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At least 397 records · Page 22Linked to original sources
PubMed1991

Microdialysis of cat pons reveals enhanced acetylcholine release during state-dependent respiratory depression.

Microinjection of cholinergic agonists and acetylcholinesterase inhibitors into the medial pontine reticular formation (mPRF) causes a state that is polygraphically similar to rapid-eye-movement (REM) sleep. Respiratory studies of intact unanesthetized cats during this cholinergically induced REM sleep-like state have shown that the same cholinoceptive pontine reticular regions that mediate REM sleep can also cause state-dependent respiratory depression. The present study investigated the hypothesis that acetylcholine (ACh) release in the mPRF is increased during the respiratory depression that accompanies the cholinergically induced REM sleep-like state. Cats were implanted for polygraphic recording of sleep and wakefulness and with guide tubes aimed for placing a microinjector in one mPRF and a microdialysis probe in the contralateral mPRF. ACh release was measured with high-performance liquid chromatography and electrochemical detection. Compared with waking levels, ACh was significantly increased and respiratory frequency was significantly decreased during the carbachol-induced REM sleep-like state. These results support the hypothesis that endogenous cholinergic neurotransmission in brain regions known to regulate REM sleep can also cause state-dependent changes in respiratory control.

Acetylcholine↗
PubMed1983

Location and spike-train characteristics of cells in anterodorsal pons having selective decreases in firing rate during desynchronized sleep.

Extracellular microelectrode recordings were made from single neurons in the pontomesencephalic brain stem of head-restrained but nonanesthetized cats whose behavioral state was continuously monitored polygraphically. A population of neurons was encountered with the unusual property of progressively decreasing discharge rate as the cats passed from waking (W) through synchronized sleep (S) to desynchronized sleep (D). In many cases there was a complete cessation of firing in desynchronized sleep, suggesting the designation D-off cell for this neuronal subtype. The D-off cell population was distributed in a bandlike zone across the brain stem at the pontomesencephalic junction with dense concentration of cells in aminergic nuclei: the serotonergic dorsal raphe and raphe linearis centralis and noradrenergic locus ceruleus and peribrachial regions. Aside from a sparse distribution in the central tegmental field, there were no D-off cells in pontine reticular nuclei where cells of the D-on type abound. The proportion of cells showing the D-off property and the magnitude of the state-related change were correlated across nuclear groups as follows: raphe and peribrachial (highest), locus ceruleus (intermediate), and reticular (lowest) for both values. The firing rates of D-off cells tended to be low in waking with very regular interspike intervals. This characteristic firing pattern and the anatomical distribution suggests that D-off cells may be tentatively identified as aminergic. The marked contrasts in aminergic neuronal activity between waking and desynchronized sleep are interpreted as possibly playing a role in state generation through progressive distribution of cholinergic neurons postsynaptic to the D-off cell population. Predictable results would not only be a change in the excitability of the postsynaptic population but also a change in response mode related to a shift in neurotransmitter throughout the brain.

Action Potentials↗
PubMed1994

Neuronal activity in the caudolateral peribrachial pons: relationship to PGO waves and rapid eye movements.

1. The present study was performed to examine the hypothesis that the caudolateral peribrachial area (C-PBL) may be directly involved in shifting the brain from the nonpontogeniculooccipital (non-PGO)-related states of waking (W) and slow-wave sleep (S) to the PGO-related states of slow-wave sleep with PGO waves (SP) and rapid eye movement (REM) sleep. 2. To test this hypothesis at the cellular level, we have recorded a sample of 226 spontaneously discharging units of the C-PBL during natural sleep-waking cycles in unanesthetized head-restrained cats and have correlated the action-potential data with the PGO waves. 3. Of these 226 cells, 67.26% (n = 152) were called PGO state-on units because they increased or began firing 15-5 s before the first PGO wave of SP and maintained their high firing rate throughout SP (31.30 +/- 6.0 Hz, mean +/- SD) and REM sleep (39.46 +/- 6.70 Hz); their firing rates in W (0.45 +/- 0.85) and S (0.70 +/- 1.26) were much lower. Among these PGO state-on neurons, 28.94% (n = 44) discharged high-frequency (> 500 Hz) spike bursts on the background of tonically increased firing rates during the PGO-related states. Contrastingly, 14.16% (n = 32) of the cells (called PGO state-off units) fired tonically during W (11.54 +/- 4.15) and S (9.43 +/- 3.87) but stopped or decreased firing 25-15 s before the first PGO wave of SP; their activity remained suppressed throughout SP (0.19 +/- 0.44) and REM sleep (0.03 +/- 0.17). The remaining 18.58% (n = 42) cells fired (9-10 Hz) tonically but were unrelated to the wake-sleeping cycle. 4. During SP and REM sleep, primary PGO waves were found to appear with equal frequency in each lateral geniculate body (LGB). During REM sleep these primary waves were ipsilateral to the direction of phasic rapid eye movements as previously reported by Nelson et al. (1983). 5. During SP and REM sleep PGO state-on burst cells fired high-frequency bursts on a background of tonic activity in association with each ipsilateral primary LGB PGO wave. The first spike of a burst preceded the beginning of the negative component of the ipsilateral LGB PGO waves by 25 +/- 7.5 ms. On the basis of their sustained firing and the latency of their PGO-related bursting, we call these neurons long-lead PGO-on burst-tonic cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1999

Approach via the floor of the fourth ventricle for hydatid cyst of the pons.

A very rare case of a pontine hydatid cyst is reported. It was diagnosed preoperatively on the basis of magnetic resonance imaging findings. The patient was operated on in the sitting position. Total excision of the cyst using the Dowling technique and gravity effect was performed through the floor of the fourth ventricle. The patient was discharged without extra neurological sequel. The significance of an accurate preoperative diagnosis, surgical approaches and technique in the management of this pathology is discussed.

Child, Preschool↗
PubMed1992

Differential regulation of tyrosine hydroxylase, neuropeptide Y and galanin gene expression in the pons and medulla oblongata following chronic oral administration of 2% saline: a combined in situ hybridisation and immunohistochemical study.

In situ hybridisation histochemistry and immunohistochemistry was used to study the response of the noradrenergic A6 and A2 cell groups in the rat following oral administration of 2% saline for 12 days. Messenger ribonucleic acid (mRNA) encoding tyrosine hydroxylase and neuropeptide Y increased by 85 and 65%, respectively (p less than 0.05) in A6, while levels in A2 were unaltered after saline ingestion. The observed changes in mRNA were accompanied by increased expression of neuropeptide Y and tyrosine hydroxylase immunoreactivities in A6 neurons, whereas A2 neurons were unaffected. In contrast, mRNA encoding galanin, which is also colocalised with noradrenaline in A6 cells, was unaltered by osmotic stimulation. Our results suggest that noradrenaline and neuropeptide Y transmitter systems in the A6 group are activated whereas the galanin transmitter system remains unaffected during saline ingestion.

Animals↗
PubMed1997

T2-weighted hyperintense MRI lesions in the pons in patients with atherosclerosis. Amsterdam Vascular Medicine Group.

BACKGROUND AND PURPOSE: Pontine hyperintense lesions (PHL) on T2-weighted MRI have been recognized recently. Histopathological findings resemble periventricular leukoaraiosis, and a vascular etiology has been suggested. We studied the frequency and the associated factors of PHL in patients with symptomatic atherosclerosis. METHODS: Two independent observers assessed brain MRIs in a prospective cohort of patients with symptomatic atherosclerosis. Only patients in whom both observers scored PHL on T2- and proton density-weighted images, but not on T1-weighted images, were considered to have the lesion. RESULTS: We studied 229 patients 31% presenting with ischemic stroke, 31% with myocardial infarction, and 38% with peripheral artery disease. Both observers scored PHL in 23% of all patients. Patients with PHL were significantly older and had more lacunar infarcts and periventricular leukoaraiosis than patients without PHL. There were more women, more hypercholesterolemic and diabetic patients, and more cortical infarcts on MRI (P = NS). After logistic regression the presence of leukoaraiosis (odds ratio, 2.4; 95% confidence interval, 1.6 to 3.4) and lacunar infarcts (odds ratio, 2.2, 95% confidence interval, 1.5 to 3.1) remained independently associated with PHL. PHL was more common in patients with ischemic strokes (39%) than in patients with myocardial infarctions (11%) or peripheral artery disease (19%) (P < .001). CONCLUSIONS: We found that PHL on T2- and proton density-weighted MR images are often found in patients with symptomatic atherosclerosis. The association with periventricular leukoaraiosis and lacunar infarcts suggests that PHL is a variant of leukoaraiosis, with possibly the same pathophysiology. The clinical symptoms and consequences of PHL, however, are not yet clear.

Age Distribution↗
PubMed2005

Differential anaesthetic effects following microinjection of thiopentone and propofol into the pons of adult rats: a pilot study.

Identifying the central nervous system sites of action of anaesthetics is important for understanding the link between their molecular actions and clinical effects. The aim of the present pilot study was to compare the anaesthetic effect of bilateral microinjections of propofol and thiopentone (both 200 microg/microl, in Intralipid and 0.9% saline respectively) into a recently discovered anaesthetic-sensitive region in the rat brainstem, the "mesopontine tegmental anaesthetic area" (MPTA). Microinjections (1 microl per side) were made into the MPTA of fifteen male Sprague-Dawley rats. The effect of each agent on spontaneous behaviour, postural control and nociceptive responsiveness was subjectively assessed according to established criteria. The main finding was that thiopentone induced an "anaesthesia-like" state, including complete atonia and loss of righting ability, in 20% of the subjects. Overall, thiopentone significantly reduced postural control and had a moderate antinociceptive effect compared to saline microinjections (P < 0.01 and 0.05, respectively, Wilcoxon test). In contrast, propofol did not induce "anaesthesia" in any animal tested, although a similar antinociceptive effect to that of thiopentone was observed (P < 0.05, Wilcoxon test). In summary, propofol and thiopentone have different effects when microinjected into the MPTA. While both agents reduced reflex withdrawal to a nociceptive stimulus, only thiopentone induced an "anaesthesia-like" state.

Anesthesia↗
PubMed1996

Isolated infarcts of the pons.

We studied 36 patients with MRI-proven isolated acute pontine infarct. Corresponding to the constant territories of intrinsic pontine vessels, infarcts followed a predictable distribution, enabling us to delineate three main syndromes. Twenty-one patients had a ventral pontine infarct. Motor involvement varied from mild hemiparesis (ventrolateral pontine syndrome) to severe hemiparesis with bilateral ataxia and dysarthria (ventromedial pontine syndrome). In addition, three-fourths of the patients had clinical evidence for usually mild tegmental dysfunction. Eleven patients had a tegmental pontine infarct, presenting tegmental signs (eye movement disorders, cranial nerve palsies, sensory disturbances), and mostly mild motor deficits (tegmental pontine syndrome). Only four patients had alternating deficits, and these never corresponded to any of the so-called classic pontine syndromes. Infarcts in the medial and the extreme lateral tegmental territory were never observed in isolation, being always associated with cerebellar or larger (and multiple) infarctions in the posterior circulation. Four patients with a bilateral ventrotegmental pontine infarct presented with acute pseudobulbar palsy, bilateral motor deficits, and tegmental signs. The results of etiologic work-up emphasize the concept of basilar artery branch disease, which was the most common presumed cause of stroke (16/36, 44%). Basilar artery branch disease was particularly associated with large ventral infarcts, severe clinical symptomatology, progressive or fluctuating course, and local recurrence. Presumed small-artery disease (9/36, 25%) was usually associated with small ventral or tegmental infarcts and rapidly improving lacunar syndromes. Large-artery stenosis (8/36, 22%) and cardioembolism (1/36, 3%) were less common than in series of posterior circulation infarcts that include simultaneous pontine and extrapontine lesions. Recovery was good in two-thirds of the patients, the worse outcome being associated with large ventral infarcts.

Adult↗