of drug.

Amino acid levels in the hypothalamus and response to N-methyl-D-aspartate and/or dizocilpine administration during sexual maturation in female rats.

Amino acid concentration in the anterior preoptic area and medial basal hypothalamus was determined by HPLC in female rats: (1) at 16 (prepubertal) vs. 30 (peripubertal) days of age and (2) after N-methyl-D-aspartate (NMDA) or dizocilpine (MK-801) administration in both groups. 30-day-old rats had higher levels of aspartate (Asp; 24%), glutamate (Glu; 49%) and glycine (Gly; 44%) and lower levels of taurine (Tau; 43%) than 16-day-old rats. In 16-day-old rats, NMDA (30 mg/kg, s.c., 10 min) increased the Glut concentration (48%). This effect was prevented by MK-801 pretreatment (1 mg/kg, s.c., 1 h), which did not modify amino acid concentrations per se. In 30-day-old rats, NMDA treatment increased Glut (24%) and asp (42%) levels. MK-801 pretreatment abolished NMDA-induced changes and reduced Tau (26%) and Gly (30%) levels. MK-801 administration alone reduced the concentration of Glut (39%), Asp (54%), Tau (33%) and Gly (31%). It is concluded that both (1) the concentration of Asp, Glu, Gly and Tau and (2) the changes induced by NMDA receptor activation or blockade are different at 16 vs. 30 days of age. The existence of a tonic (positive) control on amino acid levels linked to the NMDA receptor which would be immature or absent at 16 days of age is suggested.

Area-dependent changes in GABAergic function after acute and chronic cold stress.

(1) The function of the gamma-aminobutyric acid (GABA)ergic system in certain areas of the rat brain was investigated after acute and chronic cold stress. (2) GABA concentration, [3H]GABA uptake and the activity of the synthesis enzyme glutamate decarboxylase (GAD) were measured. (3) Acute stress: (a) reduced GABA concentration in the corpus striatum (29%); (b) decreased GAD activity (under non-saturating substrate concentration) in the olfactory bulbs (24%); (c) diminished neuronal uptake of [3H]GABA in the frontal cerebral cortex (65%), hypothalamus (86%) and olfactory bulbs (82%). (4) Chronic stress: (a) reduced the endogenous levels of GABA in the frontal cerebral cortex (51%), hypothalamus (26%) and olfactory bulbs (15%); (b) decreased GAD activity in the corpus striatum (32%) and olfactory bulbs (34%); (c) decreased neuronal uptake of [3H]GABA in the hypothalamus (83%). (5) These findings suggest that compensatory changes may develop in the GABAergic system after chronic stress.

Effects of i.c.v. lithium chloride administration on monoamine concentration in rat mediobasal hypothalamus.

We investigated the acute effects of a single i.c.v. injection of lithium chloride (LiCl) the neuroamine content of the rat mediobasal hypothalamus (MBH). The effects of lithium on amine synthesis and degradation enzymes were also studied in vitro. Noradrenaline (NA), dopamine (DA), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were reduced 10 min after i.c.v. injection of 24 nmol of LiCl and returned to control values 30 min after the injection. Two nmol of LiCl reduced the concentration of DA (10 and 30 min after injection) and 5-HIAA (30 min after injection). LiCl (0.5-10 mM) inhibited tyrosine hydroxylase activity (catecholamine synthesis) in vitro in a concentration dependent manner. The i.c.v. administration of a high dose of LiCl reduced the content of neuroamines in the MBH. This might result from and inhibition of synthesis. A possible link between the observed changes and some reported side effects of lithium therapy is discussed.

Effects of ovarian steroids on the gonadotropin response to N-methyl-D-aspartate and on hypothalamic excitatory amino acid levels during sexual maturation in female rats.

In order to evaluate the involvement of estrogen-progesterone (EP) in the effects of N-methyl-D-aspartate (NMDA) receptor stimulation on gonadotropin secretion during sexual development in female rats, NMDA (30 mg/kg sc) was administered to 16- and 30-day-old female rats pretreated with EP. NMDA administration induced increases in plasma LH concentration that were 13.6-fold and 94.5-fold higher, respectively, than those found after NMDA alone. The increase of LH levels induced by NMDA was accompanied by a significant enhancement of the content of GnRH in the anterior and preoptic hypothalamic areas and in the medial basal hypothalamus (APOA/MBH). EP potentiated this increase of GnRH induced by NMDA. NMDA increased plasma FSH levels at 16 days of age, and this increase was inhibited by EP treatment. In 30-day-old rats EP induced FSH release in response to NMDA. This release was not observed in rats treated only with NMDA. In 16-day-old rats EP induced an increase in the concentrations of aspartate, glutamate, and glycine in the anterior and preoptic hypothalamic areas and in the medial basal hypothalamus, the excitatory amino acids involved in NMDA neurotransmission. This effect was not observed in rats of 30 days of age. In summary, the present results show that during sexual maturation ovarian steroids potentiated the LH-releasing response to NMDA probably by acting at the hypothalamic level; furthermore, during sexual maturation there are changes in the response to EP of the hypothalamic concentrations of excitatory amino acids. These findings could be related to the neuroendocrine mechanisms regulating the onset of puberty and the sexual cycle in female rats.

Changes in GABAergic function after chronic chemical stress.

1. The function of the gamma-aminobutyric acid (GABA)-ergic system in certain areas of the rat brain was investigated after chronic chemical stress (exposure to either vapours 30 sec/day for 20 days). 2. GABA concentration, [3h] -GABA uptake and the activity of the synthesis enzyme glutamate decarboxylase (GAD) were measured. 3. Chronic stress: (a) reduced neuronal uptake of [3H] -GABA in the frontal cerebral cortex (43%) and increased non-neuronal uptake of [3H] -GABA in the hypothalamus (62%); (b) enhanced the activity of GAD (under subsaturating substrate concentration) in the frontal cortex (91%) and in the corpus striatum (69%); (c) did not modify GABA endogenous concentration; (d) did not affect the animals' body weight increase or produce any signs of toxicity. 4. The stimulation of GAD and reduction of [3H] -GABA neuronal uptake in the frontal cortex might suggest the stimulation of GABAergic neurotransmission induced by chronic stress in this area of the rat brain. Together with previous findings the frontal cortex would appear to be a key area in chronic stress processing.

Chemical stress and GABAergic central system.

1. The function of the gamma-aminobutyric acid (GABA)ergic system in certain areas of the rat brain was investigated after acute (30 sec) ether stress. 2. GABA endogenous concentrations, uptake of [3H]GABA and the activity of glutamate decarboxylase were measured in different brain areas. 3. After 30 sec of exposure to ether vapour, GABA concentration and total [3H]GABA uptake in the frontal cerebral cortex were increased. In contrast, stress increased GABA concentration in the hypothalamus, but reduced total [3H]GABA uptake. 4. Since the neuronal component of [3H]GABA uptake was increased in the frontal cerebral cortex this might be responsible for the increase in total [3H]GABA uptake. The increase in the endogenous concentration of GABA in the hypothalamus probably resulted from its enhanced synthesis because GAD activation was observed in the hypothalamus after stress. 5. In conclusion, the present study shows that acute ether stress induces rapid and quickly reversible changes in the GABAergic system according to the area of brain. The characteristics of these changes as related to their quick appearance and reversibility might suggest an effect upon neuronal activity due to acute stress exposure.

Acute stress and GABAergic function in the rat brain.

1. The function of the gamma-aminobutyric acid (GABA)-ergic system in certain areas of the rat brain was investigated after acute (5 min) exposure to immobilization stress. 2. The activities of glutamate decarboxylase and GABA-transaminase, GABA concentrations, GABA turnover in vivo and uptake of [3H]-GABA were measured. 3. After 5 min of immobilization stress, GABA concentrations and [3H]-GABA uptake were reduced, and GABA turnover stimulated in the olfactory bulbs. In contrast the uptake of [3H]-GABA was increased in the corpus striatum after 5 min of immobilization stress. 4. None of the parameters measured was significantly altered by acute immobilization stress in the frontal cortex, hippocampus or medio-basal hypothalamus. 5. These findings show that the olfactory bulbs and the corpus striatum are sensitive to the effects of acute stress. Since GABA in the olfactory bulbs is involved in the development of aggression and increased emotional state, it follows that neurochemical changes induced by acute stress might underlie some behavioural manifestations observed after stress.

Acute changes in 5-HT metabolism after S-adenosyl-L-methionine administration.

1. This study investigates S-adenosyl-L-methionine (SAM) (10 mg/kg, i.p.)acute effects upon 5-HT metabolism in rat brain areas. 2. One hour after SAM injection 5-HT biosynthesis was increased in the corpus striatum (55%), the hippocampus (3-fold) (82% 2 hr after SAM injection) and decreased in the olfactory bulbs (34%). 3. 5-HT levels were: (a) increased in the corpus striatum (39%), the hippocampus (44%) and the frontal cortex (27%), and oppositely reduced in the olfactory bulbs (47%) 1 hr after SAM injection; (b) increased in the hippocampus (39%) and reduced in the olfactory bulbs (35%) 1.5 hr after SAM injection; (c) increased in the hippocampus (25%) 2 hr after SAM injection. 4. 5-HIAA levels were reduced in the olfactory bulbs 27% or 21% after 1 hr or 1.5 hr from SAM injection respectively. 5. These area-related changes in 5-HT biosynthesis and metabolism might suggest a possible neurochemical substrate for the antidepressant properties of SAM.

Changes in central GABAergic function following acute and repeated stress.

1. The function of gamma-aminobutyric acid (GABA)ergic systems in response to acute and repeated stressful manipulations was evaluated in both the corpus striatum and frontal cerebral cortex of the rat. 2. In the corpus striatum the activity of the synthetic enzyme for GABA (glutamic acid decarboxylase, GAD) and the levels of GABA were reduced by acute immobilization stress (1 h). GABA turnover was reduced only by acute cold stress (3 h, 4 degrees C). 3. In the frontal cerebral cortex no changes were observed after acute stressful manipulations, but repeated stress (0.5 h immobilization per day for 14 days) enhanced both GAD activity and GABA turnover, and reduced GABA levels. 4. In conclusion, it would appear that the GABAergic system in the corpus striatum of the rat is most sensitive to acute stress and that the system in the frontal cerebral cortex area is preferentially responsive to chronic stress. It is speculated that the cortical GABAergic system is responsible for adaptive responses to the adverse conditions prevailing during chronic stress.