Biology:Basal dendrite

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A basal dendrite is a dendrite that emerges from the base of a pyramidal cell[1] that receives information from nearby neurons and passes it to the soma, or cell body. Due to their direct attachment to the cell body itself, basal dendrites are able to deliver strong depolarizing currents and therefore have a strong effect on action potential output in neurons.[2] The physical characteristics of basal dendrites vary based on their location and species that they are found in. For example, the basal dendrites of humans are overall found to be the most intricate and spine-dense, as compared to other species such as Macaques. It is also observed that basal dendrites of the prefrontal cortex are larger and more complex in comparison to the smaller and simpler dendrites that can be seen within the visual cortex.[3] Basal dendrites are capable of vast amounts of analog computing, which is responsible for many of the different nonlinear responses of modulating information in the neocortex.[4] Basal dendrites additionally exist in dentate granule cells for a limited time before removal via regulatory factors.[5] This removal usually occurs before the cell reaches adulthood, and is thought to be regulated through both intracellular and extracellular signals.[5] Basal dendrites are part of the more overarching dendritic tree present on pyramidal neurons. They, along with apical dendrites, make up the part of the neuron that receives most of the electrical signaling. Basal dendrites have been found to be involved mostly in neocortical information processing.[6]

Morphology

Basal dendrites are a feature of pyramidal neurons and emanate from the base of the soma. These neurons typically have many small basal dendrites along with one large apical dendrite.[7]There is substantial variation in Basal dendrite morphology from one brain region to another and from species to species. Studies in primates show that dendritic arbor complexity positively correlates with higher-order cortical regions.[8] In a study of macaques, it was found that the basal dendrites of layer II/III pyramidal neurons are simpler and have lower spine density in the primary visual cortex than in higher-order visual areas. This same study also found that, in macaques, the basal dendrites of the prefrontal cortex were especially large, complex, and spiny.[9]

Function

Integration of synaptic inputs

Basal dendrites of neocortical pyramidal neurons primarily receive local signals from lower-order cortical areas in bottom-up, feed-forward circuits. In the layer II/III pyramidal cells of the cortex, basal dendrites receive signals from layer IV neurons and local-circuit excitation.[10] NMDA spikes amplify the signals received simultaneously at a basal dendrite and increase the likelihood of an action potential.

Synaptic plasticity

The synapses on the proximal basal dendrites of neocortical pyramidal neurons can be potentiated by pairing EPSPs with back-propagating action potentials. Potentiation of synapses on distal basal dendrites can be initiated by a strong synaptic activation, sufficient to trigger an NMDA spike, and can be facilitated by the neuro-modulatory signal BDNF (Brain-derived Neurotrophic Factor).[11]

Caffeine has been observed to increase the length, number and branching of spines on basal dendrites of CA1 hippocampal neurons. It is believed that these effects are mediated by long-term potentiation in hippocampal synapses.[12]

A recent study posits that physical exercise contributes to the structural plasticity of the hippocampus by increasing spine density of CA1 basal dendrites. It is believed this effect is mediated by IGF-1 upregulation.[13]

Contribution to neuronal output

Basal Dendrites have been observed to experience NMDA-mediated Dendritic spikes, an ability yet to be seen in apical dendrites under certain conditions. This suggests the excitatory behavior of these two groups may differ. Dendritic Spikes are Threshold-dependent potentials generated within dendrites that influence the soma.[14] They amplify signals received by the soma and influence action potential generation. The individual branches of a basal dendrite exhibit nonlinear excitability due to the formation of NMDA spikes and have the capacity to act independently. The combined output of these individual branches is then summed at the soma.

The Basal Dendrites of Layer V pyramidal neurons in the neocortex are known to support backpropagation of Action potentials. High-frequency action potential firing from the Soma has been observed to trigger Ca2+ dendritic spikes in the Basal Dendrites due to Backpropagation.[15]

Dendritic arbor

A dendritic arbor is the branching pattern of a neuron's dendrites. Basal dendrites are part of sampling dendritic arbors.[16] These arbors are not completely space-filling, but make more than one specific, or selective, connection.[16] For example, at the CA1 pyramidal cell of a rat, there are 5 basal dendrites at the soma with 30 branch points, while space filling dendritic arbors can contain hundreds of branch points, and selective arbors can contain as few as 0 or 1.[16] Figure 2 is a representation of a CA1 pyramidal cells of a rat, showing many branch points and dendritic length.[17]

Clinical Significance

Reductions in dendritic branching and spine density in basal dendrites of pyramidal neurons in the medial prefrontal cortex has been reported to be linked with schizophrenia.[18]Other studies have also reported reduced dendritic spine volume in basal dendrites of CA3 neurons in the hippocampus. Alterations in the expression TAOK2 (thousand-and-one amino acid kinase 2), which is implicated in dendritic regulation, has been reported in both autism and schizophrenia.[19]

Gene expression

Basal dendrite growth is regulated by Semaphorin 3A and its receptor neurophilin1(NRP1). Recent studies have suggested that TAO kinase 2 (TAOK2) coordinates with NRP1 to direct basal dendrite growth by stimulating Jun Kinase (JNK). Knockdown of TAOK2 has been shown to decrease basal dendrite arborization and spinal density, whereas upregulation increases them[20]. Stimulation of JNK by TAOK2 was shown to restore basal dendrite arborization in NRP-1-deficient neurons.[21] Downregulation of Nrp1 results in a decrease in dendrite expression but this can also be rescued by overexpression of TAOK2.

References

  1. ↑ "Basilar Dendrite". Neuroscience Information Framework. August 2010. http://neurolex.org/wiki/Category:Basilar_Dendrite. 
  2. ↑ "Dynamics of action potential backpropagation in basal dendrites of prefrontal cortical pyramidal neurons". The European Journal of Neuroscience 27 (4): 923–36. February 2008. doi:10.1111/j.1460-9568.2008.06075.x. PMID 18279369. 
  3. ↑ Spruson, Nelson (February 13, 2008). "Pyramidal neurons: dendritic structure and synaptic integration". Nature Reviews Neuroscience 9 (3): 206–221. doi:10.1038/nrn2286. PMID 18270515. http://www.sci.utah.edu/~macleod/bioen/be6003/notes/W08-spruston_nature_2008.pdf. 
  4. ↑ "Location-dependent excitatory synaptic interactions in pyramidal neuron dendrites". PLOS Computational Biology 8 (7): e1002599. 2012-07-19. doi:10.1371/journal.pcbi.1002599. PMID 22829759. Bibcode: 2012PLSCB...8E2599B. 
  5. ↑ 5.0 5.1 "Differentiation of apical and basal dendrites in pyramidal cells and granule cells in dissociated hippocampal cultures". PLOS ONE 10 (2): e0118482. 2015. doi:10.1371/journal.pone.0118482. PMID 25705877. Bibcode: 2015PLoSO..1018482W. 
  6. ↑ Gordon, Urit; Polsky, Alon; Schiller, Jackie (2006-12-06). "Plasticity Compartments in Basal Dendrites of Neocortical Pyramidal Neurons". Journal of Neuroscience 26 (49): 12717–12726. doi:10.1523/JNEUROSCI.3502-06.2006. PMID 17151275. 
  7. ↑ Spruston, Nelson (March 2008). "Pyramidal neurons: dendritic structure and synaptic integration" (in en). Nature Reviews Neuroscience 9 (3): 206–221. doi:10.1038/nrn2286. ISSN 1471-0048. https://www.nature.com/articles/nrn2286. 
  8. ↑ Gilman, Morgan S. A.; Castellanos, Carlos A.; Chen, Man; Ngwuta, Joan O.; Goodwin, Eileen; Moin, Syed M.; Mas, Vicente; Melero, José A. et al. (2016-12-16). "Rapid profiling of RSV antibody repertoires from the memory B cells of naturally infected adult donors". Science Immunology 1 (6). doi:10.1126/sciimmunol.aaj1879. ISSN 2470-9468. PMID 28111638. 
  9. ↑ Gilman, Joshua P.; Medalla, Maria; Luebke, Jennifer I. (2016-03-10). "Area-Specific Features of Pyramidal Neurons—a Comparative Study in Mouse and Rhesus Monkey" (in en). Cerebral Cortex 27 (3). doi:10.1093/cercor/bhw062. ISSN 1047-3211. PMC 6059164. https://academic.oup.com/cercor/article/27/3/2078/3056318. 
  10. ↑ Granato, Alberto; Phillips, William A.; Schulz, Jan M.; Suzuki, Mototaka; Larkum, Matthew E. (2024-06-01). "Dysfunctions of cellular context-sensitivity in neurodevelopmental learning disabilities". Neuroscience & Biobehavioral Reviews 161. doi:10.1016/j.neubiorev.2024.105688. ISSN 0149-7634. https://www.sciencedirect.com/science/article/pii/S014976342400157X. 
  11. ↑ Spruston, Nelson (March 2008). "Pyramidal neurons: dendritic structure and synaptic integration" (in en). Nature Reviews Neuroscience 9 (3): 206–221. doi:10.1038/nrn2286. ISSN 1471-0048. https://www.nature.com/articles/nrn2286. 
  12. ↑ "Caffeine Consumption and Prevention of Cognitive Decline: A Focus on Mechanisms" (in en-US), Diet and Nutrition in Dementia and Cognitive Decline (Academic Press): pp. 879–889, 2015-01-01, https://www.sciencedirect.com/science/chapter/edited-volume/abs/pii/B9780124078246000811, retrieved 2026-03-29 
  13. ↑ "Brain insulin resistance impairs hippocampal plasticity" (in en-US), Vitamins and Hormones (Academic Press) 114: pp. 281–306, 2020-01-01, https://www.sciencedirect.com/science/chapter/bookseries/abs/pii/S0083672920300297, retrieved 2026-03-29 
  14. ↑ Remy, S; Beck, H; Yaari, Y (2010-08-01). "Plasticity of voltage-gated ion channels in pyramidal cell dendrites". Current Opinion in Neurobiology. Signalling mechanisms 20 (4): 503–509. doi:10.1016/j.conb.2010.06.006. ISSN 0959-4388. https://www.sciencedirect.com/science/article/pii/S0959438810001030. 
  15. ↑ Remy, S; Beck, H; Yaari, Y (2010-08-01). "Plasticity of voltage-gated ion channels in pyramidal cell dendrites". Current Opinion in Neurobiology. Signalling mechanisms 20 (4): 503–509. doi:10.1016/j.conb.2010.06.006. ISSN 0959-4388. https://www.sciencedirect.com/science/article/pii/S0959438810001030. 
  16. ↑ 16.0 16.1 16.2 Harris, Kristen M.; Spacek, Josef (2016). "Dendrite Structure". in Stuart. Dendrites (3rd ed.). Oxford University Press. https://synapseweb.clm.utexas.edu/sites/default/files/synapseweb/files/2016_dendrites_harris_spacek_dendrite_structure.pdf. 
  17. ↑ Routh, Brandy; Johnston, Daniel; Harris, Kristen; Chitwood, Raymond (October 2009). "Anatomical and Electrophysiological Comparison of CA1 Pyramidal Neurons of the Rat and Mouse". Journal of Neurophysiology 102 (4): 2288–2302. doi:10.1152/jn.00082.2009. PMID 19675296. 
  18. ↑ Copf, Tijana (2016-09-01). "Impairments in dendrite morphogenesis as etiology for neurodevelopmental disorders and implications for therapeutic treatments". Neuroscience & Biobehavioral Reviews 68: 946–978. doi:10.1016/j.neubiorev.2016.04.008. ISSN 0149-7634. https://www.sciencedirect.com/science/article/pii/S0149763415302475. 
  19. ↑ Copf, Tijana (2016-09-01). "Impairments in dendrite morphogenesis as etiology for neurodevelopmental disorders and implications for therapeutic treatments". Neuroscience & Biobehavioral Reviews 68: 946–978. doi:10.1016/j.neubiorev.2016.04.008. ISSN 0149-7634. https://www.sciencedirect.com/science/article/pii/S0149763415302475. 
  20. ↑ Copf, Tijana (2016-09-01). "Impairments in dendrite morphogenesis as etiology for neurodevelopmental disorders and implications for therapeutic treatments". Neuroscience & Biobehavioral Reviews 68: 946–978. doi:10.1016/j.neubiorev.2016.04.008. ISSN 0149-7634. https://www.sciencedirect.com/science/article/pii/S0149763415302475. 
  21. ↑ Valnegri, Pamela; Puram, Sidharth V.; Bonni, Azad (2015-07-01). "Regulation of dendrite morphogenesis by extrinsic cues". Trends in Neurosciences 38 (7): 439–447. doi:10.1016/j.tins.2015.05.003. ISSN 0166-2236. https://www.sciencedirect.com/science/article/pii/S0166223615001174. 

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