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PubMed1976

Effect of (+) amphetamine on monoamine synthesis and metabolism after axotomy in rat forebrain.

(+)Amphetamine is known to produce feedback inhibition of catecholamine-containing neurons in the central nervous system due to its indirect receptor stimulating properties. This feedback control may involve postsynaptic receptors and neuronal loops or presynaptic receptors and may be restricted to the catecholaminergic terminal system. In order to study the effect of (+)amphetamine on catecholamine synthesis and metabolism in the terminal system changes in impulse flow were eliminated by cutting the ascending monaminergic axons. Axotomy of the ascending monominergic fibers by means of a complete transverse cerebral hemisection resulted in a 3-fold increase in Dopa formation in the lesioned forebrain during 30 min after inhibition of the aromatic amino acid decarboxylase with 3-hydroxybenzylhydrazine HCl, 100 mg/kg i.p. (+)-Amphetamine sulfate, 10 mg/kg i.p. antagonized the hemisection-induced increase in Dopa formation and reduced the formation of 5-hydroxytryptophan. Pretreatment with haloperidol, 5 mg/kg i.p. failed to counteract the effect of (+)amphetamine. In the intact forebrain the stimulation of Dopa accumulation was more than additive after combined treatment with haloperidol and (+)amphetamine. Hemitransection retarded the disappearance of dopamine and noradrenaline after administration of alpha-methyl-p-tyrosine methylester HCl,300 mg/kg. (+)-Amphetamine, 10 mg/kg accelerated the utilization of dopamine on the lesioned side. Hemitransection reduced the formation of 3-methoxytyramine during 1 h after pargyline, 75 mg/kg i.p. After (+)amphetamine 3-methoxytyramine formation in the intact forebrain was 3 times higher than in the lesioned forebrain. The action of (+)amphetamine on dopamine synthesis and release appears to be dependent on the firing rate in dopamine neurons.

5-Hydroxytryptophan↗
PubMed1977

Catecholamine synthesis in rat brain after axotomy: interaction between apomorphine and haloperidol.

Axotomy of the ascending monoaminergic fibers by means of a complete cerebral hemitransection stimulated the formation of dopa during 30 min after inhibition of the aromatic amino acid decarboxylase with 3-hydroxybenzylhydrazine HCl, 100 mg/kg i.p., in c. striatum and the dopamine-rich part of the limbic system. Apomorphine, 0.5 mg/kg i.p., antagonized the accumulation of dopa not only on the intact but also on the lesioned side. Haloperidol, 2 mg/kg i.p., stimulated dopa accumulation on the intact side but could not further stimulate the increase in dopa caused by transection. When both drugs were given together, the inhibitory effect of apomorphine was fully counteracted by haloperidol on both sides. In the predominantly noradrenaline-innervated occipito-temporal cortex dopa formation was slightly higher on the lesioned than on the intact side and was not markedly influenced by apomorphine. In the rest of the hemispheres the apomorphine-induced decrease in dopa formation was more pronounced on the intact than on the lesioned side and was fully antagonized by haloperidol. The dopamine concentration was slightly higher in the lesioned c. striatum as compared to the intact side irrespective of the drugs administered. In c. striatum and the limbic system haloperidol caused a decrease in dopamine on the intact side which was not antagonized by additional treatment with apomorphine. Hemitransection caused a decrease in noradrenaline especially in the hemisphere portion. Neither apomorphine nor haloperidol or both drugs in combination changed the latter effect. In general, the tyrosine concentration tended to be higher on the lesioned than on the intact side in all brain structures investigated. The data support the view that a local receptor-mediated feedback mechanism exists which is controlling dopamine synthesis even in the absence of impulse flow.

Animals↗
PubMed1975

Effects of drugs and axotomy on acetylcholine levels in central cholinergic neurons.

Administration of cholinergic nuscarinic agonists either did not alter, or increased hippocampal Ach levels, while antagonists lowered the levels. As observed previously, placement of lesions in the medial septal area resulted in a rise in hippocampal Ach levels in the first thirty minutes. Agonist drugs administered immediately before lesion, further increased the post-lesion rise in Ach levels. With antagonists, inconsistent results were obtained in that atropine blocked the post-lesion rise, while scopolamine and quinuclidinyl benzilate (QNB) potentiated the post-lesion rise. These results suggest that there may be receptor-mediated effects on Ach synthesis or release after axotomy.

Acetylcholine↗
PubMed1976

Stereology, a complement to experimental neuropathology. I. Introduction into stereology. II. Ultrastructural-morphometric investigations (baseline data, axotomy) on the superior cervical ganglion of the rat.

This paper first gives a short introduction into the principles of stereology. It shows then its actual application to the assessment of ultrastructural-morphometric data of the normal superior cervical ganglion of the rat (base-line data) and after axotomy. In the early phase after axon transsection the volumetric composition of the superior cervical ganglionic neuron remains constant. Only the volume density of the lysosomal forms is significantly increased from 0.9--3.2%. Ultrastructural morphometric analysis of the rough endoplasmic reticulum does not provide any information on quantitative changes underlying the phenomenon of central chromatolysis.

Animals↗
PubMed1988

Axotomy-induced ornithine decarboxylase activity in the mouse dorsal root ganglion is inhibited by the vinca alkaloids.

Vinca alkaloids were used to study the role of retrograde axon transport (RT) in activating neuron perikaryal repair response to nerve transection. Mouse lumbar dorsal root ganglia (DRG) (L4-L6) were excised 48 hours after unilateral transection of the sciatic nerve and ornithine decarboxylase (ODC) activity determined. ODC activity in DRG ipsilateral to nerve transection was increased 10-20 fold over contralateral values. Typical ODC activities in ipsilateral and contralateral DRG samples were 6.18 +/- 1.4 and 0.31 +/- 0.09 pmol 14CO2 released/h/3DRG, respectively. Systemic administration of single doses of either vincristine (1 mg/kg) or vinblastine (5 mg/kg) immediately prior to axotomy attenuated ODC induction in ipsilateral DRG by 39% and 47%, respectively. A direct inhibition of ODC activity in the DRG appears unlikely since only high concentrations of vinblastine (0.5-1.0 mM) were able to inhibit ODC activity in vitro. We suggest vinca alkaloids inhibit ODC induction as a consequence of disrupting retrograde axonal transport. Interruption of this intracellular communication mechanism may be etiologically linked to the the distal axon degeneration which follows repetitive exposure to vinca alkaloids and other agents that induce toxic axonal neuropathy.

Animals↗
PubMed1979

Failure of anticholinergic drugs to antagonize the increase in dopamine seen after gammahydroxybutyric acid and axotomy.

The increase in dopamine (DA) seen either 30 or 90 min after injection of gammahydroxybutyric acid or 90 min after axotomy of the nigrostriatal DA-fibers was not affected by i.p. injections of either atropine sulfate or atropine methyl nitrate or benztropine. These increases in DA are most probably due to feedback-mechanisms which do not involve cholinergic neurons.

Animals↗
PubMed1985

Intra- and extraneuronal monoamineoxidase-A and -B activities after central axotomy (hemisection) on rats.

Hemitransection of the left side of rat brain results in a selective increase (40%) in the activity of MAO-B in the left side striatum, as compared to the right, unoperated side. This increase is shown to be the result of an increase in the activity of extraneuronal MAO-B using a "low substrate concentration method" with dopamine as substrate. This result is compatible with the hypothesis, that in certain degenerative processes such as aging, Alzheimer's disease, Huntington's disease and axotomy there is a stimulated growth of extraneuronal cells, which are relatively rich in MAO-B activity.

Aging↗
PubMed1989

JONES ganglioside expression on retinal glia increases after axotomy.

The monoclonal antibody JONES recognizes a small group of gangliosides. Within the visual system of the adult rat JONES gangliosides are found only in those regions where neuronal regeneration is known to occur, i.e. the unmyelinated retina and optic nerve head. A transient increase in JONES ganglioside expression could be observed in the retinae of adult rats after optic nerve axotomy or in the retinae of animals receiving autologous sciatic nerve grafts. The highest levels of gangliosides identified by JONES were observed five days after surgery--contemporaneous with the maximum regenerative response of the adult rat retina after crush lesions. By double-labelling experiments using antibodies against glial cell markers--glial fibrillary acidic protein, S-100 and vimentin in conjunction with JONES-JONES gangliosides were shown to be expressed on retinal glial cells in vivo and in vitro. Elimination of glial cells by intraocular injection of aminoadipic acid abolished JONES labelling in vivo.

2-Aminoadipic Acid↗
PubMed1988

Delayed astrocyte reaction following facial nerve axotomy.

Transection of the facial nerve causes a rapid increase of glial fibrillary acidic protein in reactive astrocytes and a proliferation of local microglial cells. The latter is associated with a detachment of synaptic terminals from the regenerating motor neurons. About 3 weeks following axotomy the reactive astrocytes begin to form thin, sheet-like lamellar processes which cover virtually all neuronal surfaces. A high 5'-nucleotidase enzymic activity can be demonstrated in the plasma membrane of these thin cell processes. Subsequently, the lamellar processes become arranged in stacks which persist for several months and thus isolate the regenerating motor neurons from their afferent synaptic input. It is speculated that the process may protect the motor neurons during regeneration.

5'-Nucleotidase↗
PubMed1996

Axotomy-induced loss of m2 muscarinic receptor mRNA in the rat facial motor nucleus precedes a decrease in concentration of muscarinic receptors.

The abundance of muscarinic receptors and m2 muscarinic receptor mRNA in the facial nuclei of rats was evaluated by autoradiographic procedures at various times up to 14 days after transection of the right facial nerve. Receptors were labelled by in vitro incubation of brain sections with L-[3H]quinuclidinyl benzilate, while in situ hybridization with a 35S-labelled oligonucleotide was used to identify m2 muscarinic receptor mRNA in neighbouring sections. The right and left facial nuclei of non-operated control rats appeared equivalent in abundance of muscarinic receptors (359 +/- 8 versus 376 +/- 9 fmol per mg tissue, n = 5) and the presence of m2 mRNA. Axotomy had no effect on the concentration of receptors in the contralateral facial nucleus but caused a gradual loss of receptors from the ipsilateral side. No change was detected at 1 day after nerve transection, but a 23% decrease relative to the contralateral facial nucleus had occurred by 3 days. A maximum decrease of 51% was achieved by 1 week after nerve transection. By comparison, m2 mRNA was nearly eliminated from the ipsilateral facial nucleus at 1 day post-taxonomy and remained depleted for the duration of study. Previous work has established that no significant loss of motoneurons occurs within this period. Accordingly, it is postulated that axonal injury inhibits transcription of the m2 muscarinic receptor gene, resulting in a later decrease in muscarinic receptor protein expression.

Animals↗
PubMed1975

The perineuronal glial reaction after axotomy.

The perineuronal glial reaction after axotomy of the facial nerve was examined in adult mice and rats and in newborn rabbits. The facial nerve was damaged in two ways: by crush lesions, which were followed by complete neuronal regeneration, and by transection (in mice) or evulsion (in rats and rabbits), which caused extensive nerve cell disintegration. After nerve lesions which caused irreversible damage the microglial cells encircled the degenerating neurons and ultimately phagocytosed them. After crush lesions there were great species variations in the glial reaction: the neurons of rats and rabbits showed considerable and reversible separation of the synaptic terminals by glial cells, while mice showed no significant synaptic separation. It is suggested that the main function of the microglial cells may be to serve as potential phagocytes for disintegrating neurons, and that the reversible glial changes around regenerating neurons possibly represent abortive glial reactions.

Age Factors↗
PubMed1978

alpha-Bungarotoxin-acetylcholine receptors in the chick ciliary ganglion: effects of deafferentation and axotomy.

alpha-Bungarotoxin (alpha-BuTX) binds in a saturable and practically irreversible fashion to membrane-associated receptors in the ciliary ganglion of the adult chick. The binding of toxin to receptors is competitively inhibited by nicotinic cholinergic ligands, and for these properties the receptors are regarded as acetylcholine receptors of the nicotinic type (alpha-buTX-AChRs). The rate constant of association (K1) and dissociation (K-1) of the toxin-receptor reaction has been estimated to be K1 = 7.4 x 104 M(-1) sec(-1) and K-1 = 9.6 X 10(-6) sec(-1), respectively. Light autoradiography shows that most, if not all, the receptors are related to surface membrane, probably to synaptic areas of both choroid and ciliary neurons. The choroid neurons contain more receptors than the ciliary ones. A single chick ciliary ganglion binds specifically 47 fmole of alpha-BuTX in situ corresponding to 2.83 x 1010 alpha-BuTX-AChRs/ganglion. No changes in number and distribution of the toxin receptors occur following preganglionic denervation. Conversely, postganglionic axotomy causes a rapid disappearance of the receptors in situ. Since binding experiments in vitro revealed a partial, instead of a total, loss of the receptors, it is suggested that the disappearance of the receptors in situ includes both a partial loss of the original receptors and the masking of the residual ones.

Acetylcholine↗
PubMed1979

Regeneration of normal terminal innervation patterns by central noradrenergic neurons after 5,7-dihydroxytryptamine-induced axotomy in the adult rat.

The regeneration of central adrenergic axons has been followed between 5 days and 18 months after 5,7-dihydroxytryptamine(5,7-DHT)-induced axotomy in the adult rat, using fluorescence histochemistry in combination with noradrenaline (NA) determinations and [3H]NA uptake measurements. The axonal and terminal degeneration caused by the 5,7-DHT treatment (150 micrograms intraventricularly) was, by 1--2 weeks after injection, accompanied by a 70% reduction of NA in the forebrain and 30% reduction in the brain stem, and by 43--85% reductions in the [3H]NA uptake capacity in various regions of the brain and spinal cord. Signs of sprouting of the drug-lesioned axons were evident along the terminal axon segments at 5 days after treatment. The sprouts increased rapidly in length and number during the subsequent weeks and by 2--6 months after injection new NA terminal systems of relatively normal density and distribution had been re-established in many initially denervated regions. In parallel there was a recovery of endogenous NA and [3H]NA uptake to the pre-injection levels in the brain, and to levels 50--75% of normal in the cervical and thoracic spinal cord. Four successive phases of the regeneration process are distinguished: (1) primary sprouting from the lesioned NA axon stumps, occurring within the first week after treatment; (2) seemingly random growth and proliferation of the newly formed sprouts during the second and third weeks; (3) directed, forward growth of some of the sprouts leading to a partial restoration of the original fibre paths, branching patterns and terminal networks within 3--6 months; (4) a concomitant removal of at least part of the abnormally directed sprouts. Although the original fibre architecture was quite accurately restored in many areas the regeneration was not always correct. Hyperinnervation patterns and abnormal terminal arrangements were often formed, and in the spinal cord the down-growth of the regenerating axons occurred predominantly along a route that is inconspicuous in the normal rat. It is concluded that at least certain types of central neurons regenerate very efficiently provided the conditions are favourable, and that under such conditions axonal regeneration in the mammalian CNS is subjected to regulatory mechanisms that can be very precise. The results provide evidence that the adult mammalian CNS possesses mechanisms for axonal guidance which allow the accurate regeneration of lesioned axonal tracts and branching patterns, as well as mechanisms of recognition making possible the re-establishment of the original terminal connections.

5,7-Dihydroxytryptamine↗
PubMed1979

Retinal ganglion cell response to axotomy and nerve growth factor antiserum in the regenerating visual system of the newt (Notophthalmus viridescens): an ultrastructural morphometric analysis.

One 3.0 mg dose of the nerve growth factor antiserum (anti-NGF) injected into the vitreous chamber of the eye at the time of optic nerve transection elicits significant changes in the normal newt (Notophthalmus viridescens) retinal ganglion cell body response to axotomy at 7 and 14 days postaxotomy (DPA). Light microscopic observations indicate that anti-NGF treatment significantly reduces the per cent of retinal ganglion cells demonstrating nuclear chromatin reactivity (ie., homogeneous to a more heterogeneous state) from 33.36 +/- 3.02 to 22.82 +/- 2.98%. In addition, the per cent of retinal ganglion cells demonstrating prominent nucleoli is dramatically decreased from 32.08 +/- 1.64 to 18.20 +/- 1.79% at 7 DPA. It is also important to note that the number of prominent nucleoli in the 7 DPA group is reduced to such an extent by anti-NGF treatment that the value is not significantly different from that of intact controls. Intact controls will routinely exhibit approximately half the number of prominent nucleoli that are normal for the untreated 7 DPA group. A definite dose-response relationship can be shown to exist between the per cent of nuclear reactive ganglion cells demonstrating prominent nucleoli and various anti-NGF concentrations at 14 DPA. There does not appear to be a dose-response relationship between various anti-NGF concentrations and the per cent of retinal ganglion cells demonstrating nuclear reactivity at 14 DPA. However, the degree of nuclear chromatin reactivity appears to be less at the higher anti-NGF concentrations (ie., greater than or equal to 3.0 mg/eye) at 14 DPA. Electron microscopic morphometric analysis reveals that anti-NGF treatment significantly reduces the cell perikaryal area at 7 and 14 DPA while the nuclear area remains unchanged. Therefore, there is a significant decrease in the cytoplasmic/nuclear ratios at both 7 and 14 DPA in response to anti-NGF treatment which appears more pronounced by 14 DPA. Anti-NGF treatment also significantly reduces the mitochondrial and nucleolar densities, as well as the nucleolar areas of cells at 7 and 14 DPA. There are no significant changes in Golgi field densities in response to anti-NGF treatment.

Animals↗
PubMed1981

Axotomy-induced changes in cell structure and membrane excitability are sustained in a vertebrate central neuron.

The retrograde reactions of the goldfish Mauthner neuron to axotomy 8-10 mm caudal to its soma are detectable within a few weeks and persist for more than 200 days. Morphological changes include chromatolysis, reflecting a redistribution of cytoplasmic ribosomes, and infolding of the nuclear membrane. At the time, the normally inexcitable soma-dendritic membrane becomes capable of impulse initiation; this induced excitability also persists for at least 200 days.

Action Potentials↗
PubMed1983

Granular coated vesicles in the goldfish Mauthner cell following axotomy.

Axotomy of the goldfish Mauthner cell induces a marked increase in the occurrence of granular coated vesicles in close association with axosomatic synapses. This phenomenon, which persists for over 200 days, is discussed in relation to other morphological and physiological changes which occur over the same time period.

Animals↗
PubMed1984

Deafferentation and axotomy of neurons in cat striate cortex: time course of changes in binocularity following corpus callosum transection.

Single neurons were recorded in the callosal terminal and cell zones of area 17 in the cat to assess the time course of changes in the proportion of binocular neurons produced by corpus callosum transection. The callosal terminal zone contains all the degenerating terminals in area 17 after corpus callosum transection. The callosal cell zone contains all the cells in area 17 which contribute axons to the corpus callosum. The cell zone is larger than, and partially overlaps, the callosal terminal zone. After corpus callosum transection there was an initial change in ocular dominance of neurons in both callosal zones. This initial change was followed by a reduction in the proportion of binocular neurons in both zones. This reduction became maximal 2-4 weeks after transection. In the callosal terminal zone, binocularity did not recover even at the longest postoperative periods examined (31-42 weeks). In the part of the callosal cell zone outside of the callosal terminal zone, the proportion of binocular neurons began to recover after 5 weeks and was at normal levels at the longest survival periods studied. Corpus callosum transection deafferents and axotomizes cells in the callosal terminal zone and, since central neurons do not regenerate their long-ranging axons, the combined effects of deafferentation and axotomy in this zone are permanent. The callosal cell zone outside of the callosal terminal zone contains axotomized cells and no degenerating terminals following transection. The recovery of binocularity in this region may be attributed to the transient changes which axotomized cells undergo. The zone which contains no callosal cells or terminals is unaffected by transection of the corpus callosum.

Animals↗
PubMed1984

Response to axotomy of an identified leech neuron, in vivo and in culture.

Membrane properties of identified leech neurons with non-spiking somata were studied after axotomy. Two distinct procedures were used: the section of ganglionic roots in vivo and the isolation of cell somata in culture. The results indicated that axotomized neurons progressively developed the excitability of somatic membrane, both in vivo and in culture.

Animals↗