Effects of hunger and thirst on reinforcing properties of light onset and light offset.

1968 ◽  
Vol 66 (3, Pt.1) ◽  
pp. 784-787 ◽  
Author(s):  
Jack T. Tapp ◽  
Donna M. Mathewson ◽  
Lance L. Simpson
Keyword(s):  
Light Onset

scholarly journals Triggering Slow Waves During NREM Sleep in the Rat by Intracortical Electrical Stimulation: Effects of Sleep/Wake History and Background Activity

2009 ◽  
Vol 101 (4) ◽  
pp. 1921-1931 ◽  
Author(s):  
Vladyslav V. Vyazovskiy ◽  
Ugo Faraguna ◽  
Chiara Cirelli ◽  
Giulio Tononi
Keyword(s):  
Electrical Stimulation ◽  
Field Potential ◽  
Nrem Sleep ◽  
Neuronal Population ◽  
Slow Waves ◽  
Light Onset ◽  
Naturally Occurring ◽  
Profound Influence ◽  
Electrical Pulses ◽  
Local Field Potential Lfp

In humans, non-rapid eye movement (NREM) sleep slow waves occur not only spontaneously but can also be induced by transcranial magnetic stimulation. Here we investigated whether slow waves can also be induced by intracortical electrical stimulation during sleep in rats. Intracortical local field potential (LFP) recordings were obtained from several cortical locations while the frontal or the parietal area was stimulated intracortically with brief (0.1 ms) electrical pulses. Recordings were performed in early sleep (1st 2–3 h after light onset) and late sleep (6–8 h after light onset). The stimuli reliably triggered LFP potentials that were visually indistinguishable from naturally occurring slow waves. The induced slow waves shared the following features with spontaneous slow waves: they were followed by spindling activity in the same frequency range (∼15 Hz) as spontaneously occurring sleep spindles; they propagated through the neocortex from the area of the stimulation; and compared with late sleep, waves triggered during early sleep were larger, had steeper slopes and fewer multipeaks. Peristimulus background spontaneous activity had a profound influence on the amplitude of the induced slow waves: they were virtually absent if the stimulus was delivered immediately after the spontaneous slow wave. These results show that in the rat a volley of electrical activity that is sufficiently strong to excite and recruit a large cortical neuronal population is capable of inducing slow waves during natural sleep.

Comparative Effectiveness of Behavioral Rehearsal and Verbal Reinforcement for Effecting Anger Expressiveness

1968 ◽  
Vol 22 (3_suppl) ◽  
pp. 1079-1080 ◽  
Author(s):  
Mervyn K. Wagner
Keyword(s):  
Comparative Effectiveness ◽  
Psychiatric Patients ◽  
Light Onset ◽  
Verbal Reinforcement ◽  
Behavioral Rehearsal

Psychiatric patients reinforced by light onset for increases in anger expressiveness showed greater increase in expressiveness than controls without treatment between assessments. A group experiencing behavior rehearsal between tests also increased in expressiveness.

Circadian Rhythm of Output from Neurones in the Eye of Aplysia: III. Effects of Light on Clock and Receptor Output Measured in the Optic Nerve

1977 ◽  
Vol 70 (1) ◽  
pp. 183-194
Author(s):  
JACK A. BENSON ◽  
JON W. JACKLET
Keyword(s):  
Circadian Rhythm ◽  
Optic Nerve ◽  
Circadian Clock ◽  
Light Pulse ◽  
Temperature Sensitivity ◽  
Phase Point ◽  
Light Onset ◽  
Constant Illumination ◽  
Light Pulses ◽  
East West

1. The circadian rhythm of CAP frequency recorded from the optic nerve of isolated eyes at 15 °C was damped out by constant illumination (1100 lux) after several cycles of the rhythm. During illumination (LL) the rhythm was skewed with a rapid rising phase and slow falling phase, and the period was decreased by about 1 h. It is postulated that the circadian clock was stopped by LL at its lowest phase point, and that following cessation of LL, the rhythm was reinitiated from this phase point after a latency of 6-8 h. 2. For light pulses of 80 lux and 1100 lux, the photoresponse of the dark-adapted eye to 20 min light pulses applied beginning at 2 h intervals was not influenced by the circadian clock. At 5 lux there was a periodicity in the magnitude of the photoresponse, in phase with the circadian rhythm of spontaneous CAP production. 3. Small CAPs of non-circadian frequency were recorded together with normal CAPs in about 10% of records of output from isolated eyes. The cells producing the small CAPs had a different temperature sensitivity from those producing normal CAPs. The response of these cells to short light pulses consisted of a phasic burst of activity at light onset, followed by silence during the remainder of the short light pulse, and for 1 or 2 min following cessation of illumination. These small CAPs may be the activity either of H-type receptors or of secondary cells desynchronized from the major population. Note: Laboratory of Sensory Sciences, University of Hawaii at Manoa, 1993 East-West Road, Honolulu, Hawaii 96822, U.S.A.

scholarly journals Reaccumulation of [K+]o in the toad retina during maintained illumination.

1984 ◽  
Vol 84 (3) ◽  
pp. 475-504 ◽  
Author(s):  
H Shimazaki ◽  
B Oakley
Keyword(s):  
Differential Equations ◽  
Glial Cells ◽  
Time Course ◽  
Subretinal Space ◽  
Light Onset ◽  
Müller Glial Cells ◽  
Isolated Retina ◽  
Steady Level ◽  
Spatial Buffering ◽  
Toad Bufo

Using K+-selective microelectrodes, [K+]o was measured in the subretinal space of the isolated retina of the toad, Bufo marinus. During maintained illumination, [K+]o fell to a minimum and then recovered to a steady level that was approximately 0.1 mM below its dark level. Spatial buffering of [K+]o by Müller (glial) cells could contribute to this reaccumulation of K+. However, superfusion with substances that might be expected to block glial transport of K+ had no significant effect upon the reaccumulation of K+. These substances included blockers of gK (TEA+, Cs+, Rb+, 4-AP) and a gliotoxin (alpha AAA). Progressive slowing of the rods' Na+/K+ pump (perhaps caused by a light-evoked decrease in [Na+]i) also could contribute to this reaccumulation of K+ by reducing the uptake of K+ from the subretinal space. As evidence for a major contribution by this mechanism, treatments designed to prevent such slowing of the pump reversibly blocked reaccumulation. These treatments included superfusion with 2 microM ouabain, or lowering [K+]o, PO2, or temperature. It is likely that such treatments inhibit the pump, increase [Na+]i, and attenuate any light-evoked decrease in [Na+]i. The results are consistent with the following hypothesis. At light onset, the decrease in rod gNa will reduce the Na+ influx and the resulting rod hyperpolarization will reduce the K+ efflux. In combination with these reduced passive fluxes, the continuing active fluxes will lower both [K+]o and [Na+]i, which in turn will inhibit the pump. In support of this hypothesis, the solutions to a pair of coupled differential equations that model changes in both [K+]o and [Na+]i match quantitatively the time course of the observed changes in [K+]o during and after maintained illumination for all stimuli examined.

Characterization of Spontaneous Inhibitory Synaptic Currents in Salamander Retinal Ganglion Cells

1998 ◽  
Vol 80 (4) ◽  
pp. 1752-1764 ◽  
Author(s):  
Fan Gao ◽  
Samuel M. Wu
Keyword(s):  
Retinal Ganglion Cells ◽  
Synaptic Vesicles ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Equilibrium Potential ◽  
Retinal Ganglion ◽  
Light Onset ◽  
Synaptic Currents ◽  
Postsynaptic Currents

Gao, Fan and Samuel M. Wu. Characterization of spontaneous inhibitory synaptic currents in salamander retinal ganglion cells. J. Neurophysiol. 80: 1752–1764, 1998. Spontaneous and light-evoked postsynaptic currents (sPSCs and lePSCs, respectively) in retinal ganglion cells of the larval tiger salamander were recorded under voltage-clamp conditions from living retinal slices. The focus of this study is to characterize the spontaneous inhibitory PSCs (sIPSCs) and their contribution to the light-evoked inhibitory PSCs (leIPSCs) in on-off ganglion cells. sIPSCs were isolated from spontaneous excitatory PSCs (sEPSCs) by application of 10 μM 6,7-dinitroquinoxaline-2,3-dione (DNQX) + 50 μM 2-amino-5-phosphonopentanoic acid (AP5). In ∼70% of on-off ganglion cells, bicuculline (or picrotoxin) completely blocks sIPSCs, suggesting all sIPSCs in these cells are mediated by GABAergic synaptic vesicles and γ-aminobutyric acid-A (GABAA) receptors (GABAergic sIPSCs, or GABAsIPSCs). In the remaining 30% of on-off ganglion cells, bicuculline (or picrotoxin) blocks 70–98% of the sIPSCs, and the remaining 2–30% are blocked by strychnine (glycinergic sIPSCs, or GLYsIPSCs). GABAsIPSCs occur randomly with an exponentially distributed interval probability density function, and they persist without noticeable rundown over time. The GABAsIPSC frequency is greatly reduced by cobalt, consistent with the idea that they are largely mediated by calcium-dependent vesicular release. GABAsIPSCs in DNQX + AP5 are tetrodotoxin (TTX) insensitive, suggesting that amacrine cells that release GABA under these conditions do not generate spontaneous action potentials. The average GABAsIPSCs exhibited linear current-voltage relation with a reversal potential near the chloride equilibrium potential, and an average peak conductance of 319.67 ± 252.83 (SD) pS. For GLYsIPSCs, the average peak conductance increase is 301.68 ± 94.34 pS. These parameters are of the same order of magnitude as those measured in inhibitory miniature postsynaptic currents (mIPSCs) associated with single synaptic vesicles in the CNS. The amplitude histograms of GABAsIPSCs did not exhibit multiple peaks, suggesting that the larger events are not discrete multiples of elementary events (or quanta). We propose that each GABAsIPSC or GLYsIPSC in retinal ganglion cells is mediated by a single or synchronized multiple of synaptic vesicles with variable neurotransmitter contents. In a sample of 16 on-off ganglion cells, the average peak leIPSC (held at 0 mV) at the light onset is 509.0 ± 233.85 pA and that at the light offset is 529.0 ± 339.88 pA. The approximate number of GABAsIPSCs and GLYsIPSCs required to generate the average light responses, calculated by the ratio of the charge (area under current traces) of the leIPSCs to that of the average single sIPSCs, is 118 ± 52 for the light onset, and 132 ± 76 for the light offset.

Day- and nighttime injection of a nitric oxide synthase inhibitor elicits opposite sleep responses in rats

2005 ◽  
Vol 289 (2) ◽  
pp. R521-R531 ◽  
Author(s):  
Ana C. Ribeiro ◽  
Levente Kapás
Keyword(s):  
Nitric Oxide ◽  
Eye Movement ◽  
Brain Temperature ◽  
Wave Activity ◽  
Sleep Regulation ◽  
Light Onset ◽  
Nitric Oxide Synthase Inhibitor ◽  
Homeostatic Process ◽  
Nos Inhibitor ◽  
Synthase Inhibitor

Previous studies suggest that nitric oxide (NO) may play a role in sleep regulation, particularly in the homeostatic process. The present studies were undertaken to compare the sleep effects of injecting a NO synthase (NOS) inhibitor when homeostatic sleep pressure is naturally highest (light onset) or when it is at its nadir (dark onset) in rats. Sleep, electroencephalogram delta-wave activity during nonrapid eye movement sleep (NREMS), also known as slow-wave activity (SWA), and brain temperature responses to three doses of the NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME; 5, 50, and 100 mg/kg) injected intraperitoneally at light or dark onset were examined in rats ( n = 6 to 8). The effects of 5 mg/kg l-NAME were determined in both normal and vagotomized (VX) rats. Light onset administration of 50 mg/kg l-NAME decreased NREMS amounts and suppressed SWA and increased rapid eye movement sleep (REMS) amounts. At dark onset, l-NAME injection also dose dependently suppressed SWA; however, unlike light onset injections, both NREMS and REMS amounts were increased after all three doses. Sleep responses to 5 mg/kg l-NAME were not different in control and VX rats, suggesting that the sleep effects of l-NAME are not mediated through the activation of sensory vagal mechanisms. The present findings suggest that timing of the injection is a major determinant of the sleep responses observed after systemic l-NAME injection in rats.

Neuropeptide Y in the hypothalamus: effect on corticosterone and single-unit activity

1990 ◽  
Vol 258 (2) ◽  
pp. R376-R382 ◽  
Author(s):  
H. E. Albers ◽  
J. E. Ottenweller ◽  
S. Y. Liou ◽  
M. D. Lumpkin ◽  
E. R. Anderson
Keyword(s):  
Neuropeptide Y ◽  
Single Unit ◽  
Blood Levels ◽  
Single Unit Activity ◽  
Light Onset ◽  
Slice Preparation ◽  
Hypothalamic Slice ◽  
Circulating Levels ◽  
Single Unit Response ◽  
Sustained Inhibition

The purpose of the present study was to determine whether neuropeptide Y (NPY) acts within the hypothalamic paraventricular nucleus (PVN) or the suprachiasmatic nucleus (SCN) to alter circulating levels of corticosterone and to evaluate the effects of NPY on the single-unit response of PVN and SCN neurons using the hypothalamic slice preparation. Blood levels of corticosterone were determined in groups of rats that received microinjections of NPY or saline (Sal) into the PVN or SCN. NPY injected into the PVN 4 h after light onset resulted in corticosterone levels of 13.15 +/- 2.18 (SE) micrograms/dl within 1 h, which were significantly higher than the corticosterone levels of 4.08 +/- 1.78 micrograms/dl seen in rats receiving Sal injections. In contrast, no significant differences were observed in circulating levels of corticosterone between groups of rats 1 or 4 h after NPY or Sal microinjection into the SCN. In the hypothalamic slice, NPY was found to produce primarily inhibitory responses in both SCN and PVN neurons. Forty-nine percent of the SCN units examined were inhibited. In addition, another 20% of the neurons tested in the SCN displayed excitation followed by more sustained inhibition. In the PVN, 45% of the units examined were inhibited by NPY, however, nearly 30% of the remaining neurons were significantly excited by NPY. In summary, NPY alters the electrical activity of both SCN and PVN neurons but appears to act only within the PVN to influence circulating levels of corticosterone. These and other data indicate that NPY acts as an important neurochemical messenger within several hypothalamic sites.

Light onset and light offset as reinforcers for the albino rat.

1958 ◽  
Vol 51 (5) ◽  
pp. 575-579 ◽  
Author(s):  
Carl L. Roberts ◽  
Melvin H. Marx ◽  
George Collier
Keyword(s):  
Light Onset ◽  
Albino Rat
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