Cardiorespiratory depression from brainstem seizure activity in freely moving rats.

Cardiorespiratory dysfunction during or after seizures may contribute to sudden unexpected death in epilepsy. Disruption of lower brainstem cardiorespiratory systems by seizures is postulated to impair respiratory and cardiac function. Here, we explore the effects of brainstem seizures and stimulation on cardiorespiratory function using a rat model of intrahippocampal 4-aminopyridine (4-AP)-induced acute recurrent seizures. Cardiac and respiratory monitoring together with local field potential recordings from hippocampus, contralateral parietal cortex and caudal dorsomedial brainstem, were conducted in freely moving adult male Wistar rats. Seizures were induced by intrahippocampal injection of 4-AP. Increased respiratory rate but unchanged heart rate occurred during hippocampal and secondarily generalized cortical seizures. Status epilepticus without brainstem seizures increased respiratory and heart rates, whereas status epilepticus with intermittent brainstem seizures induced repeated episodes of cardiorespiratory depression leading to death. Respiratory arrest occurred prior to asystole which was the terminal event. Phenytoin (100 mg/kg, intraperitoneal injection), administered after 4-AP intrahippocampal injection, terminated brainstem seizures and the associated cardiorespiratory depression, preventing death in five of six rats. Focal electrical stimulation of the caudal dorsomedial brainstem also suppressed cardiorespiratory rates. We conclude that in our model, brainstem seizures were associated with respiratory depression followed by cardiac arrest, and then death. We hypothesize this model shares mechanisms in common with the classic sudden unexpected death in epilepsy (SUDEP) syndrome associated with spontaneous seizures.

Changes in neural network connectivity in mice brain following exposures to palatable food.

Previously, satiated animals or human subjects can still be motivated to eat by palatable food-associated cues. However, neural circuitries of hedonic hunger have not been well investigated. This study identified neural network connectivities between major brain areas in response to chocolate-associated cues following repeated exposures to chocolate. Adult male Swiss albino ICR mice were anesthetized and implanted with intracranial electrodes in the lateral hypothalamus (LHa), nucleus accumbens (NAc), olfactory bulb (OB) and hippocampus (HP) for local field potential (LFP) recording. LFP oscillations were recorded before and after repeated exposures to chocolate for chocolate experienced group whereas control group was not exposed to chocolate. On testing days, satiated animals were individually put into a place preference-like apparatus with two opposite chambers of chocolate and normal chow scent cues, separately. The results showed that chocolate experienced group significantly increased time spent in chocolate chamber whereas control group did not. One-way ANOVA revealed significant influence of chocolate sessions on LFP spectral powers of multiple frequencies in the LHa (delta, low gamma and high gamma) and NAc (high gamma). Moreover, coherence function analyses also highlighted significant increases in LHa-NAc and LHa-OB, and decrease in LHa-HP coherent activities in response to olfactory cues of chocolate. This study demonstrated modifications of neural network connectivity and associative learning following multiple exposures to palatable food. These findings might explain why energy homeostatic hunger is overridden by hedonic hunger.