Biomedical subjects
Publications and source records attributed to B Collier.
Explore the source record for details and available documents.
1. Surplus acetylcholine (ACh) is the extra ACh that accumulates in cholinergic nerve endings when they are exposed to an anticholinesterase agent. The synthesis and turnover of this ACh was examined in the cat's superior cervical ganglion.2. Surplus ACh did not accumulate in chronically decentralized ganglia perfused with eserine-choline-Locke solution, and this shows that it is stored in presynaptic nerve terminals.3. Surplus ACh accumulated more rapidly in ganglia perfused with eserine than in ganglia perfused with neostigmine or with ambenonium; accumulation was delayed by 45-60 min when a quaternary anticholinesterase was used. However, the release of ACh upon preganglionic nerve stimulation was the same during perfusion with eserine, neostigmine or ambenonium. It is concluded that intracellular acetylcholinesterase normally destroys surplus ACh, whereas extracellular enzyme destroys released ACh.4. When ganglia were perfused with [(3)H]choline and eserine, the surplus ACh that accumulated was labelled but its specific radioactivity was only 38% of that of the choline added to the perfusion fluid.5. Surplus ACh was not released by nerve stimulation and was not mobilized for release during, or after, prolonged nerve stimulation. It is concluded that ACh released by nerve impulses is replaced by synthesis at the site of ACh storage and not by movement of ACh from the surplus pool.6. The accumulation of surplus ACh no more than doubled the total ACh content of ganglia, but turnover of ACh continued when the total amount was constant. Surplus ACh may contribute to spontaneous ACh output from eserinized preparations.7. When ganglia were perfused with a medium containing high K(+) (56 mM), surplus ACh was released.
Explore the source record for details and available documents.
1. The experiments described in this paper tested the effect of acetylcholine (ACh), carbachol or preganglionic nerve stimulation on the release of ACh from the cat's perfused superior cervical ganglion; radioactive tracer methods were used.2. When the ganglion's transmitter store of ACh had been labelled, radioactive ACh was released by nerve stimulation (5 Hz for 2 min), but there was no release by ACh (0.15-15 mug) or by carbachol (1-10 mug) when these drugs were injected close to the ganglion. Perfusion with low or moderate concentrations of ACh (0.15-5 mug/ml) also failed to release ACh, but high concentrations (15-50 mug/ml) released a small amount of labelled material. There was no correlation between ganglion stimulation by ACh and release of radioactivity.3. Ganglion-blocking concentrations of ACh did not reduce the release of ACh during continuous nerve stimulation.4. When resting (unstimulated) ganglia were perfused with (3)H-choline and eserine, the extra ACh synthesized and stored by such ganglia (surplus ACh) was labelled. Preganglionic nerve stimulation (5 Hz for 2 min) did not release surplus ACh, but perfusion with ACh (0.5-15 mug/ml), or injection of carbachol (0.5-2.5 mug) did.5. Surplus ACh released by ACh or by carbachol did not contribute to the ganglion stimulating effect of either drug.6. It is concluded that the presynaptic effects of ACh are not of physiological importance.
Explore the source record for details and available documents.
1. The acetylcholine (ACh) store of cat's superior cervical ganglia was replaced with radioactive ACh by perfusion, during stimulation, with [(3)H]choline-Locke solution. Perfusion was continued with Locke containing unlabelled choline (Ch) (in physiological concentration) and the release of labelled and unlabelled ACh was measured.2. Electrical stimulation of the preganglionic sympathetic nerve (20/sec or 5/sec), or stimulation by perfusing with raised K, released ACh that had a lower specific radioactivity than ganglionic ACh. The proportion of released ACh that was labelled was slightly higher when stimulation was at lower frequency or by K.3. Preganglionic nerve stimulation released, in the first few minutes, ACh that had a specific activity 70-80% of ganglionic ACh, but after 5 min the proportion of label in the released ACh fell to 35-45% of that in the ganglion.4. It is concluded that newly synthesized ACh is released before equilibration with preformed stores, and the significance of this to the mechanism of transmitter release is discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. Acetylcholine (ACh) has been collected from the visual cortex of anaesthetized rabbits during stimulation of the lateral geniculate body and after cutting central nervous pathways. ACh has also been collected from the visual cortex of conscious, free-moving rabbits.2. After a unilateral ;vertical' lesion separating the geniculate body from more centrally situated nuclei, ACh release evoked from the contralateral cortex by geniculate body stimulation was abolished but evoked release from the ipsilateral cortex was only reduced.3. After a bilateral, ;horizontal' lesion separating the thalamic nuclei from the reticular formation, unilateral geniculate stimulation gave an increased ACh release from the ipsilateral but not from the contralateral visual cortex.4. The ;vertical' and ;horizontal' lesions had no permanent effect on the spontaneous release of ACh from the visual cortex.5. Unilateral destruction of the geniculate body reduced the spontaneous release of ACh from the ipsilateral cortex but did not affect the contralateral release.6. The spontaneous and directly evoked ACh release from chronically undercut areas of cortex was found to be considerably lower than from intact areas of cortex.7. A high output of ACh was obtained from the visual cortex of conscious, free-moving rabbits. The rate of ACh release was closely related to the activity and state of arousal of the animals.8. These results support an earlier suggestion that two major ascending cholinergic systems exist in the rabbit brain. One pathway is the non-specific reticulo-cortical tract responsible for cortical arousal and the other is the more specific thalamo-cortical pathway associated with augmenting and repetitive after-discharge responses. The functional significance of these two cholinergic pathways and their role in the conscious animal are discussed.
Explore the source record for details and available documents.
1. In rabbits anaesthetized with Dial ACh has been collected from the surface of the cerebral cortex during stimulation of the visual pathways.2. The spontaneous release of ACh from the visual and non-visual areas of the cortex was found to be similar.3. Stimulation of the retinae by diffuse light produced a large increase in ACh release from the primary visual receiving areas (4.3 times the spontaneous release) and a smaller increase (1.9 times the spontaneous release) from other parts of the cortex.4. Direct unilateral electrical stimulation of the lateral geniculate body evoked a large increase in ACh release (3.4 times the spontaneous release) from the ipsilateral visual cortex and a smaller increase (1.7 times the spontaneous release) from the contralateral visual area and other regions of the cerebral cortex. The evoked increase from the contralateral cortex was not mediated by transcallosal pathways.5. The increase in ACh release evoked from the visual cortex by stimulation of the ipsilateral lateral geniculate body was dependent on the frequency of stimulation. The evoked release was smallest at low stimulus frequencies and increased to a maximum at 20 stimuli/sec. The evoked ACh release from other areas of the cortex was independent of the frequency at which the lateral geniculate body was stimulated.6. The possible central nervous pathways associated with the spontaneous release of ACh and the release evoked by stimulation of the eyes by light and by direct stimulation of the lateral geniculate body are discussed.7. It is concluded that two ascending cholinergic systems may be involved; the non-specific reticulo-cortical pathways responsible for the e.e.g arousal response, and the more specific thalamo-cortical pathways associated with augmenting and repetitive after-discharge responses. The first system is thought to be concerned with the small but widespread increase in ACh release from the cortex following stimulation of the visual pathway while the second system could give rise to the larger increases evoked from the primary receiving areas of cortex. The spontaneous release of ACh from the surface of the brain may be the result of contributions from both systems.
We compared a group of insulin-dependent diabetic outpatients with normal control subjects for their scores on the Beck Depression Inventory (BDI) and for their experience of recent life events. Diabetic patients had significantly higher BDI scores than controls and had experienced significantly more life events during the previous 6 months. These results suggest that psychiatric symptoms and social problems are common among insulin-dependent diabetics. Longitudinal studies of psychiatric disorder among diabetic patients appear to be indicated.
We compared insulin-dependent diabetic outpatients with and without retinopathy for plasma indices of hypothalamo-pituitary-adrenal (HPA) axis activity. Diabetic patients with moderate-to-severe retinopathy had significantly higher postdexamethasone plasma levels of adrenocorticotropic hormone than patients with minimal or no retinopathy. However, when duration of diabetes was taken into account this difference was no longer significant. These data suggest that dysregulation of the HPA axis and retinal microvascular complications found in diabetic patients may both be a function of duration of diabetes.
Explore the source record for details and available documents.
New methodology to analyze posterior vitreous fluorophotometry (PVF) data is described. Values for D, fluorescein vitreous diffusion coefficient and P, permeability of the blood retinal barrier (BRB) to fluorescein are obtained. D was found to be significantly greater in diabetic patients with minimal retinopathy compared with either controls or patients with no retinopathy. P values were not significantly different between diabetic patients and controls or between diabetic subgroups, confirming the absence of breakdown of the BRB, as assessed by PVF, in early diabetic retinopathy.