Morphology and spectral sensitivity of long visual fibers and lamina monopolar cells in the butterfly Papilio xuthus

Extensive analysis of the flower-visiting behavior of a butterfly, Papilio xuthus, has indicated complex interaction between chromatic, achromatic, and motion cues. Their eyes are spectrally rich with six classes of photoreceptors, respectively sensitive in the ultraviolet, violet, blue, green, red, and broad-band wavelength regions. Here, we studied the anatomy and physiology of photoreceptors and second-order neurons of P. xuthus, focusing on their spectral sensitivities and projection terminals to address where the early visual integration takes place. We thus found the ultraviolet, violet, and blue photoreceptors and all second-order neurons terminate in the distal region of the second optic ganglion, the medulla. We identified five types of second-order neurons based on the arborization in the first optic ganglion, the lamina, and the shape of the medulla terminals. Their spectral sensitivity is independent of the morphological types but reflects the combination of pre-synaptic photoreceptors. The results indicate that the distal medulla is the most plausible region for early visual integration.     

Synaptic pathology and cell death in the cerebellum in Creutzfeldt-Jakob disease

Prion protein (PrP(c)) is a cell membrane glycoprotein particularly abundant in the synapses. Prion diseases are characterized by the replacement of the normal PrPc by a protease-resistant, sheet-containing isoform (PrP(CJD), PrP(Sc), PrP(BSE)) that is pathogenic. Creutzfeldt-Jakob disease (CJD) in humans, scrapie (Sc) in sheep and goats, and bovine spongiform encephalopathy (BSE) in cattle are typical prion diseases. Classical CJD can be presented as sporadic, infectious or familial, whereas the new variant of CJD (nvCJD) is considered a BSE-derived human disease. Spongiform degeneration, glial proliferation, involving astrocytes and microglia, neuron loss and abnormal PrP deposition are the main neuopathological findings in most human and animal prion diseases. Yet recent data point to synapses as principal targets of abnormal PrP deposition. Loss of synapses is an early abnormality in experimental scrapie. Decreased expression of crucial proteins linked to exocytosis and neurotransmission, covering synaptophysin, synaptosomal-associated protein of 25,000 mol wt (SNAP-25), synapsins, syntaxins and Rab3a occurs in the cerebral cortex and cerebellum in sporadic CJD. Moreover, impairment of glomerular synapses and attenuation of parallel fiber pre-synaptic terminals on Purkinje cell dendrites is a cardinal consequence of abnormal PrP metabolism in CJD. Accumulation of synaptic proteins in the soma and axonal torpedoes of Purkinje cells suggests additional impairment of axonal transport. Increase in nuclear DNA vulnerability leading to augmented numbers of cells bearing nuclear DNA fragments is a common feature in the brains of humans affected by prion diseases examined at post-mortem, but also in archival biopsy samples processed with the method of in situ end-labeling of nuclear DNA fragmentation. This form of cell death is reminiscent of apoptosis found in experimental scrapie in rodents. It is not clear that all forms of cell death in human and animal prion diseases are due to apoptosis. Yet new observations have shown cleaved (active) caspase-3 (17 kDa), a main executioner of apoptosis, expressed in scattered cells in the brains of mice with experimental scrapie and in the cerebellum of patients with sporadic CJD. Together, these data suggest activation of the caspase pathway of apoptosis in human and animal prion diseases.     

Striatal glutamatergic function: Modifications following specific lesions

The effects of specific lesions of the striatum: (a) hemidecortication; (b) striatal injection of(±) ibotenate; and (c) 6-hydroxydopamine injections into the substantia nigra, were investigated on specific [³H]glutamate binding to striatal membranes. One month after decortication, there was a substantial reduction of calcium-dependent, stimulated glutamate release from striatal slices, indicating effective loss of glutamatergic fibres. Striatal glutamate binding increased by approximately 30% and this supersensitivity could be attributed solely to an increased receptor density. Ibotenate lesions which destroy target neurones for the glutamatergic fibres (sparing terminals), reduced glutamate binding in the striatum, as did nigral 6-OHDA lesions which delete striatal dopaminergic terminals. This finding supports the concept of there being glutamate receptors on pre-synaptic dopamine terminals in the striatum, involved in regulation of dopamine release. 6-OHDA lesions also result in a supersensitivity of the dopamine receptors localized on the cortico-striatal afferent terminals, as evidenced by the enhanced ability of dopamine to inhibit the K⁺-evoked, calcium-dependent release of endogenous striatal glutamate.     

An electron microscopic study of inclusion bodies in synaptic terminals of scrapie-infected animals

Summary Inclusion bodies consisting of vesicles of about 25 nm diameter and occurring in the synaptic terminals of scrapie-infected animals have been described by a number of people. In the present study these inclusion bodies were looked for in the neocortex, hippocampus and corpus callosum in a variety of strains of mice (C3H, LM, RIII, IM, VL) infected with different strains of scrapie agent (22C, 79A, ME7, 87V) after intracerebral inoculation. In plaque-bearing models of scrapie, terminals containing synaptic inclusion bodies were frequently found surrounding the amyloid plaque cores in the neocortex but not in the corpus callosum. In non-plaque-bearing models, terminals containing synaptic inclusion bodies were found in the neuropil of the neocortex and hippocampus. For all models, these bodies were either presynaptic or postsynaptic but were not, as a rule, found on both sides of the same synapse. Fibrillary material was frequently seen in the postsynaptic terminals containing the inclusion bodies in both the plaque- and non-plaque-bearing models. On one occasion fibrillary material was seen, together with the inclusion bodies, in a neuron cell body. Inclusion bodies were also seen in the neocortex of hamsters infected with the 263K strain of scrapie agent and a Cheviot sheep infected with the ME7 strain of agent. The inclusion bodies and the fibrillary material were thought to be derived from the breakdown of neurotubules.     

Dysfunction of the fusion of pre-synaptic plasma membranes and synaptic vesicles caused by oxidative stress, and its prevention by vitamin E

To define whether hyperoxia induces the dysfunction of membrane fusion between synaptic vesicles with pre-synaptic plasma membranes in the nerve terminals, and whether vitamin E prevents this abnormal event, we investigated the influence of hyperoxia on the fusion ability of isolated synaptic vesicles and the inside-out type pre-synaptic plasma membrane vesicles from rat brain using the fluorescence tracing method. The membrane fusion ability of both membranes from rats subjected to hyperoxia was markedly decreased compared with the membranes from a normal rat. Rats subjected to hyperoxia in the form of oxidative stress showed significant increases in the levels of thiobarbituric acid reactive substances (TBARS), conjugated dienes, and protein carbonyl moieties in both synaptic vesicles and pre-synaptic plasma membranes. When rats were supplemented with vitamin E, these abnormalities were inhibited even when rats were subjected to hyperoxia.     

Scrapie in the rat: an electron-microscope study

Summary Both well formed amyloid bodies showing clear concentric lamination and smaller masses of amyloid material have been found in the brains of rats suffering from scrapie. Amyloid appears to form within astrocyte processes and glial cell bodies, as well as shrunken nerve cells. Rarely, it was present in degenerate axis cylinders. The individual fibrils which make up amyloid deposits appeared to have a spiral constitution, and deposits large enough to be seen in the light microscope were commonly strikingly symmetrically located.

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Zusammenfassung In den Gehirnen von Scrapie-kranken Ratten wurden wohlgeformte Amyloidkörperchen mit deutlicher konzentrischer Schichtung und kleinere amyloide Massen gefunden. Amyloid scheint sich in Astrocytenfortsätzen und Gliazellkörpern sowie in geschrumpften Nervenzellen zu bilden. Selten ist es in degenerierten Achsenzylindern vorhanden. Die Einzelfibrillen, welche die Amyloidablagerungen aufbauen, scheinen spiralige Form zu haben. Die großen im Lichtmikroskop sichtbaren Ablagerungen sind gewöhnlich auffallend symmetrisch im Gehirn lokalisiert.

     

Cytoarchitecture,fiber connections,and ultrastructure of nucleus isthmi in a teleost (Navodon modestus) with a special reference to degenerating isthmic afferents from optic tectum and nucleus pretectalis

Cytoarchitecture and fiber connections of the nucleus isthmi in a teleost (Navodon modestus) were studied by means of Nissl, Bodian, toluidine blue, Golgi, and Fink-Heimer methods. Synaptic terminals were classified by the ultrastructural characteristics, and their origins were determined by electron microscopic degeneration experiments. The nucleus isthmi is composed of an outer cellular area or shell and an inner noncellular area or core. The shell covers anterior, dorsal, and ventral aspects of the core. The cell bodies in the shell are oval (15 × 20 μm) with an anteroposterior long axis, and have many somatic spines. Spines are also seen on the initial segment of the axon. Primary dendrites extend postermedially and branch out in the core. The core contains thin and thick myelinated fibers, which originate in the optic tectun and in the nucleus pretectalis, respectively. At least two types of axons terminal were distinguished in the nucleus isthmi: S type, containing spherical vesciles, and F type, containing flattened vesicles. S terminals are derived from thin myelinated fibers and are only seen in the core where they form asymmetric synapses with dendrites. Frequently a portion of the S terminal membrane near the usual synaptic cleft is in close apposition with the membrane of an adjacent small dendrite or spine. F terminals, which derived from thick myelinated fibers, make symmetric synaptic contacts with both cell bodies in the shell and dendrites in the core. S terminals degenerate after ipsilateral ablation of the optic tectum, whereas F terminals degenerate after destruction of the nucleus pretectalis.     

In vivo toxicity of prion protein in murine scrapie: ultrastructural and immunogold studies

Prion protein (PrP) is a cell surface, host coded, sialoglycoprotein which accumulates in excess in scrapie, Creutzfeldt‐Jakob disease, bovine spongiform encephalopathy and other transmissible spongiform encephalopathies. Infection of mice with the 87 V or ME7 scrapie strains results in distinctive and very different light microscopical patterns of vacuolation and disease specific PrP accumulation. In both of these scrapie strains immunogold electron microscopy was used to locate PrP to the plasmalemma of neurons from where it was released into the neuropil. Initial PrP accumulation around neurons and in early plaques lacking amyloid fibrils was generally not associated with morphological changes either of the neuron or dendrite releasing the PrP or in the adjacent neuropil in which excess PrP accumulated. However, accumulation of pre‐amyloid PrP in some brain areas was associated with specific degeneration of dendritic spines and axon terminals. Initial PrP aggregation into fibrils was also associated with tissue damage with both ME7 and 87 V plaques and diffuse accumulations. Tissue damage associated with fibrillogenesis was localized and would not be expected to have clinical significance. We conclude that pre‐amyloid PrP release and accumulation is not invariably toxic, either to the neuron releasing PrP or to the neuropil into which it is released. However, axon terminal degeneration and dendritic spine loss in some neuroanatomical areas may be indicative of specific PrP toxicity and may be the main cause of neurological dysfunction in murine scrapie.     

Goldfish bipolar cells and axon terminal patterns: A Golgi study

The morphology and axon terminal arrangement of Golgi stained goldfish bipolar cells were examined to understand better the organization of bipolar cells in the inner plexiform layer (IPL) of the retina. Fifteen morphological bipolar cell types were identified, representing two major cell classes: mixed input cells that receive input from rod and cone photoreceptors, and cone bipolar cells that receive input from cones only. Mixed input bipolar cells comprised six types, including two new types, characterized by large somas and terminals. The terminals of mixed input bipolar cells terminated strictly within sublamina a or b of the IPL. Cone bipolar cells comprised nine subtypes, including seven new types, characterized by small somas and from one to four small terminal bulbs along the length of the axon, each having a characteristic termination depth in the IPL. The cone bipolar cell system had a complex multilaminar organization of terminals in the IPL, but maintained a high degree of anatomical symmetry about sublamina a and b. Cone bipolar cells could be divided into three groups: cells terminating within sublamina a and having an anatomically symmetrical counterpart terminating in sublamina b; cells with anatomically similar terminals in both sublamina a and b; and cells having no anatomically symmetrical counterpart or having anatomically dissimilar terminals in sublamina a and b. Based on bipolar cell terminal arrangement, we suggest that each bipolar cell type probably has a unique set of synaptic targets in the IPL, and that several bipolar cell types may be involved in functionally equivalent circuits at more than one level in the IPL. © 1993 Wiley-Liss, Inc.     

Neurobiologieal Studies of Experimental Diphenylhydantoin Intoxication–III. Electron Microscopic Studies on Development and Disintegration Mechanism of Altered Axon Terminals and Synaptic Endings in Rat Cerebellum with Chronic Diphenylhydantoin Intoxication

Abstract: The processes of development and disintegration of axonal spheroids were electron microscopically studied in the rat cerebellum with chronic diphenylhydantoin intoxication. According to the severity and character of membrane accumulation, the whole course ranging from development to disintegration of altered axon terminals and synaptic endings in the DPH-in-toxicated rat cerebellum was classified into the following four stages–initial, moderate, advanced and terminal. The initial stage was characterized by the appearance of a small number of interconnected tubules 150 to 350 A in diameter in non-enlarged axon terminals and synaptic endings. Usually these tubular structures tended to congregate in a certain part of axoplasm so that there were no intimate relationships between them and ordinary cell organelles. The moderate stage was characterized by an increased number of interconnected tubules in slightly or moderately swollen axon terminals and synaptic endings. The advanced stage was characterized by an extraordinary number of interconnected tubules in extremely highly swollen axon terminals and synaptic endings. Membranous scrolls and/or membranous strands separated by a cleft-like space were also found in an association with interconnected tubules so that the morphological organization of spheroids in the rat cerebellum with chronic DPH intoxication was very analogous to those of infantile neuroaxonal dystrophy. The terminal stage was characterized by the following three axonal events, i.e., rarefaction and coagulation necroses, and phagocytosis of spheroids by glial elements, presumably astrocytic in origin. The formation and fate of such axonal spheroids have not as yet been shown and discussed by electron microscopists. Thus the present paper was the first to reveal the electron microscopic observations suggestive of the details of development and disintegration mechanisms of spheroids by means of animal experimentations.     

AMYLOID PLAQUES IN THE BRAINS OF MICE INFECTED WITH SCRAPIE: MORPHOLOGICAL VARIATION AND STAINING PROPERTIES

Amyloid plaques in the brains of mice infected with scrapie: morphological variation and staining properties
Cerebral amyloid deposits predominantly in the form of plaques are associated with experimental scrapie produced by particular agents in inbred mice. In this paper the staining properties and variation in the morphology of these deposits are described. At the light microscope level a discretionary classification into six types is made: shadowy plaques; amorphous plaques; stellate plaques; giant plaques; diffuse amyloid deposits; and perivascular amyloid deposits. It is shown that Masson's trichrome technique provides the most efficient staining method for identifying cerebral amyloid of all these types. A preliminary ultrastructural examination of stellate plaques confirms the presence of amyloid on the basis of characteristic fibrils and demonstrates that microglia and distended neurites are involved in the structure of the plaques. The similarities and differences between cerebral amyloid in scrapie and other forms of amyloid deposits in the brain, particularly kuru plaques and senile plaques, are discussed.     

Comparative distribution of NK1, NK2, and NK3 receptors in the rat brainstem auditory nuclei

While the distribution of substance P in the auditory system is well illustrated, the localization of its receptors has not yet been documented. The goal of our study was to characterize the distribution of the tachykinin receptors NK1-R, NK2-R and NK3-R in the brainstem auditory nuclei of the adult rat using immunohistochemical techniques. The immunoreactivity of the neurokinin receptors was found to be widely distributed in most neurons of the cochlear nucleus (CN), the lateral superior olive (LSO), the medial nucleus of the trapezoid body (MNTB) and in the inferior colliculus (IC). Immunoreactivity was generally confined to post-synaptic targets (neuronal cell body and proximal or primary dendrites) in all auditory nuclei. However, unlike brainstem nuclei, the IC showed, in addition to neuronal cell body staining, a positive axonal immunolabeling (axons and pre-synaptic terminals) with the anti-NK1-R antibody. This axonal staining, revealing a pre-synaptic expression of NK1-R, is in good agreement with the known presence of substance P in the IC neurons. The absence of axonal staining in the superior olivary complex nuclei which projects afferent to the IC indicated that the NK1-R labeled axons are rather intrinsic IC fibers or descending thalamic projections to the IC. Overall, the wide distribution of the three types of tachykinin receptors observed in the present study argues for an important role of tachykinin neuropeptides in the central auditory system.     

Functional ionotropic glutamate receptors on peripheral axons and myelin

Introduction: Neurotransmitter‐dependent signaling is traditionally restricted to axon terminals. However, receptors are present on myelinating glia, suggesting that chemical transmission may also occur along axons. Methods: Confocal microscopy and Ca²⁺‐imaging using an axonally expressed FRET‐based reporter was used to measure Ca²⁺ changes and morphological alterations in myelin in response to stimulation of glutamate receptors. Results: Activation of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) or N‐methyl‐D‐aspartate (NMDA) receptors induced a Ca²⁺ increase in axon cylinders. However, only the latter caused structural alterations in axons, despite similar Ca²⁺ increases. Myelin morphology was significantly altered by NMDA receptor activation, but not by AMPA receptors. Cu²⁺ ions influenced the NMDA receptor‐dependent response, suggesting that this metal modulates axonal receptors. Glutamate increased ribosomal signal in Schwann cell cytoplasm. Conclusions: Axon cylinders and myelin of peripheral nervous system axons respond to glutamate, with a consequence being an increase in Schwann cell ribosomes. This may have implications for nerve pathology and regeneration. Muscle Nerve 54 : 451–459, 2016     

An ultrastructural analysis of the photoreceptors of the squid and their synaptic connections. III. Photoreceptor terminations in the optic lobes

An ultrastructural investigation of the optic lobe of the squid, Loligo pealei, revealed that the optic fibers, like those of Octopus, terminated in the outer plexiform layer in long carrot-shaped bags containing small clear vesicles. The outer 4–5 μ of a terminal was devoid of conventional synapses but came into direct contiguity and specialized contacts with adjacent terminals. These specializations often included protrusions of finger-like processes from one cell into another. At contact sites the intercellular space narrowed to a minimum of about 25 Å and immediately adjacent, in the cytoplasm of each contacting cell, was a sub-membranal cistern. These contacts could be electrotonic junctions. The remainder of the receptor terminal received dendritic endings of post-synaptic cells in deep invaginations. A pre-synaptic accumulation of vesicles and increased membrane density was evident at these junctions. Neurons of the outer nuclear layer are described, as well as vertical fascicles of large pale neurites which pass through the outer nuclear and plexiform layers and which may include efferents to the retina. Specialized glial cells and a dense, intercellular material located in pools or clefts in certain regions of the cortex of the lobe are also noted.     

Scrapie inoculation of mice: light and electron microscopy of the superior colliculi

Summary Ultrastructural examination of the superior colliculi of mice intraocularly inoculated with the ME7 strain of scrapie showed vacuolation early in the course of infection. Brains were examined between 85–260 days after monocular inoculation with scrapie. The mean incubation period for the development of clinical disease was 302 days. Vacuolation was seen initially in the contralateral superior colliculus and subsequently in the ipsilateral colliculus. In coded trails light microscopical vacuolation was seen from 218 days but ultrastructural examination showed that sparse vacuoles were inconsistently present in either or both of the ipsilateral and contralateral colliculi from 85 days; frequent vacuoles were seen from 190 days. Scrapie-induced vacuoles were differentiated from vacuoles present in control tissue by the presence of loculation or by a limiting double membrane which showed protrusion or proliferation of the innermost lamella. Vacuolation was seen in neuronal perikarya, myelinated fibres, dendrites and axonal presynaptic terminals. Vacuoles of myelinated fibres were observed within myelin and possibly also in the inner tongue of oligodendroglial cytoplasm. Whorled membrane configurations were also seen. Tubulovesicular particles, 40 nm in diameter, were recognised in two scrapie-infected mice. It is suggested that some scrapie vacuoles arise as a result of incorporation of abnormal membrane into organelles, possibly mitochondria, in neuronal perikarya and neurites and probably also within oligodendroglial cytoplasm and myelin.     

The neuronal endoplasmic reticulum: its cytochemistry and contribution to the endomembrane system. II. Axons and terminals

The morphology and cytochemistry of the endoplasmic reticulum (ER) in axons and terminals of a number of different types of neurons in brains from mice were investigated ultrastructurally. The neurohypophysis received particular attention because the morphology and enzyme cytochemical activities of many of the preterminal swellings of hypothalamo-neurohypophysial axons are altered by chronic salt-stress. Membrane contrast and enzyme cytochemical staining techniques were employed to characterize the axonal reticulum and to determine if organelles representing the lysosomal system in the axon and the tubular profiles participating in the anterograde axonal transport of native horseradish peroxidase (HRP) are associated with the ER. Potential enzyme cytochemical markers for the axonal ER included glucose-6-phosphatase (G6Pase), thiamine pyrophosphatase, nucleoside diphosphatase, and acid hydroxylase activities. The anterograde transport of HRP was analyzed in undamaged hypothalamo-neurohypophysial neurons and in facial and hypoglossal motoneurons of mice receiving the protein in the lateral cerebral ventricle. The ER pervaded the axon and appeared as parallel, 20-40-nm-wide tubules interconnected by oblique anastomoses. Membrane thickness of the axonal reticulum measured 60-100 A, which is similar to that of the perikaryal ER. Enzyme cytochemical activities associated with the ER or lysosomes were not conspicuous in axons and terminals under normal conditions but became prominent in some axons and preterminal swellings manifesting an autophagic appearance within neurohypophyses from salt-stressed mice. Only G6Pase activity was a marker for the ER in these axons and preterminals. Many ER profiles in non-incubated sections and in G6Pase cytochemical preparations of salt-stressed neurohypophyses were wrapped around or interspersed among secretory granules, multilamellar bodies, and vacuoles that may represent forms of lysosomes involved in autophagy and crinophagy. Acid hydrolase activities were localized within the vacuoles as well as within 80-130-nm-wide, blunt-ended tubules in pituitary stalk axons; similar reactive tubules were confluent with large secondary lysosomes in neurosecretory cell bodies and may be derived from these lysosomes. Morphologically identical tubules transporting HRP in the anterograde direction were observed only in the salt-stressed hypothalamo-neurohypophysial neuron. The HRP-positive tubules very likely are affiliated with the lysosomal system.     

Motor nerve terminals on abdominal muscles in larval flesh flies,Sarcophaga bullata: Comparisons with Drosophila

Motor nerve terminals on abdominal body-wall muscles 6A and 7A in larval flesh flies were investigated to establish their general structural features with confocal microscopy, transmission electron microscopy, and freeze-fracture procedures. As in Drosophila and other dipterans, two motor axons supply these muscles, and two morphologically different terminals were discerned with confocal microscopy: thin terminals with relatively small varicosities (Type Is), and thicker terminals with larger varicosities (Type Ib). In serial electron micrographs, Type Ib terminals were distinguished from Type Is terminals by their larger cross-sectional area, more extensive subsynaptic reticulum, more mitochondrial profiles, and more clear synaptic vesicles. Type Ib terminals possessed larger synapses and more synaptic contact area per unit terminal length. Although presynaptic dense bars of active zones were similar in mean length for the two terminal types, there were almost twice as many dense bars per synapse for Type Ib terminals. Freeze-fractures through the presynaptic membrane showed particle-free areas indicative of synapses on the P-face, within which were localized aggregations of large intramembranous particles indicative of active zones. These particles were similar in number to those found at active zones of several other arthropod neuromuscular junctions. In general, synaptic structural parameters strongly paralleled those of the anatomically homologous muscles in Drosophila melanogaster. In live preparations, simultaneous focal recording from identified varicosities and intracellular recording indicated that the two terminals produced excitatory junction potentials of similar amplitude in a physiological solution similar to that used for Drosophila. J. Comp. Neurol. 402:197–209, 1998. © 1998 Wiley-Liss, Inc.     

Interstitial hyperosmolarity may cause axis cylinder shrinkage in streptozotocin diabetic nerve

Maximal conduction velocity values of nerves of diabetic rats 20 weeks after streptozotocin intoxication were found to be intermediate between those of onset-control and those of end-control groups. The abnormality of conduction velocity of the streptozotocin group might therefore be attributed to a failure of maturation. Detailed electron microscopic morphometry of myelinated fibers (MFs) indicates that more than lack of maturation is involved. Whereas the number of lamellae and the perimeter of axis cylinders of myelinated fibers of the three study groups suggested that growth continues, cross-sectional area of the axis cylinders of the streptozotocin group was smaller than those of either control group. Scored evaluation of fiber shape and the measured index of circularity, which related perimeter and transverse axis cylinder area, also indicated that a selective shrinkage of axis cylinders had occurred. This selective alteration in size and shape of axis cylinders is identical to that described after hyperosmolar fixation. Compared with that of controls, the serum of streptozotocin rats is hyperosmolar. It would seem reasonable to attribute the axis cylinder changes to shrinkage. Whether an additional maturational effect is operative as well cannot be resolved from our data.     

Pharmacological actions of substance P in the rat vas deferens

SP produces two different muscular responses in the isolated vas deferens of the rat. 1) A myotropic, post-synaptic effect that results from stimulation of one subtype of SP receptor, located on the membrane of the smooth muscle (NK-3 receptor). 2) A neurogenic effect at the pre-synaptic level that results from stimulation of another subtype of SP receptor, located on the nerve terminals (NK-1 receptor).     

Trophic influences of excitatory and inhibitory synapses on neurones in the auditory brain stem.

The effects of a reduction during development of excitatory and inhibitory synaptic input on CNS neurones were studied in the lateral superior olivary nucleus (LSO) of the ferret following neonatal, unilateral cochlear removal. LSO neurones normally receive excitatory input from the ipsilateral ear and inhibitory input from the contralateral ear. After cochlear removal, the ipsilateral LSO was smaller and contained fewer neurones than either the contralateral or the normal LSO. No difference was found between the volume or number of neurones in the latter nuclei. Remaining neurones in the LSO ipsilateral to the removal were smaller than those in the contralateral LSO of the same ferrets. These data show that activity in excitatory pre-synaptic terminals can be sufficient for post-synaptic target maintenance, but that activity in inhibitory terminals alone is not.