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PubMed1986

Enkephalin modulation of neural transmission in the cat stellate ganglion: pharmacological actions of exogenous opiates.

Neural ganglionic transmission was studied in vivo in the cat, using closed chest anesthetized preparations. The right stellate ganglion and its branches were exposed retropleurally and prepared for electrical stimulation of pre- and postganglionic nerve fibers. The axillary artery was cannulated allowing direct administration of drugs in the arterial blood supplying the ganglion. Stimulation of postjunctional receptors could thus be obtained by local administration of selective agents. Local administration of nicotinic, muscarinic or histaminergic agents increased heart rate and blood pressure. Opiates were given either i.v. or locally through the axillary artery: we tested the effects of morphine, Leu-enkephalin (Leu-enk), Met-enkephalin (Met-enk), [D-ala2]-Met-enkephalinamide (DAME) and etorphine. When given locally, Leu-enk (from 10 micrograms), Met-enk (from 20 micrograms), DAME (from 5 micrograms) and etorphine (from 0.2 micrograms) inhibited tachycardia induced by preganglionic stimulation and reduced the amplitude of the compound action potential recorded from the postganglionic nerve. Morphine (10-200 micrograms) had no effect. On the other hand, tachycardia induced by postganglionic nerve stimulation was unaffected by opiates in the same experimental conditions. Intravenous administration of similar doses of opiates had no effect on ganglionic transmission. When tachycardia was induced by chemical stimulation of nicotinic (DMPP), muscarinic (McN-A-343-11) or histamine receptors in the stellate ganglia, opiates were still active in reducing the effect of these chemicals. These data provide evidence that exogenous opiates exert a depressing action on postsynaptic responses of sympathetic ganglia tested in vivo, although an additional action on presynaptic terminals is not excluded. As endogenous opiates are normally present in various sympathetic ganglia, including the stellate ganglion of the cat, it is possible that they play some modulatory role on ganglionic transmission in physiological conditions.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1981

Postnatal development of ganglionic neurons in the absence of preganglionic input: morphological observations on synapse formation.

Synapse formation during postnatal development of the superior cervical sympathetic ganglion was studied in rats after neonatal ganglionic denervation, when reinnervation was either permitted or prevented. In both groups of operated animals, 90% of the synapses were lost by the fourth postoperative day. In the rats in which reinnervation was permitted, restoration of synapse numbers began by one month after surgery and reached 50% of control by two months. There was no further synapse restoration after this time. In the animals in which reinnervation was prevented, synapse numbers increased, but at all times were approximately 10% of controls. Thus the intrinsic ganglionic synapses underwent their normal postnatal developmental increase in number, but did not sprout to any significant degree in response to the massive deafferentation caused by removal of the preganglionic input. Vacant postsynaptic membrane thickenings (those not apposed by presynaptic terminals) appeared in both experimental groups. There was no significant loss of these vacant thickenings in either group over the course of 3 months. Therefore, the vacated postsynaptic sites do not appear to be recontacted during reinnervation, while the reinnervating axons appear to cause the formation of new postsynaptic sites on the ganglion cells.

Animals↗
PubMed1982

Electrophysiologic effects of acute ethanol exposure. II. Alterations in the calcium component of action potentials from sensory neurons in dissociated culture.

Dissociated dorsal root ganglion neurons were exposed to 0.05-0.50 g% ethanol. The recording medium was altered in order to produce an action potential with an increased duration which was Ca2+-dependent. Ethanol was observed to decrease the duration of sensory neuron action potentials indicating a decreased inward Ca2+ current. The ethanol induced decrease in duration was reversible and dose-dependent. No alterations in resting membrane potential, spike amplitude, or maximum rate of rise were observed during ethanol exposure. An increased threshold was also observed with application of ethanol. These findings are discussed in regard to the possible effects of ethanol on Ca2+ movement at the presynaptic terminal.

Action Potentials↗
PubMed1984

Synaptic remodelling during development and maturation: junction differentiation and splitting as a mechanism for modifying connectivity.

Morphological variation of the synaptic active zone during later development and maturation (15-224 days) has been studied in the molecular layer of the rat occipital cortex. Both E-PTA stained and osmicated tissue have been used. In the E-PTA stained material the degree of specialization of the presynaptic thickening is directly related to junction length. Junctions with well-developed dense projections (Types A and B) are longest and continue to increase in length with maturation, suggesting that active remodelling of the synaptic apposition is an ongoing process. The presence of perforated junctions, possessing two or more regions with specializations of different maturity and different curvature, raises the possibility that these junctions may arise by the addition and differentiation of new paramembranous material at an existing junction. In osmicated tissue, presynaptic terminals possessing multiple active zones have been quantitated. The maturational increase in number of simple perforated junctions (Type 1), is paralleled by a smaller increase in the number of multiple perforated junctions (Type 2). A spine apparatus is frequently observed in these perforated terminals, suggesting that it is intimately involved in the reorganization. The direction of curvature of the closely apposed junctions is predominantly negative (indenting the postsynaptic process). Other types of arrangement, with separate postsynaptic processes, are described (Types 3-5), and micrographs suggestive of sequential stages in pre- and postsynaptic terminal splitting are presented. The total length of the postsynaptic thickening of perforated terminals is twice the mean synaptic length of non-perforated terminals, again suggestive that duplication of the active zone may have occurred. Division of existing synaptic terminals by duplication and subsequent splitting would readily account for the increased dendritic spinal numbers seen in Golgi preparations of animals raised under enriched conditions. This would be a straight-forward mechanism by which reinforcement of neuronal connections could occur in response to use.

Animals↗
PubMed1990

Protein kinase C immunoreactivity in kitten visual cortex is developmentally regulated and input-dependent.

Immunocytochemistry with polyclonal antibodies directed against protein kinase C (PKC) was utilized to investigate the development of the kinase in kitten visual cortex neurons. The immunoreaction product was found at postsynaptic sites at all ages studied. However, PKC was localized in presynaptic terminals only during the first few weeks of postnatal life, during the period when the cortex is most susceptible to visual experience. The overall level of PKC immunoreactivity was high at early postnatal ages (up to 6 weeks) and declined afterwards till adulthood. This decline in reactivity was not equal across the cortex and was particularly marked in the middle cortical layers, especially layer IV. The reduction of PKC immunoreactivity in all cortical layers but layer IV was abolished by isolating a portion of cortex from its neuronal inputs early in life. Indirect evidence points to the lateral geniculate nucleus as the source of input that is required for input-dependent maturational changes in the kinase level. The results reported here suggest that the expression of PKC in kitten visual cortex in not only developmentally regulated but is also use-dependent.

Aging↗
PubMed1992

Age-related changes in binding to excitatory amino acid uptake site in temporal cortex of human brain.

The binding of D-[3H]aspartate to the specific uptake site for the excitatory amino acids glutamate and aspartate was measured in homogenates of temporal lobe cortex taken at postmortem from 76 human infant and adult brains. Binding levels were very low in brains of preterm and term infants but increased rapidly during the first 20 postnatal weeks to reach levels which exceeded those in adult brains. Linear regression analysis which compared the amount of D-[3H]aspartate binding with the age of the infant, showed a positive correlation up to 25 postnatal weeks. Saturation analysis showed that the maximum number of D-[3H]aspartate binding sites (Bmax) in temporal cortex from infants aged 20 postnatal weeks was 3 times greater than the number of sites in adult brain. The findings show that the number of excitatory amino acid uptake sites, which may be associated in part with presynaptic terminals, increase in number rapidly after birth. Furthermore, the data may indicate that a slow regression of excitatory amino acid terminals occurs during the later stages of brain development.

Aging↗
PubMed1994

The expression of GAP-43 and synaptophysin in the developing rat retina.

We have undertaken a detailed study of the expression of GAP-43 and synaptophysin immunoreactivity in the developing postnatal rat retina. We found that these two 'presynaptic' proteins have quite different expression patterns. GAP-43 was first expressed in the optic nerve and the optic fiber layer of the retina, where it disappeared between the 8th and 16th postnatal day. From the 5th postnatal day on, GAP-43 also appeared in the inner plexiform layer, where it was present in three distinct bands. This expression changed little in postnatal development and persisted in the adult retina. GAP-43 was not detected in the outer plexiform layer of the retina. Synaptophysin was absent from the optic nerve and optic fibers at all postnatal stages. It was first expressed in the developing outer plexiform and, with reduced intensity, in the outer nuclear layer between postnatal days 2 and 5. In the inner plexiform layer, synaptophysin could be first detected between postnatal days 8 and 12. The intensity of staining increased during postnatal development in both plexiform layers. The developmental sequence of synaptophysin expression can be correlated with the maturation of presynaptic terminals of photoreceptors and bipolar cells. The rather complex pattern of GAP-43 expression is not easily compatible with a single model of GAP-43 function, and suggests diverse functions of this molecule in the retina.

Animals↗
PubMed1992

Neurotransmitter transporters (plus): a promising new gene family.

Neurotransmitter transporter genes encode proteins with 12 putative transmembrane regions, which mediate Na(+)-dependent reaccumulation of released neurotransmitters into presynaptic terminals and are the sites of action of important abused and therapeutic drugs. Studies of these genes show promise for improving our understanding of transport mechanisms and modes of drug action, and may even uncover previously unanticipated neurotransmitters.

Amino Acid Sequence↗
PubMed1993

Spinules: a case for retinal synaptic plasticity.

In both vertebrate and invertebrate nervous systems, a population of synapses is characterized by having finger-like indentations of the postsynaptic membrane that project into the presynaptic terminal. These 'spinules' are often transitory structures, and their presence has been associated with increased synaptic activity. We have studied the functional role of spinules in the fish retina, where they are observed in horizontal cells invaginating cone pedicles, and in synaptic terminals of bipolar cells. In the cone-horizontal cell synaptic complex, spinules are present during light adaptation; their formation is triggered by external light stimuli as well as by endogenous factors. Pharmacologically, spinules are degraded following an increase, and formed in response to a decrease of the transmitter glutamate released by the cone cells. Dopamine, released by interplexiform cells and acting via a D1 receptor-mediated increase in cAMP, and a protein-kinase-C-based mechanism are also capable of inducing spinule formation. Functionally, the presence and absence, as well as the timecourse, of spinule formation during light adaptation is closely correlated with the development of biphasic chromatic responses in a class of cone horizontal cells and the manifestation of colour-opponency in ganglion cells. This suggests that in the outer retina of fish, spinules are mediating feedback activity essential for the coding of antagonistic colour information.

Animals↗
PubMed1996

Neural grafting of cholinergic neurons in the hippocampal formation.

The cholinergic septohippocampal system plays an important role in spatial learning and memory functions. Transections of the septohippocampal pathway have been shown to result in a near complete loss of cholinergic innervation in the hippocampus and induce severe spatial memory impairments. In this article, we have reviewed the studies which demonstrate the ability of intrahippocampal septal grafts to reinnervate the hippocampal formation and ameliorate spatial learning and memory deficits. Neuroanatomical studies suggest that grafts of cholinergic tissue can innervate the host hippocampal formation in a pattern that mimics that of the normal septohippocampal pathway. This innervation, in turn, is associated with the formation of graft-to-host synaptic connections. Neurochemical studies reveal that intrahippocampal grafts of septal cells can restore choline acetyltransferase activity, acetylcholine synthesis, and high affinity choline uptake in presynaptic terminals of grafted neurons. In addition, these grafts can normalize the upregulation of cholinergic muscarinic receptors seen postsynaptically in the hippocampus following lesions of the septohippocampal pathway. The functional nature of these grafts is also substantiated by electrophysiological recordings which demonstrate stimulus-evoked graft-to-host synaptic transmission as well as the reinstatement of EEG activity typical of septohippocampal connectivity. In addition to graft-to-host connections, behavioral and neurochemical studies also provide evidence for host-to-graft connections that can regulate the activity of grafted cholinergic neurons during the performance of specific behavioral tasks requiring spatial memory function. Together, these studies suggest that grafts of cholinergic neurons from the medial septal nucleus can become anatomically and functionally incorporated into the circuitry of the host hippocampal formation.

Animals↗
PubMed1996

Serotonergic functions in arousal and motor activity.

Changes in motor activity have long been used to characterize the effects of serotonergic manipulations. The prevailing view has been that serotonin typically inhibits motor output, often in reciprocity with catecholaminergic systems. Recent findings, however, indicate that the release of presynaptic serotonin by indirect agonists leads to a profound locomotor activation. Studies were performed in a behavioral pattern monitor (BPM). The BPM is an automated holeboard/activity apparatus measuring 30.5 x 61 cm, that allows detailed sequential analyses of both locomotor and investigatory behaviors. When tested under comparable conditions, direct agonists at both 5-HT1 and 5-HT2 receptors decrease locomotor activity in rats. With hallucinogenic 5-HT2 agonists, this effect is dependent upon the novelty of the test environment, indicating that these compounds increase the responsiveness of the animal to the threatening aspects of the novel environment. Indirect serotonin agonists, however, increase locomotor activity and decrease investigation of discrete stimuli in the environment. The activating effects of indirect agonists such as 3,4-methylenedioxy-methamphetamine (MDMA), para-chloroamphetamine (PCA), or alpha-ethyltryptamine are dependent upon the release of serotonin from presynaptic terminals and are mimicked by direct agonists at 5-HT1B receptors. Both behavioral analyses and studies with synthesis inhibitors and receptor antagonists clearly distinguish the MDMA-induced hyperactivity from that induced by amphetamine-like releasers of dopamine. Further supporting the relevance of 5-HT1B receptors to the activating effects of serotonin-releasing agents, MDMA exhibits reciprocal cross-tolerance with the 5-HT1B agonist RU 24969, but not with either 5-HT1A or 5-HT2 agonists or amphetamine. Thus, studies of locomotor and investigatory responses can be used to demonstrate and differentiate the effects of direct agonists at 5-HT1A, 5-HT1B, and 5-HT2 receptors as well as indirect serotonin agonists. The fact that the predominant effect of serotonin releasers is locomotor activation, apparently mediated via post-synaptic 5-HT1B receptors, suggests that some endogenous serotonergic systems may normally activate rather than suppress motor output.

Animals↗
PubMed1984

Synaptology of alpha-motoneurons in the chicken spinal cord.

The synaptology of alpha-motoneurons innervating the anterior and posterior latissimus dorsi muscle (ALD and PLD) in the chicken was studied electron microscopically. These motoneurons were identified by means of retrograde transport of horseradish peroxidase injected into each muscle. Presynaptic boutons on their somata and dendrites were classified as S, F, C and M types, fundamentally similar to those previously reported in the monkey, cat and rat. Besides them, the presynaptic terminals which contained dense-cored vesicles, designated as the G type collectively for practical purposes, were newly found on both the somata and dendrites of chicken alpha-motoneurons and divided into five subtypes characterized by the presence of: (1) elongated-cored vesicles and flattened clear vesicles; (2) small spherical-cored vesicles (the range of diameter, 55-100 nm) and spherical clear vesicles; (3) middle-sized spherical-cored vesicles (60-120 nm) concomitant with spherical clear vesicles; (4) large spherical cored vesicles (85-145 nm) with a few spherical clear vesicles; and (5) cored vesicles of various shapes and sizes intermingled with tubular structures with dense content in them. The frequent occurrence of the G-type boutons on alpha-motoneurons in the chickens as compared with the rat, cat or monkey may suggest that the somatic motor activity in the chicken is modulated by neuropeptides and/or biogenic amines more than in the mammals.

Animals↗
PubMed1986

Demonstration of taurine-like immunoreactive structures in the rat brain.

An antiserum was raised in a rabbit by immunization with taurine bound to bovine serum albumin. The antibody was purified by passage over an immunoabsorbent column (formyl-cellulofine-taurine) and it did not cross-react significantly with glutamate, aspartate, glycine, GABA (0.4%), glutamine, proline, cysteine, beta-alanine, cysteic acid, carnosine or homocarnosine in enzyme-linked immunosorbent assays and nitrocellulose paper immunoblots. Immunocytochemical studies employing the peroxidase-antiperoxidase immunohistochemical technique revealed that many cerebellar Purkinje cells showed taurine-like immunoreactivity. Labelled axons could be followed within the white matter up to the deep cerebellar nuclei, where numerous puncta were observed. Immunoelectron microscopic examination revealed that labelled puncta were presynaptic terminals, and axo-dendritic or axo-somatic symmetrical synapses were observed on deep cerebellar nuclear neurons.

Animals↗
PubMed1987

Presynaptic Ca-antagonist omega-conotoxin irreversibly blocks N-type Ca-channels in chick sensory neurons.

The present studies on electrophysiological and pharmacological differences of the three types of Ca-currents (N-, L- and T-types) in whole-cell clamped, cultured embryonic chick sensory neurons revealed that the majority (94%) of the Ca-currents in the nerve cells were the N-type, omega-Conotoxin (omega CTX, 5 microM), a blocker of transmitter release at the presynaptic terminals, induced a complete and irreversible blockage of Ca-currents elicited from the resting membrane potential (-60 mV) in 29 cells among 58. The Ca-currents thus irreversibly blocked by the omega CTX were determined as the N-type (neuronal), as they were insensitive to nifedipine (5 microM) or were reduced in amplitude by Bay K 8644 (5 microM). A small fraction (12%) of the total Ca-currents, which were still present after the omega CTX treatment (in the rest of 29 cells), were pure L-type (long-lasting) Ca-currents, as they were enhanced by the Bay K and were blocked by the nifedipine. omega CTX was a partial and reversible blocker of the L-type Ca-currents. Furthermore, T-type (transient) Ca-currents elicited in the hyperpolarized membrane (at -100 mV) were blocked by omega CTX in an incomplete and reversible manner. The N-type Ca-currents thus separated in the nerve cells exhibited various differences in features of the voltage-dependence and ionic selectivity from the L- and T-type Ca-currents.

Animals↗
PubMed1993

Cytosolic Ca2+ gradients, Ca2+ binding proteins and synaptic plasticity.

Trains of spikes encoded by presynaptic neurons are decoded into rises in cytosolic Ca2+ concentration both in presynaptic terminals and in postsynaptic dendrites. Intracellular [Ca2+] rises trigger neurotransmitter release and also induce short- and long-term modifications of synaptic efficacy. These modifications can be potentiation or depression depending on the intensity of stimuli. A dynamic mechanism, "dynamic decoding", is proposed to understand the multiplicity of the functions of Ca2+, based on recent knowledge of Ca2+ binding proteins and of the dynamics of Ca2+ signaling. The dynamic model is in many ways superior to static models, and may be applied to various neuronal functions including the induction of long-term plasticity in cerebral cortex.

Animals↗
PubMed1994

Phorbol ester-induced inhibition of GABA uptake by synaptosomes and by Xenopus oocytes expressing GABA transporter (GAT1).

We examined the effect of 12-O-tetradecanoylphorbol 13-acetate (TPA) on the sodium-dependent uptake of gamma-aminobutyric acid (GABA) by the synaptosomal fraction from rat cerebral cortex. Activation of protein kinase C (PKC) by 100 nM TPA inhibited the Na(+)-dependent uptake of GABA by 38.1%, whereas 4 alpha-phorbol-12,13-didecanoate (4 alpha-PDD), an inactive phorbol ester, did not alter the uptake. The inhibition was blocked by preincubation with 100 nM staurosporine, a potent inhibitor of PKC. The Eadie-Hofstee plots revealed the presence of a high affinity uptake system. The treatment with TPA increased the Km value from 6.76 microM to 18.5 microM with a trend toward a slight decrease of Vmax. In the presence of beta-alanine, TPA inhibited the GABA uptake by increasing the Km value from 8.65 microM to 15.0 microM without affecting Vmax. The molecular basis of the inhibitory effect of TPA was further examined using Xenopus oocytes expressing GAT1, a beta-alanine-insensitive and nipecotate-sensitive neuronal GABA transporter, resulting in a similar effect of TPA. The value of Km, but not Vmax, was increased by the treatment with 100 nM TPA. These results suggest that PKC may modulate the GABA uptake into presynaptic terminals through the inhibition of GAT1 activity.

Alkaloids↗
PubMedDate not supplied

Origin of the widespread N18 in median nerve SEP.

The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudal most brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.

Adult↗
PubMed1992

Synthesis and transport of GAP-43 in entorhinal cortex neurons and perforant pathway during lesion-induced sprouting and reactive synaptogenesis.

Metabolic labeling and quantitative 2D gel autoradiography were used to assess changes in the synthesis and transport of GAP-43 in entorhinal cortex (EC) neurons and perforant pathway during lesion-induced sprouting and reactive synaptogenesis. In normal adult rats, there is a high constitutive level of GAP-43 synthesis and transport in EC neurons projecting to the hippocampus. Following unilateral EC lesions, there is a 2-fold (100%) increase in the transport of newly synthesized GAP-43 to the contralateral or 'sprouting' hippocampus. The timing of this upregulation (between 6 and 15 days) suggests that changes in GAP-43 expression occur in response to the growth of presynaptic terminals during sprouting.

Animals↗