Lucía Quevedo

Dendritic morphology of neurons in medial prefrontal cortex, hippocampus, and nucleus accumbens in adult SH rats

We have studied, in spontaneously hypertensive (SH) rats at different ages (2, 4, and 8 months old), the dendritic morphological changes of the pyramidal neurons of the medial prefrontal cortex (mPFC) and hippocampus and medium spiny neurons of the nucleus accumbens (NAcc) induced by the chronic effect of high‐blood pressure. As control animals, we used Wistar‐Kioto (WK) rats. Blood pressure was measured every 2 months to confirm the increase in arterial blood pressure. Spontaneous locomotor activity was assessed, and then brains were removed to study the dendritic morphology by the Golgi‐Cox stain method followed by Sholl analysis. SH animals at 4 and 8 months of age showed decreased spine density in pyramidal neurons from the mPFC and in medium spiny cells from the NAcc. At 8 months of age as well the pyramidal neurons from the hippocampus exhibited a reduction in the number of dendritic spines. An increase in locomotion in a novel environment at all ages in the SH rats was observed. Our results indicate that high‐blood pressure alters the neuronal dendrite morphology of the mPFC, hippocampus, and NAcc. The increased locomotion behavior supports the idea that dopaminergic transmission is altered in the SH rats. This could enhance our understanding of the consequences of chronic high‐blood pressure on brain structure, which may implicate cognitive impairment in hypertensive patients. Synapse, 2010.

Some metabolic effects on lactating rats of a low-energy diet restricted in good-quality protein

Adult female Sprague-Dawley rats were fed ad libitum during pregnancy and lactation a control diet (CD; 16.1 kJ/g) or a low-energy diet with wheat gluten as the main protein source (LED; 13.3 kJ/g). Body weight, food intake, resting energy expenditure, respiratory quotient and substrate use by the mammary gland were measured. After the animals had been killed, the parametrial and retroperitoneal fat pads were weighed. The mean food intake (g) of the two groups of rats was similar, resulting in a lower energy intake by the LED rats, significantly different during the last 2 weeks of lactation. The mean body weight of both dams and pups in the LED group was lower, starting at day 9 of lactation. The resting energy expenditure increased gradually during lactation in the control group, whereas this increase was not seen in rats of the LED group in the last week of lactation. Rats that had fasted overnight had a respiratory quotient of 0.7 or less, whereas for rats that had been fed, the mean respiratory quotient was over 1.0. Under both conditions, rats showed ketonuria. The arteriovenous difference in 3-hydroxybutyrate level was higher and those for glucose, lactate and triacylglycerol were lower across the mammary glands of LED rats. The parametrial fat depot weighed less in LED rats. Reducing the increase in resting energy expenditure and using ketone bodies to a greater extent as fuels may represent important mechanisms in the LED dams to cover the energy cost of milk production.

Potentiation of the immobility response elicited by bandaging and clamping in mesencephalic rats

In earlier work, we showed that adult rats exhibit immobility response (IR) if a clamp is fastened to the skin of the nape of the neck, but not at other areas of the body, and not by bandaging. The present study characterizes IR in adult rats with complete mesencephalic transections. In the mesencephalic rats, the duration of the IR not only increased, but the stimuli capable of eliciting it were more diverse. All head and body areas clamped or bandaged were capable of inducing a profound IR. In contrast, the IR in intact rats was of shorter duration, and was only induced by clamping the neck, or by bandaging the upper or the lower torso. Furthermore, unlike the mesencephalic rats the ability of the bandaging to induce IR is reduced after the first trial and finally disappears. Only clamping the neck was able to persistently induce IR in intact rats. These data support the hypothesis that the IR control system is in the midbrain, hindbrain or spinal cord, and that systems above the mesencephalon modulate the IR. Such modulation appears to involve the ability to discriminate amongst tactile stimuli, and to integrate previous experience.

Effect of Intraperitoneal Nitroprusside and Adrenergic Agonists on Food and Water Intake

In previous works it was shown that catecholamine-induced hypodipsia is mediated by alpha1-adrenergic receptors while food intake (FI) inhibition supposes also beta-adrenergic participation. We used sodium nitroprusside (N) as a vasodilator, alone or mixed with various adrenergic agonists and measured FI and water intake (WI) in rats either deprived food and water overnight or in postprandial conditions after only 1 hour of deprivation in day time. N injected alone had no effect after overnight deprivation but diminished significantly norepinephrine (NE)-induced inhibition of both intakes, while epinephrine (E) inhibited only FI. In day time, N stimulated 30 min FI by 60% and WI by 84% in male but not in female rats. Isoproterenol (I) stimulated only WI (by 155%), while phenylephrine (P) and E inhibited it by 55%. In the presence of N, I increased WI even more (by 220%) but reduced FI. P + N and E + N increased FI by 41% and 128% as compared with P and E, respectively. Only P-induced inhibition of WI was canceled in presence of N. The results show that N, probably due to nitric oxide production, may induce hyperphagia and hyperdipsia in 1 hour-deprived male rats and also that catecholamine effects on FI and WI are differently modulated by N.

Norepinephrine inhibition of water and food intake: Comparison with vasopressin effects

UNLABELLED In a previous publication we showed that intraperitoneally (IP) injected norepinephrine (NE) induces hypodipsia (hD) in rats by an alpha 1-adrenergic effect which might be due to splanchnic vasoconstriction. In the present work we administered two vasoconstrictive hormones: NE 250 ug/kg and arginine vasopressin (VP) 550 mU/kg either by IP or intramuscular (IM) route to fasted rats in two different thirst-inducing conditions: (a) water-deprivation; or (b) induced hyperosmolarity. IP NE inhibited significantly food and water intake under both conditions. IM NE did not affect food intake and elicited significantly less hD and this only in (a). VP did not affect food intake but induced hD regardless of the route of administration in (a) but not in (b). NE administrated to anesthetized rats after food and water deprivation increased arterial pressure by both routes while VP effect was weaker and more variable. IN CONCLUSION blood pressure elevation may be implicated in the hD effect but IP NE elicits a specific splanchnic action; splanchnic-induced hypophagia is not necessarily related to water intake inhibition.

Some particularities of sodium nitroprusside stimulatory effects on food intake

It was previously shown that sodium nitroprusside (NP) stimulates food (FI) and water (WI) intakes when injected intraperitoneally (i.p.) in male rats deprived for 1-h of both food and water during day time. The present work shows that: 1) intramuscular NP increased only water intake; 2) when NP was i.p. injected simultaneously without 1-h deprivation it slightly reduced both intakes in the first 30 min but stimulated significantly FI between 30 and 60 min, and 3) it increased significantly FI even in absence of available water, while WI in absence of food was practically not affected. In conclusion NP effect on FI does originate mainly in the splanchnic area, it requires a latency of about 30 min, and stimulation of FI by NP triggers an increase in WI and not the other way around.