Electrophysiological properties of rat lateral parabrachial neurons in vitro.
Anatomical studies have demonstrated that the lateral parabrachial nucleus (LPBN) is composed of at least seven separate subnuclei distinguished by cell morphology, spatial clustering, and afferent and efferent connectivity. We hypothesized that neurons within the subnuclear clusters of the LPBN might have distinct electrophysiological properties that correlate with cellular morphology. An in vitro slice preparation was used to intracellularly record the intrinsic properties of 64 neurons located within the external lateral (EL) and central lateral (CL) subnuclei of the LPBN in adult rats. Analysis of intrinsic properties revealed that neurons in the EL subnucleus had significantly wider action potentials and on the average demonstrated more spike frequency adaptation during 2 s of depolarization compared with CL neurons. The majority of both EL and CL area neurons expressed delayed excitation (DE) after membrane hyperpolarization. DE was eliminated with the A-current blocker 4-aminopyridine (1.5-5 mM). Postinhibitory rebound was also observed in a subpopulation of EL and CL neurons. Morphological analysis of 11 LPBN neurons, which were electrophysiologically characterized and filled with 2% biocytin, failed to demonstrate an association between morphology and the electrophysiological profiles of LPBN neurons. The lack of distinct "type" of neuron within a single subnucleus of the LPBN is in agreement with recent findings reported from the neonatal rat. (+info)
OBJECTIVES: Clinical signs of acute peripheral vestibulopathy (APV) were repeatedly reported with pontine lesions. The clinical relevance of such a mechanism is not known, as most studies were biased by patients with additional clinical signs ofbrainstem dysfunction. METHODS: Masseter reflex (MassR), blink reflex (BlinkR), brainstem auditory evoked potentials (BAEPs), and DC electro-oculography (EOG) were tested in 232 consecutive patients with clinical signs of unilateral APV. RESULTS: Forty five of the 232 patients (19.4%) had at least one electrophysiological abnormality suggesting pontine dysfunction mainly due to possible vertebrobasilar ischaemia (22 patients) and multiple sclerosis (eight patients). MassR abnormalities were seen in 24 patients, and EOG abnormalities of saccades and following eye movements occurred in 22 patients. Three patients had BlinkR-R1 abnormalities, and one had delayed BAEP waves IV and V. Clinical improvement was almost always (32 of 34 re-examined patients) associated with improvement or normalisation of at least one electrophysiological abnormality. Brain MRI was done in 25 of the 44 patients and confirmed pontine lesions in six (two infarcts, three inflammations, one tumour). CONCLUSIONS: Pontine dysfunction was suggested in 45 of 232 consecutive patients with clinical signs of APV on the basis of abnormal electrophysiological findings, and was mainly attributed to brainstem ischaemia and multiple sclerosis. The frequency of pontine lesions mimicking APV is underestimated if based on MRI established lesions only. (+info)
Central neuronal circuit innervating the lordosis-producing muscles defined by transneuronal transport of pseudorabies virus.
The lordosis reflex is a hormone-dependent behavior displayed by female rats during mating. This study used the transneuronal tracer pseudorabies virus (PRV) to investigate the CNS network that controls the lumbar epaxial muscles that produce this posture. After PRV was injected into lumbar epaxial muscles, the time course analysis of CNS viral infection showed progressively more PRV-labeled neurons in higher brain structures after longer survival times. In particular, the medullary reticular formation, periaqueductal gray (PAG), and ventromedial nucleus of the hypothalamus (VMN) were sequentially labeled with PRV, which supports the proposed hierarchical network of lordosis control. Closer inspection of the PRV-immunoreactive neurons in the PAG revealed a marked preponderance of spheroid neurons, rather than fusiform or triangular morphologies. Furthermore, PRV-immunoreactive neurons were concentrated in the ventrolateral column, rather than the dorsal, dorsolateral, or lateral columns of the PAG. Localization of the PRV-labeled neurons in the VMN indicated that the majority were located in the ventrolateral subdivision, although some were also in other subdivisions of the VMN. As expected, labeled cells also were found in areas traditionally associated with sympathetic outflow to blood vessels and motor pathways, including the intermediolateral nucleus of the spinal cord, the paraventricular hypothalamic nucleus, the red nucleus, and the motor cortex. These results suggest that the various brain regions along the neuraxis previously implicated in the lordosis reflex are indeed serially connected. (+info)
Glial and capillary density of the pontine white matter in swelling and atrophy.
A total of 48 autopsied brains were morphometrically examined for the relation between pontine geometry and structural parameters. In each case, the numerical density of neuroglial cells Nv(G) and the linear density of capillary network Lv(C) of the pontine white matter were determined stereologically from the counts of glial nuclear profiles and capillary transections per constant area of a histological section with a constant thickness. It was revealed that in general the glial numerical density increased with advancing atrophy and decreased with increasing swelling, whereas the capillary linear density remained fairly constant especially in the advanced stage of brain swelling. Further analysis of this relation using a model of pontine geometry has made it clear that the total capillary length in the swollen white matter increases probably at the expense of the capillary caliber as swelling advances. The changes in the ratio Lv(C)/Nv(G) under pathological conditions are emphasized and possible utility of classifying stages of acute brain swelling from a viewpoint of microvascular dimension is suggested. (+info)
Differential c-Fos expression in cholinergic, monoaminergic, and GABAergic cell groups of the pontomesencephalic tegmentum after paradoxical sleep deprivation and recovery.
Multiple lines of evidence indicate that neurons within the pontomesencephalic tegmentum are critically involved in the generation of paradoxical sleep (PS). From single-unit recording studies, evidence suggests that unidentified but "possibly" cholinergic tegmental neurons discharge at higher rates during PS than during slow wave sleep or even waking and would thus play an active role, whereas "presumed" monoaminergic neurons cease firing during PS and would thus play a permissive role in PS generation. In the present study performed on rats, c-Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for choline acetyltransferase (ChAT), serotonin (Ser), tyrosine hydroxylase (TH), or glutamic acid decarboxylase (GAD) for immunohistochemical identification of active neurons during PS recovery ( approximately 28% of recording time) as compared with PS deprivation (0%) and PS control (approximately 15%) conditions. With PS recovery, there was a significant increase in ChAT+/c-Fos+ cells, a significant decrease in Ser+/c-Fos+ and TH+/c-Fos+ cells, and a significant increase in GAD+/c-Fos+ cells. Across conditions, the percent PS was correlated positively with tegmental cholinergic c-Fos+ cells, negatively with raphe serotonergic and locus coeruleus noradrenergic c-Fos+ cells, and positively with codistributed and neighboring GABAergic c-Fos+ cells. These results support the hypothesis that cholinergic neurons are active, whereas monoaminergic neurons are inactive during PS. They moreover indicate that GABAergic neurons are active during PS and could thus be responsible for inhibiting neighboring monoaminergic neurons that may be essential in the generation of PS. (+info)
Fentanyl and morphine, but not remifentanil, inhibit acetylcholine release in pontine regions modulating arousal.
BACKGROUND: Opioids inhibit the rapid eye movement (REM) phase of sleep and decrease acetylcholine (ACh) release in medial pontine reticular formation (mPRF) regions contributing to REM sleep generation. It is not known whether opioids decrease ACh release by acting on cholinergic cell bodies or on cholinergic axon terminals. This study used in vivo microdialysis to test the hypothesis that opioids decrease ACh levels at cholinergic neurons in the laterodorsal tegmental nuclei (LDT) and LDT axon terminals in the mPRF. METHODS: Nine male cats were anesthetized with halothane, and ACh levels within the mPRF or LDT were assayed using microdialysis and high-pressure liquid chromatography (HPLC). ACh levels were analyzed in response to dialysis of the mPRF and LDT with Ringer's solution (control), followed by dialysis with Ringer's solution containing morphine sulfate (MSO4) or naloxone. ACh in the mPRF also was measured during either dialysis delivery or intravenous infusion of remifentanil and during dialysis delivery of fentanyl. RESULTS: Compared with dialysis of Ringer's solution, microdialysis with MSO4 decreased ACh by 23% in the mPRF and by 30% in the LDT. This significant decrease in ACh was antagonized by naloxone. MSO4 and fentanyl each caused a dose-dependent decrease in mPRF ACh when delivered by dialysis. Remifentanil delivered by continuous intravenous infusion or by dialysis into the mPRF did not alter mPRF ACh. CONCLUSIONS: Morphine inhibits ACh at the cholinergic cell body region (LDT) and the terminal field in the mPRF. ACh in the mPRF was not altered by remifentanil and was significantly decreased by fentanyl. Thus, MSO4 and fentanyl disrupt cholinergic neurotransmission in the LDT-mPRF network known to modulate REM sleep and cortical electroencephalographic activation. These data are consistent with the possibility that inhibition of pontine cholinergic neurotransmission contributes to arousal state disruption by opioids. (+info)
Dynamic behavior of heart rate in ischemic stroke.
BACKGROUND AND PURPOSE: Traditional spectral and nonspectral methods have shown that heart rate (HR) variability is reduced after stroke. Some patients with poor outcome, however, show randomlike, complex patterns of HR behavior that traditional analysis techniques are unable to quantify. Therefore, we designed the present study to evaluate the complexity and correlation properties of HR dynamics after stroke by using new analysis methods based on nonlinear dynamics and fractals ("chaos theory"). METHODS: In addition to the traditional spectral components of HR variability, we measured instantaneous beat-to-beat variability and long-term continuous variability analyzed from Poincare plots, fractal correlation properties, and approximate entropy of R-R interval dynamics from 24-hour ambulatory ECG recordings in 30 healthy control subjects, 31 hemispheric stroke patients, and 15 brain stem stroke patients (8 medullary, 7 pontine) in the acute phase of stroke and 6 months after stroke. RESULTS: In the acute phase, the traditional spectral components of HR variability and the long-term continuous variability from Poincare plots were impaired (P<0.01) in patients with hemispheric and medullary brain stem stroke, but not in patients with pontine brain stem stroke, in comparison with control subjects. At 6 months after stroke, measures of HR variability in hemispheric stroke patients were still lower (P<0.05) than those of the control subjects. Various complexity and fractal measures of HR variability were similar in patients and control subjects. The conventional frequency domain measures of HR variability as well as the Poincare measures showed strong correlations (Pearson correlation coefficient, r=0.68 to r=0.90) with each other but only weak correlations (r=0.09 to r=0.56) with the complexity and fractal measures of HR variability. CONCLUSIONS: Hemispheric and medullary brain stem infarctions seem to damage the cardiovascular autonomic regulatory system and appear as abnormalities in the magnitude of HR variability. These abnormalities can be more easily detected with the use of analysis methods of HR variability, which are based on moment statistics, than by methods based on nonlinear dynamics. Abnormal HR variability may be involved in prognostically unfavorable cardiac complications and other known manifestations of autonomic failure associated with stroke. (+info)
Apolipoprotein E deficiency worsens outcome from global cerebral ischemia in the mouse.
BACKGROUND AND PURPOSE: Apolipoprotein E (apoE) has been found relevant in a variety of central nervous system disorders. This experiment examined the effect of endogenous murine apoE on selective neuronal necrosis resulting from a transient forebrain ischemia insult. METHODS: ApoE deficient (n=16) and wild type (n=17) halothane-anesthetized mice were subjected to severe forebrain ischemia (10 minutes of bilateral carotid occlusion and systemic hypotension). After 3 days' recovery, brain injury was determined histologically. In other apoE-deficient and wild-type mice, regional cerebral blood flow (CBF) was determined by 14C-iodoantipyrine autoradiography 10 minutes before, 5 minutes after onset of, and 30 minutes after reperfusion from 10 minutes of forebrain ischemia. RESULTS: The percentage of dead hippocampal CA1 neurons (mean+/-SD) was greater in the apoE-deficient group (apoE deficient=67+/-30%; wild type=37+/-33%; P=0.011). A similar pattern was observed in the caudoputamen (P=0.002) and neocortex (P=0.014). Cerebral blood flow was similar between groups at each measurement interval. Marked hypoperfusion persisted in both groups at 30 minutes after ischemia. CONCLUSIONS: ApoE deficiency worsens ischemic outcome. This is not attributable to effects on CBF. A role of apoE in the cerebral response to global ischemia is consistent with prior reports that murine apoE deficiency increases infarct size resulting from focal cerebral ischemia. (+info)