To test the possibility that glutamate (Glu) and aspartate (Asp) are transmitters at geniculo-cortical synapses in the visual cortex of the cat, we studied the release of amino acids from the striate cortex consequent upon visual and electrical stimulation of the dorsal lateral geniculate nucleus (LGN) and of the optic tract, using push-pull cannulae. We perfused a discrete region that included layer IV of the cortex with an artificial cerebrospinal fluid (aCSF) and analysed the amino acid content of these perfusates by high-performance liquid chromatography (HPLC). Significant increases only of Glu and Asp were obtained among all 17 amino acids measured, except for gamma-aminobutyric acid (GABA), during electrical stimulation of the afferent pathways. Visual stimulation by stroboscopic diffuse flashes of light increased the level of Glu released, but did not change that of Asp significantly. The level of GABA released did not change during diffuse flash stimulation, suggesting that the increase in Glu was not derived from cortical neurons. The increases in release of Glu/Asp were not seen when the perfusion medium was replaced with a Ca2(+)-free, high-Mg2(+)-containing solution. The basal (resting) release of Glu/Asp in the absence of stimulation also was decreased during perfusion with Ca2(+)-free/high-Mg2+ solutions. Intraocular injections of a sodium channel blocker, tetrodotoxin (TTX), resulted in a remarkable decrease in the basal release of Glu. These results suggest that Glu is released as in excitatory synaptic transmitter at least from terminals of geniculo-cortical afferents and Asp from axons of a certain type of visual cortical neuron.
1. We investigated the effect of unilateral vestibular stimulation on histamine release from the anterior hypothalamic area of urethan-anesthetized rats in vivo, using a brain microdialysis method coupled with high-performance liquid chromatography fluorometry. 2. The histamine release was increased to approximately 180% of the basal release by the electrical stimulation of the inner ear with 1 Hz, 500 microA, and 200 ms for 20 min. This effect was dependent on the current intensity. 3. Activation of the unilateral horizontal semicircular canal by middle ear irrigation for 15 min with 45 degrees C water increased the histamine release to approximately 200% of the basal release. 4. Irrigation of the middle ear with ice water for 15 min increased the histamine release to approximately 190% of the basal release. 5. The histamine release was not changed by the irrigation of the middle ear with 37 degrees C water and the irrigation of the auricle with ice water, which suggests that neither somatosensory stimulation to the middle ear nor nonspecific cold stress affects the histamine release. 6. All these findings suggest that the sensory mismatch signals induced by caloric stimulation and unilateral electrical vestibular stimulation activate the histaminergic neuron system in the brain.
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