Effects of adenosine and adenine nucleotides on synaptic transmission in the cerebral cortex.

Adenosine and the adenine nucleotides have a potent depressant action on cerebral cortical neurons, including identified corticospinal cells. Other purine and pyrimidine nucleotides were either weakly depressant (inosine and guanosine derivatives) or largely inactive (xanthine, cytidine, thymidine, uridine derivatives). The 5'-triphosphates and to a lesser extent the 5'-diphosphates of all the purine and pyrimidines tested had excitant actions on cortical neurons. Adenosine transport blockers and deaminase inhibitors depressed the firing of cortical neurons and potentiated the depressant actions of adenosine and the adenine nucleotides. Methylxanthines (theophylline, caffeine, and isobutylmethylxanthine) antagonized the depressant effects of adenosine and the adenine nucleotides and enhanced the spontaneous firing rate of cerebral cortical neurons. Intracellular recordings showed that adenosine 5'-monophosphate hyperpolarizes cerebral cortical neurons and suppresses spontaneous and evoked excitatory postsynaptic potentials in the absence of any pronounced alterations in membrane resistance or of the threshold for action potential generation. It is suggested that adenosine depresses spontaneous and evoked activity by inhibiting the release of transmitter from presynaptic nerve terminals. Furthermore, the depressant effects of potentiators and excitant effects of antagonists of adenosine on neuronal firing are consistent with the hypothesis that cortical neurons are subject to control by endogenously released purines.     

Cytochemistry and morphology of synaptic structures in the cerebral cortex of rat

Summary Glycogen synthetase and phosphorylase activities in the paraboloid glycogen of the accessory cone of the chick retina were studied electron histochemically, while the paraboloid glycogen was observed by electron microscopy.Some of the paraboloid of the accessory cone of the chick retina contained abundant glycogen granules, but some showed no glycogen granules. Some inner segments of the accessory cones were occupied by deposition of glycogen granules.Polyglucose particles synthesized by glycogen synthetase activity in the chick paraboloid were demonstrated in fine granular form with diameter from 70 to 130 Å. These particles were less stainable with lead citrate than native glycogen granules. Synthesized polyglucose particles were located in the cytoplasmic matrices and expanded them. Lamellar and membrane structures were not related to synthesized polyglucose.Polyglucose particles synthesized by phosphorylase activity in the chick paraboloid were located in the cytoplasmic matrices and expanded them widely. Tubular structure appeared to be flattened by deposition of synthesized polyglucose particles. These features showed the resemblance to the inner segment of the accessory cone filled with a great amount of glycogen granules. Synthesized polyglucose was demonstrated in macromolecular form with diameter from 200 to 500 Å. There were no relationships between lamellar or membrane structures and polyglucose.The present study suggests that the chick paraboloid not only is a field for active glycogen metabolism, but also becomes a storage of glycogen.     

Cytochemistry and morphology of synaptic structures in the cerebral cortex of rat.

Studies have been carried out on the synapses in the cerebral cortex of rat by using impregnation with ethanolic solution of phosphotungstic acid, contrast staining with ruthenium red and impregnation with bismuth iodide, with or without subsequent uranyl acetate and lead citrate staining. It has been established that dense projections are adequately visualized with methods demonstrating basic chemical groups (phosphotungstic acid and bismuth iodide), whereas the synaptic vesicles are stained by techniques demonstrating acid chemical groups (ruthenium red and uranyl acetate and lead citrate). On the basis of these observations a hypothesis is forwarded concerning the mechanisms of migration of synaptic vesicles towards the presynaptic membrane. Measurements of the parameters of the dense projections suggest that the configuration of the presynaptic vesicular grid is not uniform along the presynaptic areas.     

Comparative characteristics of the methods of calculating numerical synaptic density in the cerebral cortex

The number of axon synaptic terminals (AT) in 1 mm3 of the acoustic (A1) and associative (field 5b) cerebral cortex in cat has been determined. Results from this determination obtained by different methods have been compared.     

Interaction of psychotropic preparations with the synaptic membranes of the cerebral cortex in rats

Interaction of psychotropic drugs with synaptosomal membranes from rat brain cortex was investigated by fluorescent probes. The data obtained indicate that all studied drugs change the state of membrane's surface. Tranquilizers, unlike antidepressants and neuroleptics, decreased fluorescence of the probe. Neuroleptics, unlike other drugs, penetrated deeper into the membranes hydrophobic core.     

Redistribution of synaptic vesicle antigens is correlated with the disappearance of a transient synaptic zone in the developing cerebral cortex

To examine the distribution of synaptic vesicle antigens during development of the cerebral cortex, antibodies against synapsin I and p65 were used on sections of cat cerebral cortex between E40 and adulthood. In the adult, the layers of the cerebral cortex are immunoreactive for each of these antigens, while the white matter is free of staining. In contrast, the fetal and neonatal pattern of immunostaining is reversed: the cortical plate (future cortical layers) is devoid of immunoreactivity, while the marginal (future layer 1) and the intermediate zones (future white matter) are stained. Electron microscopic immunohistochemistry shows that immunolabeling is associated with presynaptic nerve terminals in the adult and during development. These observations suggest that during development the white matter is a transient synaptic neuropil and that a global redistribution of synapses takes place as the mature pattern of connections within the cerebral cortex emerges.     

NMDA受体参与小鼠的前额扣带回的神经突触传递

谷氨酸性突触是哺乳动物神经系统的主要兴奋性突触。在正常条件下,大多数的突触反应是由谷氨酸的AMPA受体传递的。NMDA受体在静息电位下为镁离子抑制。在被激活时,NMDA受体主要参与突触的可塑性变化。但是,许多NMDA受体拮抗剂在全身或局部注射时能产生行为效应,提示NMDA受体可能参与静息状态的生理功能。此文中,我们在离体的前额扣带回脑片上进行电生理记录,发现NMDA受体参与前额扣带回的突触传递。在重复刺激或近于生理性温度时,NMDA受体传递的反应更为明显。本文直接显示了NMDA受体参与前额扣带回的突触传递,并提示NMDA受体在前额扣带回中起着调节神经元兴奋的重要作用。     

Specifics of post-theta modification of synaptic transmission in thalamo-cortical input of the rat's barrel cortex

The possibility of the development of either the long-term posttetanic potentiation or the depression of focal evoked potentials in identified columns of the barrel somatic cortex of unanaesthetized rats during stimulation of their specific thalamocortical afferent fibers was shown. Phase-dependent potentiation developed after burst tetanization with the frequency of theta rhythm at the negative phase of a theta wave, whereas the stimulation at the positive phase produced the depression. Potentiation after continuous tetanization was observed only at the optimal selection of stimuli amplitude and duration. Excessively intense tetanization more frequently caused the depression of tested responses probably due to the involvement of recurrent inhibition.     

Ultrastructure of the synaptic apparatus of the cerebral cortex during iontophoretic application of acetylcholine

An ultrastructure comparison of presynaptic and postsynaptic components of axodendritic synapses of the fifth layer of rats neocortex sensomotor region after microionophoresis of acetylcholine and physiological solution has been carried out. The absence of true differences is considered as an adequacy indicator of application mediator regime.     

Effects of the corticoliberin on synaptic transmission in the rat olfactory cortex slices in water-immersion model depression

Corticoliberin (corticotrophin-releasing hormone, CRH) regulated of endocrine, autonomic and immune response to stress and is a mediator of anxiety in behavioral response. We studied the effect of corticoliberin on neuronal activity after microstimulation of olfactory cortex slices. Wistar rats strain were selected in T-maze labyrinth according to active and passive strategy of the adaptive behavior. The rats were exposed to water-immersions stress and after 10 days from their brain the olfactory cortex slices were prepared. The evoked focal potential were registered after perfusion with 0.1 mcM of CRH. It was revealed that in 60% of the slices of the active rats CRH induced the small decrease of excitatory amplitude but the increase amplitude inhibitory postsynaptic potential. In 40%, CRH induced the depression of synaptic transmission. Addition of CRH in incubation medium of the passive rat slices related, blockade the synaptic transmission.     

Oxytocin suppresses basal glutamatergic transmission but facilitates activity-dependent synaptic potentiation in the medial prefrontal cortex

Both oxytocin and oxytocin receptors are implicated in neuropsychiatric disorders, particularly autism which involves a severe deficit in social cognition. Consistently, oxytocin enhances social cognition in humans and animals. The infralimbic medial prefrontal cortex (IL-mPFC) is believed to play an important role in the regulation of social cognition which might involve top-down control of subcortical structures including the amygdala. However, little is known about whether and how oxytocin modulates synaptic function in the IL-mPFC. The effect of oxytocin on excitatory neurotransmission in the IL-mPFC was studied by examining both the evoked and spontaneous excitatory neurotransmission in the IL-mPFC layer V pyramidal neurons before and after perfusion with oxytocin. To investigate the effect of oxytocin on synaptic plasticity, low-frequency stimulation-induced long-lasting depression was studied in oxytocin-treated brain slices. Oxytocin produced a significant suppression of glutamatergic neurotransmission in the IL-mPFC layer V pyramidal neurons which was mediated by a reduction in glutamate release. Activation of the cannabinoid CB1 receptors was involved in this pre-synaptic effect. Treatment of brain slices with oxytocin for 1?h converted long-lasting depression into long-lasting potentiation of glutamatergic neurotransmission. This oxytocin-mediated plasticity was NMDA receptor-dependent and was mediated by the synaptic insertion of calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors. The aforementioned suppression of basal glutamatergic neurotransmission and facilitation of activity-dependent synaptic plasticity in the IL-mPFC might be critical for the effect of oxytocin on social cognition.     

Separation of synaptic junctional complexes from thin layers of rabbit cerebral cortex

Synaptic junctional fractions were separated from rabbit brain by procedures based on combining the methods of Cotman and Taylor [4], Orosz et al. [16, 17] and Lisman et al. [13]. Thin layers of cerebral cortices were homogenized to obtain a crude mitochondrial-synaptosomal fraction. The sedimentation rates of mitochondria and mitochondria containing synaptosomes were increased by raising the density of mitochondria with an insoluble dense formazan deposit inside mitochondria after iodo-nitrotetrazolium treatment. The synaptic plasma membrane fraction isolated by this method contained no mitochondrial contamination. After Triton X-100 treatment the insoluble residues of the detergent were centrifuged through discontinuous sucrose gradients. A great enrichment of morphologically identifiable intact synaptic junctions was observed in some of the obtained interface layers.