A minimum of 3 months of dietary fish oil supplementation is required to raise amygdaloid afterdischarge seizure thresholds in rats--implications for treating complex partial seizures.

Complex partial seizures, which typically originate in limbic structures such as the amygdala, are often resistant to antiseizure medications. Our goal was to investigate the effects of chronic dietary supplementation with n-3 polyunsaturated fatty acids (PUFAs) derived from fish oil on seizure thresholds in the amygdala, as well as on blood and brain PUFA levels. The acute effects of injected n-3 PUFAs--eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)--were also tested in the maximal pentylenetetrazol (PTZ) seizure model. In amygdala-implanted subjects, fish oil supplementation significantly increased amygdaloid afterdischarge thresholds, as compared with controls at 3, 5, and 7 months after the start of supplementation. Fish oil supplementation also increased serum EPA and DHA concentrations. DHA concentration in the pyriform-amygdala area increased in the fish-oil treated group by 17-34%, but this effect did not reach statistical significance (P=0.065). DHA significantly increased the latency to seizure onset in the PTZ seizure model, whereas EPA had no significant effect. These observations suggest that chronic dietary fish oil supplementation can raise focal amygdaloid seizure thresholds and that this effect is likely mediated by DHA rather than by EPA.

Tactile, acoustic and vestibular systems sum to elicit the startle reflex.

The startle reflex is elicited by intense tactile, acoustic or vestibular stimuli. Fast mechanoreceptors in each modality can respond to skin or head displacement. In each modality, stimulation of cranial nerves or primary sensory nuclei evokes startle-like responses. The most sensitive sites in rats are found in the ventral spinal trigeminal pathway, corresponding to inputs from the dorsal face. Cross-modal summation is stronger than intramodal temporal summation, suggesting that the convergence of acoustic, vestibular and tactile information is important for eliciting startle. This summation declines sharply if the cross-modal stimuli are not synchronous. Head impact stimuli activate trigeminal, acoustic and vestibular systems together, suggesting that the startle response protects the body from impact stimuli. In each primary sensory nucleus, large, second-order neurons project to pontine reticular formation giant neurons critical for the acoustic startle reflex. In vestibular nucleus sites, startle-like responses appear to be mediated mainly via the vestibulospinal tract, not the reticulospinal tract. Summation between vestibulospinal and reticulospinal pathways mediating startle is proposed to occur in the ventral spinal cord.