Is thalamocortical tract injury responsible for memory impairment in a patient with putaminal hemorrhage?

Prior to development of diffusion tensor imaging （DTI）, there were many difficulties in visualization and estimation of the Papez circuit in the live human brain （Papez, 1995）. Diffusion tensor tractography （DTT）, derived from DTI, allows for identification and visualization of neural tracts in the Papez circuit （Concha et al., 2005; Kwon et al., 2010; Granziera et al., 2011; Jang and Yeo, 2013; Jang et al., 2014a）. In the current study, using DTT, we report on a patient who showed injured thalamocortical tract between the anterior thalamic nuclei and the cingulate gyrus following a putaminal hemorrhage.

Thalamocortical Circuit Controls Neuropathic Pain via Up-regulation of HCN2 in the Ventral Posterolateral

The thalamocortical(TC)circuit is closely asso-ciated with pain processing.The hyperpolarization-activated cyclic nucleotide-gated(HCN)2 channel is predominantly expressed in the ventral posterolateral thalamus(VPL)that has been shown to mediate neuropathic pain.However,the role of VPL HCN2 in modulating TC circuit activity is largely unknown.Here,by using optogenetics,neuronal trac-ing,electrophysiological recordings,and virus knockdown strategies,we showed that the activation of VPL TC neurons potentiates excitatory synaptic transmission to the hindlimb region of the primary somatosensory cortex(S1HL)as well as mechanical hypersensitivity following spared nerve injury(SNI)-induced neuropathic pain in mice.Either pharmaco-logical blockade or virus knockdown of HCN2(shRNA-Hcn2)in the VPL was sufficient to alleviate SNI-induced hyperalgesia.Moreover,shRNA-Hcn2 decreased the excitability of TC neurons and synaptic transmission of the VPL-S1HL circuit.Together,our studies provide a novel mechanism by which HCN2 enhances the excitability of the TC circuit to facilitate neuropathic pain.

Neuronal nociceptive responses in thalamocortical pathways

The sensation of pain is critical for the survival of animals and humans. However, the brain mechanisms underlying pain perception remain largely unknown. How does the brain decode the pain-evoked activity into a particular sensory experience？ Over the past decade, attempts have been made to answer these questions by employing electrophysiological, functional brain imaging, and behavioral approaches, and some basic properties of pain formation have been revealed. Researchers have gradually recognized that there exists a distributed neural network that participates in the transmission and processing of pain information. These studies will further guide the development of more effective treatment for many disorders such as chronic pain.

Is the pain in chronic pancreatitis of neuropathic origin? Support from EEG studies during experimental pain

AIM: To prove the hypothesis that patients with chronic pancreatitis would show increased theta activity during painful visceral stimulation. METHODS: Eight patients and 12 healthy controls underwent an experiment where the esophagus was electrically stimulated at the pain threshold using a nasal endoscope. The electroencephalogram (EEG) was recorded from 64 surface electrodes and "topographic matching pursuit" was used to extract the EEG information in the early brain activation after stimulation. RESULTS: A major difference between controls and patients were seen in delta and theta bands, whereas there were only minor differences in other frequency bands. In the theta band, the patients showed higher activity than controls persisting throughout the 450 ms of analysis with synchronous brain activation betweenthe channels. The main theta components oscillated with 4.4 Hz in the patients and 5.5 Hz in the controls. The energy in the delta (0.5-3.5 Hz) band was higher in the controls, whereas the patients only showed scattered activity in this band. CONCLUSION: The differences in the theta band indicate that neuropathic pain mechanisms are involved in chronic pancreatitis. This has important implications for the understanding and treatment of pain in these patients, which should be directed against drugs with effects on neuropathic pain disorders.

Altered thalamic subregion functional networks in patients with treatment-resistant schizophrenia

BACKGROUND The thalamus plays a key role in filtering information and has extensive interconnectivity with other brain regions.A large body of evidence points to impaired functional connectivity(FC)of the thalamocortical pathway in schizophrenia.However,the functional network of the thalamic subregions has not been investigated in patients with treatment-resistant schizophrenia(TRS).AIM To identify the neural mechanisms underlying TRS,we investigated FC of thalamic sub-regions with cortical networks and voxels,and the associations of this FC with clinical symptoms.We hypothesized that the FC of thalamic subregions with cortical networks and voxels would differ between TRS patients and HCs.METHODS In total,50 patients with TRS and 61 healthy controls(HCs)matched for age,sex,and education underwent resting-state functional magnetic resonance imaging(rs-fMRI)and clinical evaluation.Based on the rs-fMRI data,we conducted a FC analysis between thalamic subregions and cortical functional networks and voxels,and within thalamic subregions and cortical functional networks,in the patients with TRS.A functional parcellation atlas was used to segment the thalamus into nine subregions.Correlations between altered FC and TRS symptoms were explored.RESULTS We found differences in FC within thalamic subregions and cortical functional networks between patients with TRS and HCs.In addition,increased FC was observed between thalamic subregions and the sensorimotor cortex,frontal medial cortex,and lingual gyrus.These abnormalities were associated with the pathophysiology of TRS.CONCLUSION Our findings suggest that disrupted FC within thalamic subregions and cortical functional networks,and within the thalamocortical pathway,has potential as a marker for TRS.Our findings also improve our understanding of the relationship between the thalamocortical pathway and TRS symptoms.

Selective and constructive mechanisms contribute to neural circuit formation in the barrel cortex of the developing rat

The cellular strategy leading to formation of neuronal circuits in the rodent barrel cortex is still a matter of controversy. Both selective and constructive mechanisms have been proposed. The selective mechanism involves an overproduction of neuronal processes and synapses followed by activity dependent pruning. Conversely, a constructive mechanism would increase the number of axons, dendrites, and synapses during development to match functionality. In order to discern the contributions of these two mechanisms in establishing a neuronal circuit in the somatosensory cortex, morphometric analysis of dendritic and axonal arbor growth was performed. Also, the number of synapses was followed by electron microscopy during the first month of life. We observed that axonal and dendritic arbors retracted distal branches, and elongated proximal branches, resulting in increased arbor complexity. This neuronal remodeling was accompanied by the steady increase in the number of synapses within barrel hollows. Similarly, the content of molecular markers for dendrites, axons and synapses also increased during this period. Finally, cytochrome oxidase activity rose with age in barrels indicating that the arbors became more complex while synapse density and metabolic demands increased. Our results support the simultaneous use of both selective and constructive mechanisms in establishing the barrel cortex circuitry.

Neuronal activity controls the development of interneurons in the somatosensory cortex

BACKGROUND： Neuronal activity in cortical areas regulates neurodevelopment by interacting with defined genetic programs to shape the mature central nervous system. Electrical activity is conveyed to sensory cortical areas via intracortical and thalamocortical neurons, and includes oscillatory patterns that have been measured across cortical regions. OBJECTIVE： In this work, we review the most recent findings about how electrical activity shapes the developmental assembly of functional circuitry in the somatosensory cortex, with an emphasis on intemeuron maturation and integration. We include studies on the effect of various neurotransmitters and on the influence of thalamocortical afferent activity on circuit development. We additionally reviewed studies describing network activity patterns. METHODS： We conducted an extensive literature search using both the PubMed and Google Scholar search engines. The following keywords were used in various iterations： ＂intemeuron＂, ＂somatosensory＂, ＂development＂, ＂activity＂, ＂network patterns＂, ＂thalamocortical＂, ＂NMDA receptor＂, ＂plasticity＂. We additionally selected papers known to us from past reading, and those recommended to us by reviewers and members of our lab. RESULTS： We reviewed a total of 132 articles that focused on the role of activity in interneuronal migration, maturation, and circuit development, as well as the source of electrical inputs and pattems of cortical activity in the somatosensory cortex. 79 of these papers included in this timely review were written between 2007 and 2016. CONCLUSIONS： Neuronal activity shapes the developmental assembly of functional circuitry in the somatosensory cortical interneurons. This activity impacts nearly every aspect of development and acquisition of mature neuronal characteristics, and may contribute to changing phenotypes, altered transmitter expression, and plasticity in the adult. Progressively changing oscillatory network patterns contribute to this activity in the early postnatal period, although a direct requirement for specific patterns and origins of activity remains to be demonstrated.

Molecular guidance cues in the development of visual pathway

70%-80% of our sensory input comes from vision. Light hit the retina at the back of our eyes and the visual information is relayed into the dorsal lateral geniculate nuclei （dLGN） and primary visual cortex （V1） thereafter, constituting the image-forming visual circuit. Molecular cues are one of the key factors to guide the wiring and refinement of the image-forming visual circuit during pre- and post-embryonic stages. Distinct molecular cues are involved in different developmental stages and nucleus, suggesting diverse guidance mechanisms. In this review, we summarize molecular guidance cues throughout the image-forming visual circuit, including chiasm determination, eye-specific segregation and refinement in the dLGN, and at last the reciprocal con- nections between the dLGN and VI.