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The activity of neurons in the dorsolateral pontine nucleus (dlpn) was studied in two awake rhesus monkeys trained to participate in a variety of visual and oculomotor tests. The visual and eye movement related responses of 73 neurons encountered in the more caudal part of the dlpn were analyzed. Thirty eight of these could be assigned to one of the three following groups. Visual-only neurons (Type 1, n = 10) responded to movement of a broad range of visual stimuli in certain preferred directions. Their receptive fields were usually large, not restricted to the contralateral visual field and always included the fovea. Visual-tracking (VT) neurons (n = 28) discharged in relation to smooth pursuit of a small target in particular preferred directions. Nine of these (Type 2) did not respond to visual stimulation during stationary fixation. Nineteen VT-cells (Type 3) discharged in relation to both visual tracking and visual stimulation. In 9 of the Type 3 neurons, the preferred directions for visual stimulation and tracking were opposite, whereas they were the same in the other 10. Visual responses of Type 3 neurons were indistinguishable from those of Type 1 neurons. Testing of an additional 9 neurons driven by either visual-tracking or pattern movement was not sufficient to allow a definite assignment to one of the groups 1, 2 or 3. The distribution of preferred directions for both visual stimulation and visual tracking was widely scattered between 0 and 360 deg. Our results suggest that the dlpn is a constituent in a cerebro-cerebellar loop important for the generation of smooth pursuit eye movements.

(MR). A homogeneous population of 11 patients with progressive non-enhancing LGG was prospectively studied. Imaging was done at 6-months intervals starting six months, and in a second series starting three months after treatment initiation. F-18 fluoro-ethyl-l-tyrosine (FET) uptake was quantified with PET as metabolically active tumor volume, and was compared with the tumor volume on MR. Response was defined as ≥10% reduction of the initial tumor volume. Eight patients showed metabolic responses. Already 3 months after start of chemotherapy the active FET volumes decreased in 2 patients to a mean of 44% from baseline. First MR volume responses were noted at 6 months. Responders showed a volume reduction to 31 ± 23% (mean ± SD) from baseline for FET, and to 73 ± 26% for MR. The time to maximal volume reduction was 8.0 ± 4.4 months for FET, and 15.0 ± 3.0 months for MR. The initial metabolic response correlated with the best volume response on MR (Spearman Rank P = 0.011). Deactivation of amino acid transport represents an early indicator of chemotherapy response in LGG. Response assessment based on MR only has to be reconsidered. The time window obtained from PET may assist for individual treatment decisions in LGG patients. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Wyss page 2 AbstractBackground: Amino acid transport and protein synthesis are important steps of tumor

1. In the alert monkey, 74 neurons in the vestibular nuclei were investigated during sinusoidal rotation about a vertical axis at frequencies between 0.003 and 0.5 Hz. Phase and gain were determined by a fast Fourier analysis program. 2. Phase advance, relative to turntable velocity, was small between 0.05 and 0.5 Hz. At lower frequencies phase advance increased to 45 degrees at 0.007--0.02 Hz, and 90 degrees at 0.003--0.005 Hz. In agreement with the phase characteristics, a gain decrease of -3 dB was determined between 0.007 and 0.02 Hz. Assuming a linear system, time constants of 9.5, 11.9, and 24.5 s were calculated for three different monkeys. 3. Simultaneously recorded nystagmus exhibited similar time constants as the central vestibular neurons for each monkey. 4. Frequency responses of 11 neurons were recorded from the same monkeys while they were under general anesthesia and the time constants were reduced to 4--7 s. This is the range of time constants seen in the peripheral nerve. 5. The longer time constants in the alert state are due to an integration process, which provides a low-frequency compensation, and is thought to be achieved through a feedback loop involving the reticular formation. 6. In the alert and anesthetized state, monkeys were also exposed to velocity trapezoids. Time constants of decay of neuronal activity were in good agreement with the data obtained during sinusoidal stimulation. 7. A transfer function of the primary vestibular afferents is expanded to include the described low-frequency compensation found in central vestibular neurons in the alert animals.

Evidence for an intrinsic effect of insulin on the central nervous system is accumulating. To test the hypothesis that insulin per se may modulate neuroendocrine counterregulation, hypoglycemia perception, and cerebral function in insulin-dependent diabetes mellitus, we examined 27 patients without any sign of classical autonomic neuropathy or evidence of so-called hypoglycemia unawareness. We used the hyperinsulinemic (0.67 vs. 2.00 mU/kg.min), stepped hypoglycemic (5.6/3.5/2.4/2.0 mmol/L) clamp technique to assess the patient's awareness of and response to equivalent hypoglycemic stimuli under different degrees of physiological hyperinsulinemia (approximately 270 vs. approximately 810 pmol/L) after an overnight euglycemic clamp (5.6 mmol/L). Simultaneously, the patient's cerebral function was assessed from his electrophysiological activity and neuropsychological skills. Higher degrees of physiological hyperinsulinemia caused enhanced neuroendocrine response (adrenaline, P < 0.05; noradrenaline, P < 0.03; GH, P < 0.02; beta-endorphin, P < 0.03; ACTH, P = 0.12; cortisol, P = 0.06; PRL, P = 0.08) and symptom awareness (total symptoms, P < 0.04; autonomic symptoms, P < 0.02; neuroglycopenia symptoms, P < 0.05; sweating, P < 0.05; heart pounding, P < 0.02; trembling, P < 0.01; lack of concentration, P < 0.02) to occur. Deteriorations of electrophysiological activity (middle latency auditory-evoked potentials, P < 0.04; Pa peak latencies, P < 0.05; Pa-V interpeak latencies, P = 0.08) and neuropsychological skills (Stroop test, P < 0.05; trail making, P = 0.12) were more pronounced the higher the insulin level, but at similar blood glucose concentrations. We conclude that insulin-associated modulation of neuroendocrine counterregulation, hypoglycemia perception, and cerebral function may occur in insulin-dependent diabetes mellitus, which indicates an intrinsic effect of insulin on the human brain.