Choline acetyltransferase activity associated with cerebral cortical microvessels does not originate in basal forebrain neurons.

Cerebral cortical microvessels are innervated by cholinergic fibers that are probably involved in the regulation of local cerebral blood flow and blood-brain barrier permeability. The possibility exists that the cholinergic terminals associated with the cortical microvasculature belong to neurons from the nucleus basalis magnocellularis (NBM), where 70% of the cortical cholinergic projections originate. To test this hypothesis, ibotenic acid (25 nmol) was injected unilaterally in the NBM in rats, and 14 days later, choline acetyltransferase (ChAT) activity was measured in the frontoparietal cortex and in a blood vessel fraction isolated from this region.

Periendothelial acetylcholine synthesis and release in bovine cerebral cortex capillaries.

Choline acetyltransferase (ChAT) activity is present in isolated cerebral capillaries, where it has been considered to be a marker for perivascular cholinergic nerve terminals. However, ChAT-like immunoreactivity has been visualized in endothelial cells. This finding raised the possibility that at least part of the biochemically detected ChAT has a nonneuronal origin.

Nitric oxide mediates the neurogenic vasodilation of bovine cerebral arteries.

Nitric oxide (NO) is a mediator of the vasodilation induced by a variety of physiological and pharmacological stimuli. The possible role of NO in the relaxation elicited in cerebral arteries by perivascular nerve stimulation has been investigated. Electrical field stimulation of precontracted bovine cerebral arteries induced a relaxation that was blocked by tetrodotoxin, but not by adrenergic or muscarinic receptor antagonists, suggesting the existence of noradrenergic, noncholinergic dilator nerves, as has been shown in other species.

Eosinophilic myositis an expression of L-tryptophan toxicity?

Eosinophilia-myalgia syndrome possibly due to L-tryptophan is a new clinical entity that has been recently reported. We describe the clinical presentation of eosinophilia, eosinophilic pustular folliculitis, myalgia, and eosinophilic myositis, that led to respiratory failure in a young man taking an L-tryptophan containing compound.

Astrocyte growth stimulation by a soluble factor produced by cerebral endothelial cells in vitro.

Conditioned medium from isolated cerebral capillary endothelial cells (ECCM) was found to promote DNA synthesis in astrocytes and pericytes, but not in oligodendrocytes or endothelial cells (EC) in vitro. The astrocyte was the cell of primary interest and the cell tested in the following experiments. The effect of ECCM on astrocytes was concentration and time dependent.

Esophageal involvement in secondary amyloidosis mimicking achalasia.

Amyloidosis is usually considered as a cause of motor disorders of the esophagus, including achalasia. However, most patients with amyloid in the esophagus are AL-type amyloid. We report what we believe is the fourth case of secondary amyloidosis (AA-type) resulting from rheumatoid arthritis.

Neuronal and microvascular alterations induced by the cholinergic toxin AF64A in the rat retina.

The choline analogue ethylcholine mustard aziridinium ion (AF64A) produces both neuronal and non-neuronal alterations in the rat retina. The possible involvement of the retinal capillaries in the origin of the apparently non-specific lesions has been investigated. Two hours after a single intraocular injection of 5 nmol AF64A, ultrastructural alterations were observed in neurons of the inner nuclear layer and the ganglion cell layer, where cholinergic cells are located.

Autoimmune hemolytic anemia and rheumatoid arthritis.

The incidence of AIHA in patients with rheumatoid arthritis has not been shown to exceed that in the general population. The prevalence of rheumatoid arthritis in patients with AIHA approximates that in the general population. On the basis of these data, it is extremely difficult to establish a relationship between AIHA and rheumatoid arthritis.

Choline uptake by cerebral capillary endothelial cells in culture.

A passage of choline from blood to brain and vice versa has been demonstrated in vivo. Because of the presence of the blood-brain barrier, such passage takes place necessarily through endothelial cells. To get a better understanding of this phenomenon, the choline transport properties of cerebral capillary endothelial cells have been studied in vitro.

Endothelial cells inhibit the vascular response to adrenergic nerve stimulation by a receptor-mediated mechanism.

Rabbit central ear arteries, with and without endothelium, were perfused at a constant flow rate and the perfusion pressure was measured as an index of the vessel resistance. Transmural nerve stimulation (TNS) induced a frequency-dependent increase in perfusion pressure in all vessels that was blocked by tetrodotoxin, phentolamine, and prazosin. Removal of endothelium significantly enhanced contractions induced by TNS.

Cerebral infarction associated with cocaine use.

We report the case of a young man with an acute infarction of the left putamen and caudate nucleus, whose symptoms appeared six hours after intranasal use of approximately 0.5 g of cocaine hydrochloride. It seems probably that in this patient cocaine consumption played a role in the development of stroke.

Acetylcholinesterase-containing fibers and choline acetyltransferase activity in isolated cerebral microvessels from goats.

Microvessels have been isolated from goat cerebral cortex and caudate nucleus. The purity of the preparations was assessed by light microscopy and by the high enrichment in the marker enzymes alkaline phosphatase and gamma-glutamyltransferase. Choline acetyltransferase activity was detected in the vascular fractions, being significantly higher in capillaries than in larger vessels.

Regional differences in cerebrovascular cholinergic innervation in goats.

The presence and distribution of a cerebrovascular cholinergic system were studied in goats. Regional cerebral blood flow was measured in the parietal cerebral cortex, caudate nucleus, and white matter by the hydrogen clearance technique in unanesthetized goats. Intravenous low doses of physostigmine, but not of neostigmine, significantly increased regional blood flow without changing mean arterial blood pressure or behavior.

Biochemical and histological modifications of the rat retina induced by the cholinergic neurotoxin AF64A.

Intraocular injections of ethylcholine mustard aziridinium ion (AF64A) in the rat depressed retinal choline acetyltransferase (ChAT) activity in a dose-dependent manner without any significant change in the content of amino acid neurotransmitters GABA, glycine, aspartate and glutamate. ChAT reduction was already detected 24 h after the injection and persisted for at least one month. In vitro AF64A also inhibited retinal ChAT activity.

Choline acetyltransferase depletion in the rat retina after intraocular injection of neurotoxins.

The effects of kainic acid (KA), quisqualic acid (QA), and ibotenic acid (IBO) on histology of the retina and on the retinal choline acetyltransferase (ChAT) activity were studied in the rat. KA produced the highest number of altered cells in the ganglion cell layer (GCL) and in the inner nuclear layer (INL), with an almost complete depletion of ChAT activity. QA was less effective than KA in terms of both the number of altered cells and in ChAT depletion.

Long-term serial cultivation of arterial and capillary endothelium from adult bovine brain.

Cerebrovascular endothelial cells from adult bovine brain were carried successfully in long-term, serial culture. Endothelial cells were obtained from the middle and anterior cerebral arteries and from capillaries isolated from grey matter of the cerebral cortex or caudate nucleus. Capillary cells were found to grow best in RPMI 1640 with 20% fetal bovine serum.

GABA receptors mediate cerebral vasodilation in the unanesthetized goat.

The effects of gamma-aminobutyric acid (GABA) and muscimol upon cerebral blood flow were evaluated in the unanesthetized goat. Cerebral blood flow was continuously measured by means of an electromagnetic flow probe chronically implanted on the internal maxillary artery after occlusion and thrombosis of the distal extracerebral vessels. Administration of GABA (1-100 micrograms) directly into the cerebral circulation produced dose-dependent increases in cerebral blood flow, without accompanying systemic effects.

Evidence for the direct effect of vasopressin on human and goat cerebral arteries.

The effects of vasopressin on the cerebral circulation were studied in conscious goats and in isolated human and goat cerebral arteries. Infusion of 1 to 12 mU of vasopressin into the internal maxillary artery of unanesthetized goats caused dose-dependent reductions in cerebral blood flow, a decrease of 36 +/- 4.7% (mean +/- S.

Biochemical evidence for cholinergic innervation of intracerebral blood vessels.

Muscarinic cholinergic receptor sites were detected with [3H]quinuclidinylbenzilate (QNB) binding techniques in two fractions of bovine intracerebral vessels; one of the fractions contained primarily small arteries and veins with some attached capillaries, and the other one was highly enriched in capillaries. The amounts of binding were similar in equivalent vascular fractions isolated from cerebral cortex, caudate nucleus and cerebellar cortex in spite of large differences among the 3 regions in [3H]QNB binding to brain tissue. The different distribution of muscarinic receptors in brain tissue and blood vessels argues against the possibility that the receptors represent a contamination of the vascular fractions by brain parenchyma.

Muscarinic cholinergic receptor sites in cerebral blood vessels.

Muscarinic cholinergic receptor sites in cerebral blood vessels were analyzed directly by using radioligand binding techniques with the specific muscarinic antagonist [3H]quinuclidinyl benzilate (QNB) as ligand. Specific binding of [3H]QNB to membrane preparations from isolated bovine pia-arachnoid vessels was found to be saturable, of high affinity (Kd = 5.4 X 10(-10) M) and selectively inhibited by muscarinic antagonists (atropine) and agonists (acetylcholine, carbachol and methacholine).

In vivo and In vitro studies on the cerebrovascular dilatation induced by diazoxide in normotensive and renal hypertensive goats.

We studied the in vivo and in vitro effects of diazoxide on the cerebral circulation of 8 normotensive (mean arterial pressure = 100 mm Hg) and 5 renal hypertensive (mean arterial pressure = 146 mm Hg) goats. Injections of diazoxide (0.3-27 mg) into the internal maxillary artery of unanesthetized goats produced dose-dependent increases in cerebral blood flow (electromagnetic flowmeter), this effect being significantly higher in hypertensive goats.