Ventrobasal complex
| Ventrobasal complex | |
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| Details | |
| Latin | nuclei ventrobasales |
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| TA | Lua error in Module:Wikidata at line 744: attempt to index field 'wikibase' (a nil value). |
| TH | {{#property:P1694}} |
| TE | {{#property:P1693}} |
| FMA | {{#property:P1402}} |
| Anatomical terminology
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The ventrobasal complex ("'VB"') is a relay nucleus of the thalamus for nociceptive stimuli received from nociceptive nerves. The VB consists of the Ventral posteromedial nucleus (VPM) and the Ventral posterolateral nucleus (VPL). In some species the ventral posterolateral nucleus, pars caudalis is also a part of the VB.[1] The VB gets inputs from the Spinothalamic tract, Medial lemniscus, and corticothalamic tract.[2][3] The main output of the VB is the primary somatosensory cortex.
The VB serves as the main relay for nociceptive stimuli and the modulation of that stimuli to the primary somatosensory cortex. The modulation occurs through different types of receptors present in the VB.
Contents
VB Inputs
Spinothalamic Tract (STT) cells that project from laminae I and V in the lumbrosacral area of the spinal cord project to the VPL in the VB.[2] STT cells located in the cervical area of the spinal cord are the densest and project from the neck of the dorsal horn to the VPL of the VB. Most projections to the VB are contralateral while only a few projections to the VB are ipsilateral.[2]
Excitatory inputs to the VB are medial lemniscal (ML) and corticothalamic (CT) glutamatergic synapses. The ML is a sensory afferent input and the CT is from layer VI of the primary sensory cortex.[3]
The VB also gets inputs from areas in the brain stem which release Acetylcholine (ACh) that can modulate activity in the VB.[3]
VB Outputs
The VB has outputs to the primary somatosensory cortex.
VB Neurons
There is two types of nociceptive neurons that provide input to the VB: nociceptive specific (NS) neurons and Wide dynamic range neuron (WDR).
NS neurons respond specifically to a noxious mechanical stimuli, whereas WDR neurons respond to a graded mechanical stimuli. NS and WDR neurons within the VB are somatotopically organized. NS neurons are located more caudally in the VB, while WDR neurons are located more rostrally. All inputs into the VB are contralateral and have two different receptive fields within the VB. The VPM receptive field receives input from the contralateral trigeminal nerve and the VPL receptive field receives input from the contralateral spinal nerve. Each have NS and WDR neurons but terminate either caudally or rostrally respectively.[1]
VB Modulation
Nicotinic ACh Receptors
Nicotinic acetylcholine receptor (nAChRs) are present in the VB. Each nAChR can be made up of different subunits which can cause the receptor to respond to different stimuli.[3] In the VB nAChRs can contain the subunits α4, α5, α7, and β2. nAChRs that are made up of (α4β2)2α5 are of interest because they decrease neurotransmitter release for corticothalamic (CT) synapses. When nAChRs are activated there is a decrease in synaptic transmission of glutamate from CT neurons. When CT synaptic transmission is decreased by activation of the nAChRs then the activated nAChRs in the VB can selectively enhance information[further explanation needed] to the somatosensory cortex through the medial lemniscal tract.[3]
Mu-opioid Receptors
Lua error in package.lua at line 80: module 'strict' not found.mu Opioid receptor (MORs) are inhibitory receptors that can cause a decrease in pain if activated and are expressed in the VB especially in the VPL.[4] When MORs are activated, can be activated by an agonist like DAMGO, pain related behaviors are decreased for a certain amount of time. After 45 minutes rats that were given DAMGO show signs of increased pain behaviors suggesting that opiates activate a pronociceptive system which can lead to increased pain sensitivity after only having one dose of opiates administered.[4] Decrease in pain related behaviors can be attributed to the activation of MORs in the VB which activates an inhibitory circuit for pain by decreasing the amount or quality of information relayed to the somatosensory cortex.[4] However, there is a complex mechanism between MORs and other receptors in the VB that can lead to a decrease in pain related behaviors and thus further research is needed to understand exactly how this mechanism works.
GABAB Receptors
GABAB receptors is located in the VB. If the receptor is located presynaptically then when activated it causes the suppression of neurotransmitter release. If the receptor is located postsynaptically then when activated the receptor causes Inhibitory postsynaptic potential.[5] When GABAB receptors are activated or blocked by baclofen (agonist) or CGP35348 (antagonist) respectively there is a decrease in pain related behaviors in a dose-dependent manner.[further explanation needed][5] That is if a higher dose is given then there is less pain related behaviors. It is not known if this mechanism is presynaptically or postsynpatically occurring. Further research is needed to distinguish between where the inhibition is being mediated.
References
- ↑ 1.0 1.1 Natsu Koyama, Yasuo Nishikawa, Toshikatsu Yokota. Distribution of nociceptive neurons in the ventrobasal complex of macaque thalamus. Neuroscience Research 31 (1998) 39-51.
- ↑ 2.0 2.1 2.2 W.D. Willis Jr. et al. Projections from the marginal zone and deep dorsal horn to the ventrobasal nuclei of the primate thalamus. Pain 92 (2001) 267-276.
- ↑ 3.0 3.1 3.2 3.3 3.4 Yasuyuki Nagumo, Yuichi Takeuchi, Keiji Imoto, Mariko Miyata. Synapse- and subtype-specific modulation of synaptic transmission by nicotinic acetylcholine receptrs in the ventrobasal thalamus. Neuroscience Research 69 (2011) 203-213.
- ↑ 4.0 4.1 4.2 Daniel Humberto Pozza et al. Nociceptive behaviour upon modulation of mu-opioid receptors in the ventrobasal complex of the thalamus of rats. Pain 148 (2010) 492-502.
- ↑ 5.0 5.1 Catarina Soares Potes, Fani Lourenca Neto, Jose Manuel Castro-Lopes. Inhibition of pain behavior by GABAB receptors in the thalamic ventrobasal complex: Effect on normal rats subjected to the formalin test of nociception. Brain Research 1115 (2006) 37-47.
