Brain Research

Raw data of experiments shown in main manuscript and statistical results of ANOVA shown in Figure 6.

Electron microscopy morphometric analysis raw data for the Scn1a gene variant model of Dravet syndrome and littermate controls aged P50 (n=4 per group).

EEG files: We collected 8 h of continuous electrophysiological data from narcoleptic mice of the orexin/ataxin-3 line, and their wildtype littermates, starting at lights-out. Using the electroencephalographic and electromyographic information, 12 s epochs were manually scored into either wake, nrem or rem states using the ICELUS software according to the Radulovacki criteria. Each eeg file contains the information for one state (wake, nrem or rem), and each row represents a continuous bout in seconds. Recorded_behavior file: Animals of each group were recorded for 4 h starting at lights out with the aid of a CCTV infrared video camera. Behaviors were then classified into categories of either behavioral arrest, sleep, grooming, eating, drinking, climbing, and otherwake and the duration of each behavior logged.

The sequence raw data for the study.

Wilkinson et al, Brain Research. Contact corresponding (F. Colbourne) or first author (C. Wilkinson) for additional details or data.

Statistical data of behavioral experiments

Data of unit recording from monkeys that performed information seeking tasks. Data obtained from monkeys S (Data_table_Nakamura1) and R (Data_table_Nakamura2). Each sheet stores data concerning one neuron. Entries of A1 and A2 are the sites of the neuron on rostral-caudal and dorsal-ventral axes, respectively. The i-th entries in columns C and D are times at onset of the six dots and the second onset of the central cross fixation in the i-th trial of task A, respectively. All values of time in these tables indicate times after onset of the computer program that presents visual stimuli of the behavioral tasks and detects monkeys’ eye movements. Value 0 indicates that monkeys ended the trial before the corresponding event. The i-th entry in column E is the firing time of the i-th spike of the neuron in task A. The i-th entries in columns G, H, and I are times at onset of the six dots, the second onset of the central cross fixation, and the third onset of the central cross fixation in the i-th trial of task B, respectively. The i-th entry in column J is the firing time of the i-th spike of the neuron in task B. The i-th entries in columns K and L are times at onset of the six dots and the second onset of the central cross fixation in the i-th trial of task C, respectively. The i-th entry in column M is the firing time of the i-th spike of the neuron in task C. The i-th entries in column O are times at onset of the six dots in the i-th trial of task D, respectively. The i-th entry in column P is the firing time of the i-th spike of the neuron in task D.

This study explores the effect of diabetes on norepinephrine release in the paraventricular nucleus of the hypothalamus and its relationship to circulating corticosterone. Leptin treatment helps to partially reverse the increase in noradrenergic activity in diabetic rats. Adrenergic agonists were used to reverse the effect of leptin. It was found that while the alpha adrenergic agonist clonidine reversed the effect of leptin on norepinephrine release towards the end of the observation period, the beta adrenergic agonist, isoproterenol, did not have a similar effect. We conclude that the hypothalamus remains sensitive to alpha adernergic agonists in diabetes, but not to beta adrenergic agonists. Leptin treatment produces a dramatic drop in circulating corticosterone indicating that the adrenals remain sensitive to leptin during diabetes. Moreover, both adrenergic agonists were able to counter leptin's effects on corticosterone. These results indicate that the adrenals continue to be sensitive to both adrenergic receptors in diabetes.