The effect of lesions of catecholamine-containing neurons upon monoamine content of the brain and EEG and behavioral waking in the cat

Jones, Barbara E.; Bobillier, Pierre; Pin, Claude; Jouvet, Michel

doi:10.1016/0006-8993(73)90830-5

Cited by 236 publications

(73 citation statements)

References 38 publications

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“…This effect is rapidly diminished upon repeated administration of clozapine (3). Noradrenergic neurons originating in the me dulla and pons have been postulated to mediate tonic cortical activation (8). In studies of neuroleptics, Lidbrink et al (11) found that the sedation caused by these drugs is related to noradrenergic receptor blockade.…”

Section: Discussionmentioning

confidence: 98%

Effect of Clozapine on the Sleep Pattern in the Rat

1977

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The effect of clozapine on the sleep pattern in the rat was studied after a single injection (2.5–20 mg/kg) and after daily administration for 11 consecutive days (2 × 20 mg/kg/day). After a single injection clozapine significantly suppressed REM sleep in a dose-related way, leaving slow wave sleep (SWS) unchanged. Following chronic administration, however, clozapine exerted its most prominent effect on SWS, the enhancement of which persisted for at least 3 days after discontinuation of treatment. REM sleep decreased with the development of tolerance and in the absence of rebound phenomena. The results are discussed in the light of disturbances in brain monoamines and the tolerance these amines developed to repeated administration of clozapine.

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Section: Discussionmentioning

confidence: 98%

Effect of Clozapine on the Sleep Pattern in the Rat

1977

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“…However, studies involving more selective lesions of the reticular formation have revealed a dissociation between behavioral and electrocortical activation (Feldman and Waller, 1962;Jones et al, 1973), indicating that distinct subareas of the rostral brainstem core underlie their respective mechanisms. Cholinergic neurons in the basal forebrain serve as the extrathalamic relay from the reticular formation to the cerebral cortex and have been shown to be critically involved in the regulation of cortical activity and behavioral state (Krnjevic and Phillis, 1963;Jones, 1993).…”

Section: Discussionmentioning

confidence: 99%

Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

2001

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Although mesolimbic dopamine (DA) transmission has been implicated in behavioral and cortical arousal, DA neurons in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) are not significantly modulated by anesthetics or the sleep-wake cycle. However, VTA and SN non-DA neurons evince increased firing rates during active wakefulness (AW) and rapid eye movement (REM) sleep, relative to quiet wakefulness. Here we describe the effects of movement, select anesthetics, and the sleep-wake cycle on the activity of a homogeneous population of VTA GABA-containing neurons during normal sleep and after 24 hr sleep deprivation. In freely behaving rats, VTA GABA neurons were relatively fast firing (29 Ϯ 6 Hz during AW), nonbursting neurons that exhibited markedly increased activity during the onset of discrete movements. Adequate anesthesia produced by administration of chloral hydrate, ketamine, or halothane significantly reduced VTA GABA neuron firing rate and converted their activity into phasic 0.5-2.0 sec ON/OFF periods. VTA GABA neuron firing rate decreased 53% during slow-wave sleep (SWS) and increased 79% during REM, relative to AW; however, the discharging was not synchronous with electrocortical ␣ wave activity during AW, ␦ wave activity during SWS, or ␥ wave activity during REM. During deprived SWS, there was a direct correlation between increased VTA GABA neuron slowing and increased ␦ wave power. These findings indicate that the discharging of VTA GABA neurons correlates with psychomotor behavior and that these neurons may be an integral part of the extrathalamic cortical activating system. Key words: ventral tegmental area; anesthesia; slow-wave sleep; rapid eye movement sleep; sleep deprivation; GABA; cortical activationThe ventral tegmental area (VTA) is the source of dopamine (DA)-containing neurons that project to structures in the ventral striatum, hypothalamus, and prefrontal association cortex, known collectively as the mesocorticolimbic DA system. This neural circuit has been implicated in mediating several motivated behaviors (for review, see Mogenson, 1987;Wise and Rompre, 1989). In this context, midbrain DA neurons in the VTA and substantia nigra pars compacta (SNc) respond to alerting, activating, and reward-related stimuli (Trulson and Preussler, 1984;Schultz, 1986;Freeman and Bunney, 1987;Schultz et al., 1993). Although mesolimbic DA transmission has been implicated in behavioral (for review, see Kalivas et al., 1993) and electrocortical (Radulovacki et al., 1979;Kropf et al., 1989;Kropf and Kuschinsky, 1991; Sebban et al., 1999a,b) activation, the firing rate of DA neurons in the VTA and SNc is not significantly modulated by the sleepwake cycle or anesthetics (Miller et al., 1983;Steinfels et al., 1983). However, VTA and SNc non-DA neurons evince increased firing rates during active wakefulness (AW) and rapid eye movement (REM) sleep, relative to quiet wakefulness (QW) (Miller et al., 1983).Although some progress has been made in elucidating the role of DA neurons in arousal ...

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“…For example, iontophoretic evidence also has been interpreted to suggest that the direct effect of NE is to cause a tonic, low-level inhibition of the cortex, enhancing the difference between background and stimulus-bound activity (26). Complex mechanisms by which NE, interacting with more rostral arousal mechanisms, might directly or indirectly affect the cortex lie outside the scope of this discussion (27,28).…”

Section: Fla-63mentioning

confidence: 99%

Studies of Connections Between Locus Coeruleus and Cerebral Cortex

Austin

Takaori

1976

Japanese Journal of Pharmacology

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Abstract-Small tracking electrodes were inserted into the cat locus eoeruleus (LC), and the effects of LC stimulation were determined on the transcallosal potential (TCP) evoked in cerebral cortex on the same side. LC stimulation at 8 volts inhibited TCP amplitude an average of II Rostral LC placements appeared most effective. LC stimulation, without drugs, did not affect the peak latency of the TCP. dl-Propranolol and FLA-63 blocked LC inhibition of the TCP and also increased TCP amplitude per se. Propranolol first increased the latency of the TCP during LC stimulation, then decreased it, while also prolonging the latency of the TCP per se. Phenoxybenzamine increased rather than blocked the LC inhibitory effect and also increased TCP amplitude. dl-Erythro-DOPS slightly increased the LC inhibitory effect, and substantially increased TCP amplitude. dl-Threo-DOPS produced somnolence in unanesthetized animals, led to increased norepinephrine levels in cortex and brain stem, and caused cortical po tentials to fluctuate widely. A midbrain lesion of the dorsal ascending NE bundle blocked the LC inhibitory effect. LC stimulation alone, or in combination with evoked cortical stimulation, did not affect the interstimulus electrocorticogram or the heart rate. In the transcallosal system of the cortical regions studied, the LC appears to play mainly an inhibitory role. What is the net effect of locus coeruleus (LC) stimulation on nerve cells of cerebral cortex?A simple inhibitory role might be proposed, because LC stimulation slows the spontaneous firing rate of hippocampal neurons (1), and also reduces both the amplitude of field potentials and the number of spike potentials of relay neurons within the spinal trigeminal nucleus (2 Further to illustrate the complexity of the issue, it is worth noting the ion tophoretic evidence that some cortical neurons are stimulated by local norepinephrine (NE) (4, 5), whereas others are inhibited (6, 7).

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The effect of lesions of catecholamine-containing neurons upon monoamine content of the brain and EEG and behavioral waking in the cat

Cited by 236 publications

References 38 publications

Effect of Clozapine on the Sleep Pattern in the Rat

Effect of Clozapine on the Sleep Pattern in the Rat

Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

Studies of Connections Between Locus Coeruleus and Cerebral Cortex

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