[3] The apical dendrites in these regions contribute significantly to memory, learning, and sensory associations by modulating the excitatory and inhibitory signals received by the pyramidal cells.
[5] Individual pyramidal cells in the CA3 region have burst properties due to high densities of calcium channels in their proximal dendrites.
Usually curtailed by the hyperpolarizing local inhibition (due to the excitatory collateral system), this can lead to gradual recruitment of CA3 neurons and result in synchronized burst discharges.
[4] In the CA3, the temporoammonic (TA), commissural (COM), associational (ASSOC), and mossy fiber (MF) afferents all make excitatory glutamatergic (Glu) synapses on pyramidal cell dendrites (both apical and basal).
[4] In contrast, only slow signals from the distal dendrites are efficiently transferred to the soma, suggesting a modulatory role on the resting potential of the cell.
[4] The major trigger for CA3 discharge is the afferent input from the dentate gyrus granule cells, from which mossy fiber terminals create very complex synapses on the proximal part of the CA3 apical dendrite in the stratum lucidum.
[2] Mossy fiber input to CA3 exhibits different plasticity than that of typical long term potentiation because it is dependent on (or at least sensitive to) monoaminergic (see monoamine) activation of the cAMP 2nd messenger system.
Interneuron cell types show unique dendritic arborization patterns and region specific targeting by axon collaterals.
[2] Recent experiments show that this modulation of pyramidal cells may differentially activate an interneuron subpopulation located in the distal reaches of the apical dendrites.
[9] The inhibitory system, by contrast, possess several (10) different types of synapses originating from specifically differentiated cells and are much more difficult to track.
[9] There is insufficient information to precisely distinguish between excitatory and inhibitory pathways contributing to the alterations in neurotransmitter expression and cell structure changes.
[10] Dendritic arbor formation for pyramidal neurons in the cortices occurs progressively beginning in late embryonic stages of development and extending well into post-natal periods.
Action potential changes in the retina, hippocampus, cortex, and spinal cord provide activity-based signals both to the active neurons and their post-synaptic target cells.
Spontaneous activity originating within neuronal gap junctions, the cortex sub-plate, and sensory inputs are all involved in the cell signaling that regulates dendrite growth.
[3] Useful models of dendritic arbor formation are the Xenopus tadpoles, which are transparent in early stages of larval development and allow for dye-labeled neurons to be repeatedly imaged in the intact animal over several weeks.
For example, in optical tectal neurons, dendrite arbor growth occurs approximately at the onset of retinal input.
[3] CaMKII mRNA is targeted to dendrites and both protein synthesis and enzyme activity are increased by strong synaptic input.
[15] Dendritic spines, post-synaptic structures receiving mainly excitatory input, are sensitive to experiences in development including stress episodes or drugs.
Studies have shown that prenatal stress reduces complexity, length, and spine frequency of layer II/III pyramidal apical dendrites in rat and primate models.
[17] Stress hormones in small doses do not themselves cause damage but magnify effects of other dangerous agents, including excitotoxins, hypoglycemia, hypoxia and ischemia.
Lesions in rat prefrontal cortices impair spontaneous alternation, radial maze performance, and passive avoidance.
[5] The apical dendrites, however, show a significant redistribution in stress-hormone treated animal brains, which is measured using Scholl analysis.
[16] In neurometabolic diseases, distended storage neurons are markedly swollen and pear shaped, with the nucleus and the nissl bodies displaced toward the apical dendrites.
The hypothesis is that this phenomenon creates a situation in which fast sodium spikes in the soma back-propagate into the dendrites, whereby they detonate bursting.
[21] These receptors are most dense in sectors CA3 and CA2 of the hippocampus, where nanomolar (nM) concentrations of kainic acid have been associated with pronounced and persistent depolarization of CA3 pyramidal neurons.
[21] This involving the conduction of excitatory activity along the mossy fiber projections from the area dentate granule cells to the CA3 neurons.
[2] Hyperventilation leads to a marked surface negative direct current shift due to depolarization of the apical dendritic trees of the cortical pyramidal cells.
[2] In the same model, the aforementioned upregulation of t-type calcium channels also has been shown to result in increased burst behavior in neurons in the hippocampus.
[2] However, measurements from both somatic and dendritic patch recordings show that the peak membrane potential deflection during a paroxysmal depolarizing shift (PDS) is 10mV greater in the apical trunk (supragranular location) than the soma.
[22] However, time-lapsed photography and two-photon microscopy have revealed dendrites as living, constantly changing tissues which are motile on a rapid time scale.