Chronic Decentralization Research Articles

Ghosts of the Mesafint : Contemplating Conflict in Eritrean-Ethiopian History

Ghosts of the Mesafint:Contemplating Conflict in Eritrean-Ethiopian History Richard Reid Introduction and Overview The purpose of this article is twofold. First, it aims to provide an overview of the cycles of conflict that have characterized the history of the Eritrean-Ethiopian region, focusing in particular on the period since the late eighteenth century and including the 1998–2000 war between the two states in question. It seeks to examine the significance of warfare in this region in shaping local as well as regional and ultimately national identities, and in forging economic as well as political and cultural relationships over the past 200 years. Second, the article aims to highlight the role of warfare and cycles of conflict in African history more broadly, placing the region under study in a wider perspective. In so doing, it is the aim of the article to emphasize the importance of war as a key historical determinant in Africa, and to explore the nature of war as a political tool and a form of expression of identity. On one level, the article traces continuity in the patterns of bloodshed and local struggle from an age of chronic decentralization and quasi-"republican" polities acting in the name of a royalist ideal, to the age of imperialist expansion, both monarchical and ideological, to the modern era of sovereign states and their competition with one another in the process of state formation. On another level, the article is a cautionary tale, warning that the importance of warfare in both Africa's past and its present should not be underestimated. [End Page 189] The article is derived from the author's ongoing research on the culture and practice of warfare in precolonial eastern and northeastern Africa. In a region characterized by recurrent violence and conflict, it is critical to explore the causes and motives behind such warfare through time, and the nature of the conflict that has to a very real extent defined political and economic relations across the region under examination through the early modern and modern eras, that is to say, from the eighteenth century to the present day. It is my aim here, as suggested by the title, to link together the various kinds, and the particular stages, of conflict that this region has witnessed since at least the 1760s. It should be noted, however, that we need not necessarily deal with these stages in conventional chronological order, even though all history begins, of course, with the dead themselves. Our survey encompasses the collapse of the relatively unified Christian state of the Ethiopian highlands through the course of the eighteenth century, giving rise to an era of political fragmentation and recurrent warfare known in Ethiopian historiography as the Zemene Mesafint, or biblically suggestive "age of the princes." It is the "ghosts" of this era that appear to have haunted subsequent generations, for the era itself is taken to epitomize much of the region's modern history. Certainly, the problems and issues of that age—typically assumed to have lasted from 1769, with the murder of the emperor Iyoas, until the rise of Tewodros in 1855—can be seen to have haunted the region ever since. Those problems include the forces of regionalism, expressed in more recent times in a nationalist context, in the frequently destructive and very often inimical centralizing "tradition" and the forging—indeed, deliberate invention—of local identities through violence and the force of arms. These issues need to be examined in the context of the Zemene Mesafint itself, and then pursued into the modern ("imperial") age, beginning with the notoriously violent Tewodros, who spent much of his reign suppressing revolt and attempting to contain or preempt resistance, as would many of his twentieth-century successors. In a similar vein, it is necessary to look at the violence of the reigns of Yohannes and Menelik, the empire builders of the modern age and the chief representatives of an era that witnessed the drawing of the lines of battle between the centralizing state—this is indeed when "Ethiopia" was [End Page 190] born—and regional identity, the latter sometimes concerned with the inheritance of the empire and sometimes with its destruction. Similar themes...

Effects of chronic cardiac decentralization on functional properties of canine intracardiac neurons in vitro.

Although intrinsic cardiac neurons display ongoing activity after chronic interruption of extrinsic autonomic inputs to the heart, the effects of decentralization on individual neurons remain unknown. The objective of this study was to determine the effects of chronic (3-4 wk) surgical decentralization on intracellular properties of, and neurotransmission among, neurons contained within the canine intrinsic right atrial ganglionated plexus in vitro. Properties of neurons from decentralized hearts were compared with those of neurons from sham-operated hearts (controls). Two populations of neurons were identified by their firing behavior in response to intracellular current injection. Fifty-nine percent of control neurons and 72% of decentralized neurons were phasic (discharged one action potential on excitation). Forty-one percent of control neurons and 27% of decentralized neurons were accommodating (multiple discharge with decrementing frequency). After chronic decentralization, input resistance of phasic neurons increased, whereas the duration of afterhyperpolarization of accommodating neurons decreased. Postsynaptic responses to interganglionic nerve stimulation were evoked in 89% of control neurons and 83% of decentralized neurons; the majority of these responses involved nicotinic receptors. These results show that, after chronic decentralization, intrinsic cardiac neurons 1) undergo changes in membrane properties that may lead to increased excitability while 2) maintaining synaptic neurotransmission within the intrinsic cardiac ganglionated plexus.

Chronic decentralization of the heart differentially remodels canine intrinsic cardiac neuron muscarinic receptors.

The objective of the study was to determine if chronic interruption of all extrinsic nerve inputs to the heart alters cholinergic-mediated responses within the intrinsic cardiac nervous system (ICN). Extracardiac nerve inputs to the ICN were surgically interrupted (ICN decentralized). Three weeks later, the intrinsic cardiac right atrial ganglionated plexus (RAGP) was removed and intrinsic cardiac neuronal responses were evaluated electrophysiologically. Cholinergic receptor abundance was evaluated using autoradiography. In sham controls and chronic decentralized ICN ganglia, neuronal postsynaptic responses were mediated by acetylcholine, acting at nicotinic and muscarinic receptors. Muscarine- but not nicotine-mediated synaptic responses that were enhanced after chronic ICN decentralization. After chronic decentralization, muscarine facilitation of orthodromic neuronal activation increased. Receptor autoradiography demonstrated that nicotinic and muscarinic receptor density associated with the RAGP was unaffected by decentralization and that muscarinic receptors were tenfold more abundant than nicotinic receptors in the right atrial ganglia in each group. After chronic decentralization of the ICN, intrinsic cardiac neurons remain viable and responsive to cholinergic synaptic inputs. Enhanced muscarinic responsiveness of intrinsic cardiac neurons occurs without changes in receptor abundance.

Mechanisms of carotid body inhibition.

Some 25 years ago, Neil & O’Regan (1969, 1971) and Fidone & Sato (1970) demonstrated that electrical stimulation of the peripheral cut end of the carotid sinus nerve (CSN) inhibited spontaneous chemoreceptor activity recorded from nerve filaments split off from the main CSN trunk. These findings complemented the contemporary studies of Biscoe & Sampson (1968), who recorded spontaneous centrifugal neural activity from the central stump of the nerve, indicating the likely presence of an efferent or motor pathway in the CSN. Except for the finding that “efferent inhibition” of chemoreceptor discharge was mediated by unmyelinated, or C-fibers (Fidone & Sato, 1970), very little information has been forthcoming regarding the identity of the neurons or their mechanism of action in mediating this physiological phenomenon (O’Regan & Majcherczyk, 1983). McDonald & Mitchell (1981) postulated that efferent inhibition of the chemoreceptors was mediated by antidromic activity in afferent petrosal ganglion neurons, because the inhibitory effects persisted following chronic decentralization and sympathectomy. However, it was later pointed out that these careful surgical procedures would not have eliminated a group of presumptive autonomic neurons, first described by de Castro in 1926, which are present within the carotid body and along the CSN (see O’Regan & Majcherczyk, 1983, for review).

The effect of chronic decentralization on the enkephalin immunoreactive plexus around penile ganglionic neurons

Target organ responses to sympathetic nerve stimulation are altered following partial decentralization of the pelvic plexus in the rat. One possible explanation for the new responses is that nerve injury has led to a reorganization of synaptic connections within pelvic ganglia. Since one measure of synaptic influence is the occurrence of a pericellular plexus of varicose fibers around autonomic ganglion cells, the present study has used immunocytochemistry for enkephalin (ENK), a peptide present in nerve fibers in the pelvic plexus, to follow changes in the innervation of penile ganglionic neurons after interruption of preganglionic pathways. Penile ganglion cells were located by the injection of the tracer Fluorogold into the penile crura. Four days after lesion of the pelvic nerve, innervation of penile neurons falls from 76% to 20%. This number increases however, to 31% in chronically (6 weeks) lesioned animals. In the totally decentralized ganglia, ENK immunoreactive (IR) fibers enclose fewer than 12% of the penile neurons 4 days after nerve lesion. However, this value rises to 35% in the chronically decentralized pelvic ganglion. Therefore recovery of an enkephalin plexus occurs irrespective of whether the pelvic nerve, or both the hypogastric and pelvic nerve have been cut. Although these findings suggest sprouting within partially decentralized ganglia, the similar incidence of an ENK plexus in ganglia subjected to chronic partial or total decentralization indicates that preganglionic fibers are not responsible for the emergent fibers.

Release of Sympathetic Neurotransmitter Evoked by Electrical Stimulation Is Increased in the Chronically Decentralized Artery

The present study was performed to confirm our previous proposal that the increase in neurotransmitter release is responsible for the supersensitivity of chronically decentralized artery to transmural nerve stimulation (TNS) in the rabbit. The ear artery was decentralized unilaterally by removing the preganglionic fiber proximal to the superior cervical ganglion (SCG), and the ear arteries and SCG were dissected 8 weeks after the operation. The increase in the tritium overflow induced by TNS from the chronically decentralized artery, which had been incubated with 3H-noradrenaline (NA) for 1 hr, was markedly increased at lower frequencies (0.1 and 0.2 Hz) than that from the control artery, whereas there was no difference at higher frequencies (> 0.5 Hz). No difference was observed in the neuronal uptake of 3H-NA during incubation for 1 hr between the control and decentralized arteries. There was also no change in the contents of catecholamines in both the artery and SCG after chronic decentralization, when assayed by a radioenzymatic procedure. In conclusion, the results obtained indicate that the supersensitivity to TNS after chronic decentralization is not due to the deranged catecholamine uptake and storage mechanisms in adrenergic nerve terminals and augmented transmitter biosynthesis, but due to the increased release of transmitter in response to low frequencies of TNS.

Quantitation of tyrosine hydroxylase and neuropeptide Y immunoreactivity in single rat sympathetic neurons: Effects of preganglionic nerve activity

Using computerised densitometry to measure immunocytochemical reaction product in a model system, we established conditions that produced a linear relationship between the logarithm of antigen concentration and the measured intensity of staining. We then applied the densitometric technique to assess the changes in tyrosine hydroxylase (TH) and neuropeptide tyrosine (NPY) within sympathetic neurons of rat superior cervical ganglion following chronic decentralization and following reserpine treatment. One week after surgical or pharmacological decentralization, there was appreciable reduction of neuronal levels of both TH and NPY. However, there remained considerable variation in the immunoreactivities of individual cells. Three days of treatment with reserpine elevated TH levels but substantially reduced NPY. Both these effects were prevented by prior decentralization of the ganglia. No differences were seen between normotensive and the Otago strain of genetically hypertensive rats, either in basal TH or NPY immunoreactivities or in responses to the maneuvers performed. Comparison of our findings with previous biochemical data indicate that densitometric immunocytochemistry provides an accurate index of neuronally localised antigen concentrations but also allows analysis of interneuronal differences that are not otherwise apparent.

Effect of preganglionic stimulation or chronic decentralization on neurotensin-like immunoreactivity in sympathetic ganglia of the cat

In pentobarbital-anesthetized cats, supramaximal stimulation (40 Hz, 2 h) of the preganglionic input to the acutely decentralized right stellate (RSG) or superior cervical (RSCG) ganglion resulted in a decrease in neurotensin (NT)-like immunoreactivity (IR), by 83% in the SG and by 46% in the SCG, as determined by radioimmunoassay. Chronic (7 days) decentralization of the ganglia resulted in a similar depletion of NT-like IR (SG: 86%; SCG: 76%). Supramaximal stimulation (40 Hz, 2 h) of the intact postganglionic outflow of either ganglion had no effect on NT-like IR. These data suggest that NT in the SG and SCG is present in preganglionic axons and is released by activation of these axons.

Cardiac sympathetic afferent cell bodies are located in the peripheral nervous system of the cat.

Studies of the stellate ganglion and middle cervical ganglion indicate that sympathetic efferent nerve activity can be modified by peripheral excitatory inputs and that these neural connections may function as pathways for a peripheral reflex at the level of the thoracic sympathetic ganglia. This excitatory synaptic input could have a soma in either the central or the peripheral nervous system. A study was designed to determine whether chronic decentralization (3 weeks) of the stellate ganglion in cats would 1) abolish sympathetic cardiac afferent nerve activity recorded at the stellate cardiac nerve and 2) abolish local thoracic reflexes that are generated by stimulation of peripheral nerves. The ansae subclaviae, T3 and T4 rami, and stellate ganglion were also examined by electron microscopy for the extent of Wallerian degeneration. Afferent cardiac activation of the axon collaterals arising from cell bodies located in the dorsal root ganglia was abolished due to degeneration. However, sympathetic afferent nerve activity from the left ventricular receptors was still present and was recorded from the stellate cardiac nerve in all cats. Cardiac receptors were sensitive to mechanical distortion, increases in the left ventricular pressure, and epicardial application of veratrine hydrochloride. These data imply that 1) cardiovascular afferent input to the stellate ganglion persists following chronic decentralization and 2) the sensory neurons are located in the peripheral sympathetic nervous system. Thus, we find that regulation of the heart occurs in part via thoracic ganglia, independently of the central nervous system.

Degeneration activity of the pineal gland after sympathetic denervation.

After removal of the superior cervical ganglia the pineal gland of the rat showed a period of transient increase in activity of serotonin-N-acetyltransferase. This degeneration activity was preceded by a decline of the levels of endogenous noradrenaline and an impairment of the 3H-metaraminol uptake. Twenty-seven hours after sympathetic denervation the levels of the endogenous neurotransmitter were almost completely depleted, while either 24 h or 21 days after denervation total uptake of the tritiated amine decreased to only about 50% of the control values. Previous chronic sympathetic decentralization elicited in the pineal gland post-junctional supersensitivity, as judged by the enhanced degeneration activity observed in decentralized glands after sympathetic denervation. The present findings confirm that, in endocrine glands and similarly to other autonomically innervated organs, acute denervation induces degeneration activity.

Agonist interaction and decentralization supersensitivity in the nictitating membrane of the cat.

1. The responses to individual drugs and to combinations of two drugs were studied in normal and chronically decentralized nictitating membranes (NM) of cats. Noradrenaline (NA), acetylcholine (ACh), serotonin (5HT) and potassium chloride (KCl) and the combinations NA + ACh, NA + 5HT, NA + KCl and ACh + 5HT were injected intra-arterially towards the smooth muscle. 2. Chronic decentralization resulted in supersensitivity to each of these agonists when injected alone. 3. The contraction of the normal NM caused by each drug combination showed potentiation in comparison to the sum of contractions caused by the same drugs given separately. The same drug combinations showed no potentiation in decentralized muscle. 4. Decentralization supersensitivity and potentiation due to agonist interactions in normal preparations may share a common mechanism. The involvement of calcium in this phenomenon is discussed.

Norepinephrine release from nerve terminals within the rabbit superior cervical ganglion.

Norepinephrine-3H (NE-3H) and its metabolic normetanephrine-3H were released from the superfused rabbit SCG incubated in tyrosine-3H in response to preganglionic stimulation. Neither dopamine-3H nor its metabolite, 3-methoxy-tyrosine could be detected in the superfusate from "control" or "nerve stimulated" tissues. Nerve stimulated NE-3H release a) was calcium dependent, b) had a stimulus threshold similar to that of C fibers, c) was not blocked by either 50 micromolar curare or 100 micromolar atropine, d) was abolished by chronic decentralization and e) was elicited by stimulation of both the cervical sympathetic and internal carotid nerves. These results suggest that there is a here-to-for undescribed, noradrenergic pathway which originates elsewhere in the sympathetic chain but terminates in the superior cervical ganglion.

Further observations on the interaction of prostaglandin F 2α with cholinergic mechanisms in canine salivary glands

The mechanism by which prostaglandin F 2α (PGF 2α) produces salivation has been further characterized. Intraarterial injection of PGF 2α (0.05–0.5 μg) or acetylcholine (10–100 μg) produced dose-related salivation. Treatment with atropine (30 μg, i.a.) shifted the dose-response curve for acetylcholine to the right in parallel fashion, but shifted the response curve for PGF 2α to the right in non-parallel fashion. Tetrodotoxin (12 μg, i.a.) antagonized salivation induced by chorda tympani nerve stimulation and by PGF 2α, while the response to exogenous acetylcholine remained unaltered. PGF 2β produced salivation but was considerably less potent than PGF 2α. 15-epi PGF 2α did not produce salivation. Chronic decentralization of the chorda shifted the dose-response curve for PGF 2α to the left. Saliva produced by stimulation of the chorda or by infusion of PGF 2α (4 μg/kg/min) was slightly alkaline, rich in sodium, and contained low concentrations of potassium and total protein. These results are consistent with the previous suggestion that PGF 2α produces salivation by liberation of endogenous acetylcholine.

Chronic decentralization prevents α-receptor mediated regulation of noradrenaline release in the field stimulated rat iris

Chronic decentralization prevents α-receptor mediated regulation of noradrenaline release in the field stimulated rat iris

Sensitivity of the nictitating membrane of the cat to succinylcholine after decentralization and denervation.

Seven days after decentralization or denervation, the nictitating membrane of the cat becomes supersensitive to succinylcholine. The supersensitivity to succinylcholine is of a moderate degree (2-3 fold) and there is little difference between the supersensitivity induced by decentralization or denervation. In this respect, it is similar to the decentralization type of supersensitivity observed for other agonists which are not taken up by the adrenergic nerve endings (e.g. acetylcholine and methoxamine). Since succinyloholine causes an apparent contraction of the nictitating membrane through its action on the extraocular muscle and no effect on the nictitating membrane itself, it is concluded that both chronic decentralization and denervation produced a decentralization type supersensitivity in the extraocular muscles. The results suggest that supersensitivity in the extraocular muscles may contribute significantly to the decentralization supersensitivity of the nictitating membrane of the cat, in vivo, especially for those agonists which cause contractions of both the nictitating membrane and the extraocular muscle.

Pharmacological studies on the hypogastric ganglion of the rat and guinea-pig.

1. Preparations were developed whereby the hypogastric ganglion of the rat or guinea-pig was perfused through its vasculature with saline solutions. Drugs were injected into the perfusion stream, and their effects were indicated by contractions of the vas deferens. The base of this organ could be ligated to prevent the drugs reaching the smooth muscle via the blood vessels. For comparison, experiments were also performed on fully isolated preparations of the rat and guinea-pig hypogastric nerve-vas deferens, where the vas deferens was held in an inner bath, so that drugs added to the outer bath could act only on the ganglion. Attempts were made to demonstrate non-nicotinic receptors in these preparations.2. It was shown that the perfused hypogastric ganglion of the guinea-pig would respond repeatedly to several nicotinic stimulants, though autodesensitization eventually occurred. The fully isolated preparation behaved similarly, but desensitized much more rapidly. In contrast, the rat ganglion, either perfused or fully isolated, was remarkably insensitive to nicotinic stimulant drugs.3. Neither species responded well to non-nicotinic stimulants; that from the guinea-pig gave small contractions to methacholine in about 33% of cases, but did not respond to (4-m-chlorophenyl-carbamoyloxy)-2-butynyl trimethylammonium chloride (McN-A-343). With the rat, the situation was opposite.4. The guinea-pig ganglion did not become more sensitive to non-nicotinic stimulants after some treatments known to sensitize the cat superior cervical ganglion. These include preganglionic tetanization, chronic decentralization, and removal of all potassium. Sensitization did occur, however, in the presence of physostigmine, after tachyphylaxis to dimethyl phenyl piperazinium iodide (DMPP) had developed, and when the preparation was perfused with a suspension of washed erythrocytes.5. It is concluded that the responses of sympathetic ganglia vary from one species to another, and according to whether the organs are perfused or fully isolated.

Monoamine oxidase activity of the cat nictitating membrane and superior cervical ganglion under various experimental conditions

Monoamine oxidase activity of the cat nictitating membrane and superior cervical ganglion was studied using a fluorimetric technique after chronic decentralization and denervation and pretreatment with reserpine and pheniprazine. Catecholamine content of the cat nictitating membrane and superior cervical ganglion was measured by using a fluorimetric technique after reserpine and pheniprazine pretreatments. Monoamine oxidase activity of the nictitating membrane was reduced in all procedures studied, while enzyme activity of the superior cervical ganglion was unchanged by sectioning of the preganglionic fiber (decentralization). Catecholamine content of the nictitating membrane was unchanged by pheniprazine treatment, while that of the superior cervical ganglion increased. Results are discussed in terms of the possible differences in the turnover rates of norepinephrine in the nictitating membrane and superior cervical ganglion. The effect of monoamine oxidase inhibition on reserpineinduced depletion of catecholamines in the cat nictitating membrane and in rat heart was also studied. The Catecholamine content of the cat nictitating membrane 18–24 hr after treatment with reserpine or with pheniprazine plus reserpine was reduced to the same extent. Similar results were obtained with the rat heart. The data support the concept that monoamine oxidase inhibition does not prevent the reserpine-induced release of catecholamines.