An electron microscopic study of lesion-induced synaptogenesis in the dentate gyrus of the adult rat. I. Magnitude and time course of degeneration

Two distinct types of thalamic nucleus are proposed on the basis of the afferent fibres that they receive from ascending pathways and from the cerebral cortex. 'First order nuclei' receive primary afferent fibres, definable on the basis of their origin and their intrathalamic synaptic relationships, from ascending pathways. These nuclei receive corticothalamic afferents from pyramidal cells in cortical layer 6, which also send branches to the thalamic reticular nucleus and appear to have a modulatory function. 'Higher order nuclei' receive most or all of their 'primary afferents' from pyramidal cells in cortical layer 5. These resemble the ascending primary afferents in the first order nuclei in terms of fine structure, synaptic relationships and in lacking a branch to the thalamic reticular nucleus. The higher order nuclei also receive modulatory afferents from layer 6. It is proposed that the higher-order nuclei are largely concerned with transmitting information about the output of one cortical area to another cortical area, and that they are likely to play a key role in corticocortical communication and higher cortical functions.

Anatomical evidence concerning the role of the thalamus in corticocortical communication: a brief review

The synaptic input of interneurons with horizontal dendrites in stratum oriens of the CA1 region was investigated, with particular attention to the portion of synapses originating from local pyramidal cells. Most of these GABAergic interneurons are known to contain somatostatin, and terminate on pyramidal dendrites in conjunction with entorhinal afferents in stratum lacunosum-moleculare. A smaller number of horizontal cells in this layer are immunoreactive for calbindin, and project to the medial septum. Selective ischaemic degeneration was used to label local axon collaterals of CA1 pyramidal cells, and immunostaining for mGluR1 or calbindin to visualise somatostatin- and calbindin-containing horizontal interneurons, respectively, at the stratum oriens-alveus border. The number of degenerating and intact synaptic boutons was counted on mGluR1- as well as on calbindin-positive dendrites and somata, whereas in another group of animals the proportion of GABA-immunoreactive synapses was estimated on calbindin-positive dendrites. On average, > 60% of the total presynaptic elements of both cell types were degenerating, i.e. originated from CA1 pyramidal cells, whereas GABA-positive boutons, which are known to survive ischaemia, are likely to account for a large proportion of non-degenerating boutons. Thus the vast majority of presumed excitatory synapses on somatostatin- and calbindin-containing horizontal neurons derives from local collaterals of CA1 pyramidal cells. The remaining GABA-negative synapses surviving ischaemia may also originate from CA1 pyramidal cells, e.g. from those in the ventral hippocampus, which are rarely damaged by global forebrain ischaemia. Alternative sources may include subcortical afferents known to innervate interneurons, or ipsi- and contralateral CA3 pyramidal cells, which, according to the present results, may account only for a negligible number of synapses on these interneurons types. We conclude that somatostatin-containing neurons at the oriens-alveus border of CA1, which are likely to mediate an inhibitory control of the efficacy and/or plasticity of entorhinal synapses on pyramidal cell dendrites, are driven primarily in a feed-back manner. The source of afferent excitation for calbindin-containing horizontal neurons in this region is very similar, suggesting that the GABAergic hippocamposeptal feed-back is also activated by local pyramidal cell collaterals.

Synaptic input of horizontal interneurons in stratum oriens of the hippocampal CA1 subfield : structural basis of feed-back activation

Colchicine, which inhibits axoplasmic transport and induces organelle alterations in nerve terminals, was injected intraocularly in pigeons. Electrical stimulation of the optic nerve yielded normal evoked potentials in retinotectal fibers, whereas postsynaptic responses recorded in the tectum were reduced. Postsynaptic depression suggests a deficit of synaptic transmission, presumably dependent on colchicine interference with migrating material.

https://science.sciencemag.org/content/sci/175/4026/1140.full.pdf

Synaptic Transmission Depressed by Colchicine Blockade of Axoplasmic Flow

Publisher Summary The existence of axoplasmic flow—that is, the longitudinal translocation of materials in axons, is generally recognized. This chapter describes axoplasmic flow in the nerves of mature animals. Such nerves are usually opaque and axoplasmic flow in them eludes direct observations. Indirect methods have to be used to detect the flow in this material. The existence of movements of neuronal components in axons in situ was first inferred from the effects of nerve section and subsequent regeneration. Since the peripheral effects of nerve section are much more conspicuous than the central effects, attention was focused almost exclusively on the transport of substances from the cell body to the nerve endings. This chapter reexamines the divergent descriptions of axoplasmic flow and the ways by which they were arrived at. It describes the advantages and shortcomings of various methods of detection and measurements of flow.

O.L. Vaccarezza

Papers

Temporal course of synaptic degeneration in the lateral geniculate nucleus: Its dependence on axonal stump length