An electron microscopic study on the development of synapses in the rat carotid body

The number of types 1 and 2 synapses on chief cells per unit area in the rat carotid body were compared throughout pre- and postnatal periods. Chief cells are postsynaptic in type 1 synapses and presynaptic in type 2 synapses. Type 2 synapses increased in number rapidly as development proceeded, while type 1 synapses remained few. By the 50th postnatal day the numerical density of synapses of both types reached a plateau, where type 2 synapses were approximately 22 times more numerous than type 1 synapses. The present findings suggest that nerve fibers innervating chief cells of the carotid body are basically sensory.     

Monoaminergic synapses,including dendro-dendritic synapses in the rat substantia nigra

Summary Intraventricular administration of 1 or 2 mg of the osmiophilic false transmitter 5-hydroxydopamine (5-OHDA) was used to label monoamine storage and release sites in the rat substantia nigra. Vesicles containing unusually dense cores indicative of the presence of the marker were seen forming from the Golgi apparatus in the cell bodies of medium-sized neurons of the substantia nigra, pars compacta, and from smooth endoplasmic reticulum in the dendrites of those neurons and in small unmyelinated axons of unknown origin. In serial sections, both axons and dendrites containing synaptic vesicles marked with 5-OHDA were seen to form synapses en passage in pars compacta, and some presynaptic dendrites containing vesicles filled by the marker were also observed to form contacts with dendrites in pars reticulata. The only identified postsynaptic elements engaging in monoaminergic synapses in the substantia nigra were dendrites of medium-sized pars compacta neurons.     

Transport-mediated synapses in the retina

Most synapses rely on regulated exocytosis for determining the concentration of transmitter in the synaptic cleft. However, this mechanism may not be universal. Several synapses in the retina appear to use a synaptic machinery in which transmitter transporters play an essential role. Two types of transport-mediated synapses have been proposed. These synapses have been best observed in horizontal cells and cones of nonmammalian retinas. Horizontal cells use a transporter to mediate a bidirectional shuttle, whose balance point is set by ion concentrations and voltage. Nonmammalian cones combine exocytosis and the activity of a transporter. Because exocytosis is voltage independent over most of a cone's physiological voltage range, a voltage-dependent transporter determines the concentration of transmitter in the synaptic cleft. These two synapses may be models for transport-mediated synapses that operate in other parts of the brain.     

Microtubules in synapses of the retina

Summary Using a new method, microtubules can be seen running up to, and lying in close relationship with, the synaptic ribbons in the outer and inner plexiform layers of the frog retina. In the inner plexiform layer microtubules can be seen running up to the terminal membrane in the non-ribbon synapses. Unlike non-ribbon C.N.S. synapses (frog and rat) processed by the same method, there is no clear association between synaptic vesicles and microtubules in the approach regions.     

Leaky synapses: regulation of spontaneous neurotransmission in central synapses

The mechanisms underlying spontaneous neurotransmitter release are not well understood. Under physiological as well as pathophysiological circumstances, spontaneous fusion events can set the concentration of ambient levels of neurotransmitter within the synaptic cleft and in the extracellular milieu. In the brain, unregulated release of excitatory neurotransmitters, exacerbated during pathological conditions such as stroke, can lead to neuronal damage and death. In addition, recent findings suggest that under physiological circumstances spontaneous release events can trigger postsynaptic signaling events independent of evoked neurotransmitter release. Therefore, elucidation of mechanisms underlying spontaneous neurotransmission may help us better understand the functional significance of this form of release and provide tools for its selective manipulation. For instance, our recent investigations indicate that the level of cholesterol in the synapse plays a critical role in limiting spontaneous synaptic vesicle fusion. Therefore, alterations in synaptic cholesterol metabolism can be a critical determinant of glutamatergic neurotransmission at rest. This article aims to provide a closer look into our current understanding of the mechanisms underlying spontaneous neurotransmission and the signaling triggered by these unitary release events.     

Microvesicles in developing synapses

Laboratory of Brain Ultrastructure, Brain Research Institute, Academy of Medical Sciences of the USSR, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 9, pp. 227–229, September, 1991.     

Alkaline phosphatase and 5'-nucleotidase enzymes in the carotid rete-cavernous sinus complex of sheep and goats

12 sheep and 4 goats were used to detect the presence of alkaline phosphatase (A.P.) and 5'-nucleotidase (5'-N) enzymes in the carotid rete-cavernous sinus structure. Different methods of preservation were used. The calcium and the lead methods were used to detect the presence of A.P. and 5'-N, respectively. Best results in their detection were obtained with liquid nitrogen preservation. A.P. enzyme was found in and around areas in which blood capillaries were present, indicating active transport of materials through the capillary membrane. Slight enzymatic activity was seen on the endothelial surface of the rete branches, while the enzyme seemed to be absent from the cavernous sinus. 5'-N was discernible in the tunica adventitia and in the endothelial cells, while the tunica media of the rete branches was apparently devoid of this enzyme. Possible role of these enzymes in the vascular wall metabolism of this structure has been discussed.     

Electrical synapses coordinate activity in the suprachiasmatic nucleus

In the suprachiasmatic nucleus (SCN), the master circadian pacemaker, neurons show circadian variations in firing frequency. There is also considerable synchrony of spiking across SCN neurons on a scale of milliseconds, but the mechanisms are poorly understood. Using paired whole-cell recordings, we have found that many neurons in the rat SCN communicate via electrical synapses. Spontaneous spiking was often synchronized in pairs of electrically coupled neurons, and the degree of this synchrony could be predicted from the magnitude of coupling. In wild-type mice, as in rats, the SCN contained electrical synapses, but electrical synapses were absent in connexin36-knockout mice. The knockout mice also showed dampened circadian activity rhythms and a delayed onset of activity during transition to constant darkness. We suggest that electrical synapses in the SCN help to synchronize its spiking activity, and that such synchrony is necessary for normal circadian behavior.     

Electrotonic synapses in the spinal cord of mammals

Translated from Arkhiv Anatomii, Gistologii i Émbriologii, Vol. 91, No. 7, pp. 13–20, July, 1986.     

Creation of AMPA-silent synapses in the neonatal hippocampus

In the developing brain, many glutamate synapses have been found to transmit only NMDA receptor-mediated signaling, that is, they are AMPA-silent. This result has been taken to suggest that glutamate synapses are initially AMPA-silent when they are formed, and that AMPA signaling is acquired through activity-dependent synaptic plasticity. The present study on CA3-CA1 synapses in the hippocampus of the neonatal rat suggests that AMPA-silent synapses are created through a form of activity-dependent silencing of AMPA signaling. We found that AMPA signaling, but not NMDA signaling, could be very rapidly silenced by presynaptic electrical stimulation at frequencies commonly used to probe synaptic function (0.05-1 Hz). Although this AMPA silencing required a rise in postsynaptic Ca(2+), it did not require activation of NMDA receptors, metabotropic glutamate receptors or voltage-gated calcium channels. The AMPA silencing, possibly explained by a removal of postsynaptic AMPA receptors, could subsequently be reversed by paired presynaptic and postsynaptic activity.