Blockade of spreading depression in chronic epileptic rats: reversion by diazepam

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As several other factors, nutritional deficiency and sensory input hyperactivation can influence the mammalian brain development. This work investigated the effects of repeated episodes of early peripheral electrostimulation (PE), associated or not with early malnutrition, on cortical spreading depression (CSD) propagation. From postnatal days 7-28, well-nourished and malnourished Wistar rat pups (whose mothers were fed a 23 and 8% protein diet, respectively) received daily sessions of repetitive PE (2 or 60 Hz-square-wave pulses, 1.5 ms duration, 10-40 V intensity), delivered by two electrodes attached to the left paws. At postnatal days 35-45, under anesthesia, KCl-elicited spreading depression was monitored at two cortical points of both hemispheres. In the well-nourished rats, 2 Hz, but not 60 Hz PE was associated with slower spreading depression propagation in the hemisphere contralateral to the stimulated body-side, as compared to the ipsilateral hemisphere. In the malnourished rats, this effect was found for both 2 and 60 Hz stimulation frequencies. In the sham-stimulated controls, which received similar paw-electrodes, but were not stimulated, no inter-hemispheric spreading depression differences were seen. The results indicate an impairing effect of early PE on spreading depression propagation, which is frequency-dependent and can be influenced by the animal's nutritional status. Data raise the question whether brain plasticity changes consequent to the interaction between sensory input activation and malnutrition would be involved in the here described spreading depression effects.

Section: Nutrition and Developing Body And Brain Weightssupporting

confidence: 82%

Nutrition-dependent influence of peripheral electrical stimulation during brain development on cortical spreading depression in weaned rats

Monte-Silva

Assis

Leal

et al. 2007

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“…38 In the neocortex of normal laboratory animals, under certain conditions there may be a direct relationship between excitability and CSD susceptibility. However, when the tissue undergoes exaggerated increased excitability (which is the case of the epileptic brain), it may became more resistant to CSD, as documented by our laboratory, 13,39 as well as by others. 40 Considering the above-mentioned possibility of excitability changes in several brain regions due to L-arginine administration, it can be concluded that the present results represent one of those situations in which Larginine-nitric oxide relationships influence brain electrical activity in the neocortex.…”

Section: Discussionsupporting

confidence: 60%

“…8,9 CSD is considered as a phenomenon related to brain excitability and, as such, has been causally associated with important human diseases like migraine, 10 brain ischemia, 11 and epilepsy. 7,12,13 The developing brain can easily suffer morphological and electrophysiological changes as a consequence of early malnutrition. Depending on its intensity and duration, nutritional deficiency early in life can modify histological 14 and biochemical 15 patterns of developmental processes in the brain, influencing its functions.…”

Section: Introductionmentioning

confidence: 99%

L-Arginine administration during rat brain development facilitates spreading depression propagation: evidence for a dose- and nutrition-dependent effect

Maia

Amâncio-dos-Santos

Duda-de-Oliveira

et al. 2009

L-Arginine (ARG) is the precursor of the nitric oxide (NO) synthesis. NO-mediated signaling seems to be involved in the phenomenon of cortical spreading depression (CSD). Here, well-nourished and malnourished rats were treated, by gavage, with 150, 300 or 450 mg/kg/day of L-arginine from postnatal days 7-28, and CSD propagation was analyzed at 30-40 days. Compared to non-treated ('naïve') and water-treated controls, ARG-treated rats dose-dependently displayed higher CSD-velocities (P<0.05). In the malnourished rats, only the highest ARG-dose (450 mg/kg/day) increased CSD velocities. The mean +/- SD CSD-velocities (in mm/min) were: for well-nourished rats, 3.77 +/- 0.15, 3.78 +/- 0.23, 4.03 +/- 0.16, 4.36 +/- 0.19 and 4.41 +/- 0.26, in the naïve-, water-controls, 150, 300 and 450 mg/kg/day ARG-groups, respectively; for the same conditions in the malnourished rats, the velocities were 4.18 +/- 0.13, 4.22 +/- 0.09, 4.24 +/- 0.10, 4.27 +/- 0.21 and 4.64 +/- 0.22, respectively. Results demonstrate a dose- and nutrition-dependent CSD-facilitation by L-arginine administered during brain development. It is suggested that this effect is due to the modulation of nitric oxide synthesis.

“…41,42 Since CSD is considered a phenomenon related to brain excitability, it has been causally associated with some human diseases, for example, brain ischemia, 43 migraine 44 and epilepsy. 38,45,46 The brain susceptibility to CSD is considered increased when the CSD-velocity of propagation becomes higher as compared to the control situation, and vice-versa. CSD has been characterized in laboratory animals under conditions of pharmacological, nutritional and environmental manipulation.…”

Section: Introductionmentioning

confidence: 99%

Lasting facilitatory effects of neonatal vibrissae removal on the propagation of cortical spreading depression: an electrophysiological study in well-nourished and early-malnourished adult rats

Tenório¹,

Moura²,

Silva³

et al. 2009

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Early malnutrition interferes with the formation of somatosensory pathways and reduced sensory input activity during brain development can induce morphological and physiological changes in the cerebral cortex, altering their response properties in the long-term. Here, we investigated cortical spreading depression (CSD) propagation in male adult rats submitted to unilateral vibrissae removal, at postnatal days 2-3, and malnourished during lactation followed by nutritional recovery until adulthood (90-120 days), when CSD was recorded. Compared to nutrition-matched non-lesioned controls, CSD-propagation was increased in the hemisphere contralateral to the vibrissae removal. The findings indicate that vibrissae removal during brain development enhances CSD-propagation, and early malnutrition did not modify this effect. Considering that CSD-facilitation persisted until adulthood, we suggest that this effect is permanent. The data might contribute to the understanding of the mechanisms by which sensory input deprivation-induced plasticity modifies cerebral electrophysiological responses in the developing brain.