Basal dendrite

Pyramidal neurons

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. In mammals, the basal dendrites of pyramidal neurons are typically short tufts but can vary in size, shape, and spine density depending on location. In macaques, the basal dendrites of pyramidal neurons are especially large in the prefrontal cortex relative to other regions. 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.

Synaptic inputs and integration

Dendrites of pyramidal neurons, both basal and apical, typically receive excitatory glutamatergic signals, whereas the soma receives inhibitory GABAergic signals. Basal dendrites often receive inputs from cell populations that are distinct from those connected to distal apical dendrites. In many pyramidal neurons, basal and proximal apical dendrites receive inputs from local neural circuits, whereas distal apical dendrites receive inputs from more distant cell populations. In many mammalian CA1 pyramidal neurons, basal and proximal apical dendrites will receive input primarily from CA3 pyramidal neurons, whereas the distal apical dendrites will receive input from neurons in the entorhinal cortex and thalamic nucleus reuniens.

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. NMDA spikes amplify the signals received simultaneously at a basal dendrite and increase the likelihood of an action potential.

Excitability and plasticity

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).

It is theorized that the organization of inputs across basal, proximal, apical dendrites, and distal apical dendrites may be functionally significant. The arrangement of signals from distant sources on distal apical dendrites and local signals on basal and proximal apical dendrites may contribute to the pyramidal neuron’s coincidence detection. Alternatively, it is postulated that this arrangement is meant to modulate responsiveness to local signals.

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.

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.

Contribution to neuronal output

Basal dendrites of pyramidal neurons have been observed to experience NMDA-mediated Dendritic spikes, an ability yet to be seen in the 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. 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.

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. 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.

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. Stimulation of JNK by TAOK2 was shown to restore basal dendrite arborization in NRP-1-deficient neurons. Downregulation of Nrp1 results in a decrease in dendrite expression but this can also be rescued by overexpression of TAOK2.