Pyramidal neurones

Neurodegeneration. Figure 3 Illustration of synaptic (neuritic) apoptosis. A pyramidal neuron is depicted with cortical afferents synapsing on its dendrites. Localized apoptotic mechanisms lead to the release of cytochrome c from the mitochondria and an increase in the concentration of activated caspase-3 in a presynaptic terminal that is synapsing on a dendritic spine. Increased caspase-3 activity results in a localized breakdown of this nerve terminal and its synapse. Subsequently, the postsynaptic dendritic spine retracts and disappears (Figure modified from Glantz et al. [5] [3]). 

Pyramidal neurons are the principal long-projecting cells of the cerebral cortex and hippocampus. They are so named because of the characteristic large apical dendrite, giving them a pyramidal shape. 

Kang N, Xu J, Xu Q, Nedergaard M, Kang J (2005) Astrocytic glutamate release-induced transient depolarization and epileptiform dischaiges in hippocampal CAl pyramidal neurons. J Neurophysiol... 

Figures 2.5 and 2.6 shows some experimental records illustrating the function of these channels. Figure 2.5 illustrates the function of SKca channels in a hippocampal pyramidal neuron. In the record marked control in Fig. 2.5(b) the neuron was depolarised by injecting a 1-s long depolarising current. This makes it fire action...

There is a good deal of evidence that the therapeutic effects of antidepressants could involve adaptive changes in 5-HTia receptors. Postsynaptic 5-HTia receptor responses became implicated because the hyperpolarisation of hippocampal CA3 pyramidal neurons that follows ionophoretic administration of 5-HT was found to be increased after chronic treatment with most (but not all) antidepressants (Chaput, de Montigny and Blier 1991). Others suggested that antidepressants attenuate postsynaptic 5-HTja responses because the hypothermia, evoked by their activation, is diminished by antidepressants (Martin et al. 1992). 

Hesen, W. Joels, M. (1996). Modulation of 5-HTia responsiveness in CAi pyramidal neurons by in vivo activation of corticosteroid receptors. J. Neuroendocrinol. 8, 433-8. 

Intracerebroventricular injection of kainic acid has been shown to result in a well-characterized pattern of neuronal cell damage. In the hippocampus, kainic acid causes a selective lesion of the CA3 pyramidal neurons, an area rich in KA1 and GluR6 receptors. The lesion does not compromise passing axons, which is why this type of (excitotoxic) lesion is often referred to as axon-sparing . Kainic acid injection into the hippocampus also leads to epileptiform discharges in cells normally innervated by the damaged pyramidal neurons. 

FIGURE 24-1 Phosphotyrosine staining of a hippocampal neuron. A cultured rat hippocampal pyramidal neuron is stained with an antiphosphotyrosine antibody and detected by a secondary antibody conjugated to rhodamine. The staining reflects the presence of tyrosine-phosphorylated proteins throughout the neuron, including the cell body and synaptic regions. 

Englund, U., Bjorldund, A., Wictorin, K., Lindvall, O. and Kokaia, M. Grafted neural stem cells develop into functional pyramidal neurons and integrate into host cortical circuitry. Proc. Natl Acad. Sci. U.S.A. 99 17089-17094,2002. 

CA3 pyramidal neurons receive the mossy fiber input from the granule neurons of the dentate gyrus. This connection is part of the 3-cell circuit of the hippocampus that is believed to be involved in learning and memory. 

Chronic corticosterone treatment or repeated restraint stress promotes atrophy of apical dendrites of CA3 pyramidal neurons. 

Adrenalectomy causes neurons of the dentate gyrus to die and to be replaced by new neurons, whereas pyramidal neurons are unaffected. 

FIGURE 52-10 Summary of adrenal steroid effects on neurons of the hippocampus, illustrating their ability to protect and stabilize the population of the dentate granule neurons and to potentiate damage caused by excitatory amino-acid release upon pyramidal neurons. E, estrogen. (From [41], with permission.)... 

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