Suckling in litters with different sizes, and early and late swimming exercise differentially modulates anxiety-like behavior, memory and electrocorticogram potentiation after spreading depression in rats.

OBJECTIVE: Analyze the hypothesis that swimming exercise, in rats suckled under distinct litter sizes, alters behavioral parameters suggestive of anxiety and recognition memory, and the electrocorticogram potentiation that occurs after the excitability-related phenomenon that is known as cortical spreading depression (CSD). METHODS: Male Wistar rats were suckled in litters with six or 12 pups (L6 and L12 groups). Animals swam at postnatal days (P) 8-23, or P60-P75 (early-exercised or late-exercised groups, respectively), or remained no-exercised. Behavioral tests (open field - OF and object recognition - OR) were conducted between P77 and P80. Between P90 and P120, ECoG was recorded for 2 hours. After this 'baseline' recording, CSD was elicited every 30 minutes over the course of 2 hours. RESULTS: Early swimming enhanced the number of entries and the percentage of time in the OF-center (P < 0.05). In animals that swam later, this effect occurred in the L6 group only. Compared to the corresponding sedentary groups, OR-test showed a better memory in the L6 early exercised rats, and a worse memory in all other groups (P < 0.05). In comparison to baseline values, ECoG amplitudes after CSD increased 14-43% for all groups (P < 0.05). In the L6 condition, early swimming and late swimming, respectively, reduced and enhanced the magnitude of the post-CSD ECoG potentiation in comparison with the corresponding L6 no-exercised groups (P < 0.05). DISCUSSION: Our data suggest a differential effect of early- and late-exercise on the behavioral and electrophysiological parameters, suggesting an interaction between the age of exercise and the nutritional status during lactation.

The facilitating effect of unfavorable lactation on the potentiation of electrocorticogram after spreading depression in awake and anesthetized adult rats.

OBJECTIVES: Cortical spreading depression (CSD) is a brain excitability-related phenomenon that can be affected by unfavorable conditions of lactation and by anesthetic agents. We have previously demonstrated that after CSD the electrocorticogram (ECoG) amplitude increases significantly (ECoG potentiation). Here, we investigated this potentiation in awake and anesthetized adult rats that were previously suckled among different lactation conditions. METHODS: Newborn rats were suckled in litters with 6 pups or 12 pups (L6 or L12 condition, respectively). At adulthood, we evaluated the ECoG potentiation after CSD at two cortical points (one point near, and another remote to the CSD-eliciting site). The amplitude of the ECoG waves was averaged with the support of an algorithm implemented in Matlab™ software. In both L6 and L12 condition, awake animals were compared with anesthetized groups that received either tribromoethanol- or urethane + chloralose-anesthesia. RESULTS: L12 rats presented significantly lower body- and brain weights than L6 rats (P < 0.01), indicating a nutritional deficiency. The anesthetized L6 groups presented with ECoG potentiation (P < 0.05) only in the near cortical recording point (28.0% and 32.6% increase for the tribromoethanol and urethane + chloralose groups, respectively), whereas the L12 groups displayed ECoG potentiation in both near (67.0% and 55.0%) and remote points (37.0% and 20.0%), in comparison with the baseline values (before CSD). DISCUSSION: The results suggest a facilitating effect of unfavorable lactation on the potentiation of ECoG after spreading depression in anesthetized adult rats. The potential implications for the human neurological health remain to be investigated.

Anesthetic agents modulate ECoG potentiation after spreading depression, and insulin-induced hypoglycemia does not modify this effect.

Cortical spreading depression (CSD) is characterized by reversible reduction of spontaneous and evoked electrical activity of the cerebral cortex. Experimental evidence suggests that CSD may modulate neural excitability and synaptic activity, with possible implications for long-term potentiation. Systemic factors like anesthetics and insulin-induced hypoglycemia can influence CSD propagation. In this study, we examined whether the post-CSD ECoG potentiation can be modulated by anesthetics and insulin-induced hypoglycemia. We found that awake adult rats displayed increased ECoG potentiation after CSD, as compared with rats under urethane+chloralose anesthesia or tribromoethanol anesthesia. In anesthetized rats, insulin-induced hypoglycemia did not modulate ECoG potentiation. Comparison of two cortical recording regions in awake rats revealed a similarly significant (p<0.05) potentiation effect in both regions, whereas in the anesthetized groups the potentiation was significant only in the recording region nearer to the stimulating point. Our data suggest that urethane+chloralose and tribromoethanol anesthesia modulate the post-CSD potentiation of spontaneous electrical activity in the adult rat cortex, and insulin-induced hypoglycemia does not modify this effect. Data may help to gain a better understanding of excitability-dependent mechanisms underlying CSD-related neurological diseases.