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The amplitude of backpropagating action potentials (BAPs) is attenuated, either activity- or neurotransmitter-dependently in the apical dendrite of hippocampal pyramidal neurons. To test the possibility that this BAP attenuation may contribute to regulating the inducibility of long-term potentiation (LTP), BAPs evoked by theta-burst stimulation (TBS), a standard protocol for LTP induction, to apical dendrite synapses were subjected to perturbation by conditioning stimuli to basal dendrite synapses. During this conditioned TBS (cTBS), the amplitude of BAPs was noticeably attenuated, but that of somatic action potentials was not. In the distal dendrite area, cTBS-induced LTP was much smaller than that induced by TBS. By contrast, no difference was observed between TBS- and cTBS-induced LTP in the proximal dendrite area. These findings suggest that the activity-dependent attenuation of BAPs, propagating along the apical dendrite, may serve to regulate hippocampal synaptic plasticity.

Dendritic morphology was studied in human hippocampal dentate granule cells (DGCs) by intracellularly-injecting biocytin in slice preparations that were obtained from temporal lobe epilepsy patients who underwent a surgical treatment for medically-intractable seizures. These DGCs had a fan-shaped dendritic domain of 54.1 degrees +/- 4.1 S.E.M. with 13.8 +/- 1.1 branch points and an estimated total dendritic length of 11535.6 microns +/- 3045.4. Dendritic spines were counted, and spine density was calculated to be 0.25 spines/microns +/- 0.16 S.E.M.. However, when the cells were categorized into two groups based on the presence or absence of the aberrant mossy fiber collaterals, the number of dendritic branches was significantly lower and spine density was significantly higher in DGCs that had aberrant collaterals. In particular, in the proximal dendrite, the spine density was 5 times higher in DGCs whose own mossy fibers were reorganized sending aberrant collaterals to this dendritic region (0.750 spines/microns +/- 0.203 S.E.M.: P0.01) than the DGCs without such collaterals (0.082 spines/microns +/- p.021 S.E.M.). These results suggest that the axonal reorganization may have an effect on the morphology of DGC dendrites directly or indirectly in such a way that dendritic structure and spines could be protected from seizure-induced excitotoxic cell damage.

Although the majority of mRNAs expressed in neurons are confined to the perikaryon, a growing number appear to be transported into dendrites. It is likely that this allows for the local regulation of protein synthesis within discrete subcellular compartments. Here, three different subcellular distribution patterns are demonstrated for four mRNAs that encode proteins highly expressed in Purkinje cells and their dendrites; mRNAs are found in the perikaryon only, perikaryon and proximal dendrite, or perikaryon and proximal plus distal dendrites. Further, it is shown that transport of an mRNA into the dendrites increases its sensitivity to translational inhibition by diphtheria toxin. These data suggest a simple model whereby the transport machinery can regulate the translation of selected mRNAs. Thus, environmental signals that generally affect translational efficiency in concert with the selectivity provided by the transport machinery could provide a means to locally regulate the synthesis of a restricted pool of proteins.

To examine synaptic input and association of terminals containing dopamine and other transmitters to rat striatal nitric oxide synthase-expressing neurons, an electron microscopic study using tyrosine hydroxylase (TH) immunohistochemistry combined with histochemistry for NADPH-diaphorase (NADPHd) was performed. NADPHd-positive neurons had medium-sized cell bodies containing a highly invaginated nucleus and received relatively sparse synaptic input; 3.6% of boutons apposed to the NADPHd-positive neurons were TH-immunoreactive. Of these TH-immunoreactive boutons, two synaptic contacts showing symmetrical synaptic specializations were found on a cell body and a proximal dendrite of a NADPHd-positive neuron. Other nonsynaptic TH-immunoreactive boutons were occasionally associated with unlabeled terminals adjacent to the NADPHd-positive dendrites and also forming asymmetric synaptic contacts with unlabeled spinous or dendritic profiles. These results suggest that activity of the striatal neurons that release nitric oxide may be regulated by direct synaptic input from dopaminergic neurons and also suggest that the TH-immunoreactive terminals associated with the dendrites of nitric oxide synthase-expressing neurons provide the sites where nitric oxide influences dopamine release from neighboring terminals.

The Mg 2+ -dependent depolarizing action of N- methyl- d -aspartate (NMDA) was intrasomatically investigated, in comparison with quisqualate (QA), in Purkinje cells in cerebellar slices from adult guinea pigs. NMDA applied iontophoretically to the proximal dendritic region (about 100 μm from the Purkinje cell soma) induced depolarizations and spike firings in about the half of the Purkinje cells tested in nominal Mg 2+ -free medium (contaminated with 4–11 μM Mg 2+ ), and 1 mM Mg 2+ almost completely blocked this NMDA action. Application of NMDA onto the distal dendritic region (about 200 μm from the soma) caused no depolarization at all even in the Mg 2+ -free medium. QA applied onto either the proximal or distal dendritic region consistently showed Mg 2+ -independent depolarization The amplitude of NMDA-induced depolarization in the Mg 2+ -free medium was non-linearly related to the membrane potential, i.e. smaller at a hyperpolarized potential level. 2-Amino-5-phosphonovalerete blocked the NMDA action partially but more selectively than the QA action, while the reverse was the case for glutamic acid diethylester. These results suggest that the Mg 2+ -dependent, NMDA-sensitive receptor, which is distinct from the QA receptor and probably similar to the well-known NMDA receptor, is present on the proximal dendrite of the cerebellar Purkinje cell of the guinea pig.

Electron microscopic examination of the lateral geniculate nucleus in monkeys reveals the consistent occurrence of triadic synaptic arrangements where a retinal axon terminal is presynaptic to both a principal cell (P-cell) and a non-axonal portion of an interneuron (I-cell) containing flattened vesicles, which in turn is presynaptic to the same P-cell element. These ‘triads’ are found within glomeruli where the P-cell participates with a dendritic protrusion and the I-cell with a dendritic appendage (type 1 triad), and also outside the glomerulus where the P-cell is represented by its soma or very proximal dendrite (type 2 triad), or the I-cell profile is the soma which again contains synaptic vesicles (type 3 triad). The most parsimonious interpretation of the functional significance of the triadic synapse is to consider it as a device for the inhibitory phasing of the P-cell discharge resulting from the release of I-cell inhibitory transmitter by excitation of the interneuron through the same retinal afferent which causes the initial tonic activity of the P-cell. Further roles of the I-cell are discussed on the basic of a model which considers a random geometry of dendritic (long) and axonal (short) arborizations. The model suggests 3 possible I-cell actions: (1) local inhibition limited to the triadic arrangement; (2) inhibition at a distance through an axonal mechanism; and (3) inhibition at a distance by way of the presynaptic dendrites.

The secondary transneuronal effect of bilateral, dorsal column lesion (T12) on the frequency of boutons on cells in the lateral ventroposterolateral nucleus (VPL) was studied. Rats were killed 1, 2, 3, 7, 14, 30, 45, 60, 90, or 120 days postoperative (DPO), and bouton counts (Rasmussen stain) were made on the soma, or along 5- and 10-μm segments of the proximal dendrite branching from soma, in the rostral two-thirds of the VPL. The soma diameter also was measured of those neurons chosen for bouton counts on the circumference of the soma. Significant, increased afferentiation along a 5-μm segment of the proximal dendrite occurred during the first 3 days postlesion compared with longer survival times. Along the 10-μm segment, as at 5 μm on the proximal dendrite, bouton counts at 2 DPO were significantly higher than at 30 and 120 DPO. This rapid change in afferentation during the first week postlesion mirrors similar effects reported in the nucleus gracilis of these same cases. Bouton counts along the 5-μm segment of the proximal dendrite decreased significantly to less than normal at 30 and 120 DPO, indicating the nonstable and protracted character of afferentation after the distal cord lesion. A significant, positive correlation was obtained between boutons on the soma and proximal dendrite (5 μm segment) in cases with lesions, suggesting parallel innervation patterns for these adjacent neuronal components during 120 postoperative days. There was no significant change in the bouton counts or diameter of the soma during postoperative days. These results suggest that lesion of the thoracic dorsal column may result in subsequent rapid bouton patterning on the lateral VPL neurons, presumably mediated by their medial lemniscal afferent fibers. The postlesion source(s) of afferentation remains an intriguing, and as yet unanswered, question.