Animals ; Apoptosis ; Humans ; Ischemia ; pathology ; Neurons ; pathology ; Signal Transduction ; physiology

Alzheimer Disease/pathology* ; Animals ; C9orf72 Protein/metabolism* ; Mice ; Microglia/pathology* ; Neuronal Plasticity ; Neurons/pathology* ; Synapses/pathology*

Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future pathogen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host-microbe interactions.
Animals ; Humans ; Infection ; complications ; etiology ; pathology ; Neurons ; pathology ; Pain ; etiology ; pathology ; Pruritus ; etiology ; pathology

Stroke leads to a variety of pathophysiological conditions such as ischemic infarct, cerebral inflammation, neuronal damage, cognitive decline, and depression. Many endeavors have been tried to find the therapeutic solutions to attenuate severe neuropathogenesis after stroke. Several studies have reported that a decrease in the neuropeptide regulator ‘galanin’ is associated with neuronal loss, learning and memory dysfunctions, and depression following a stroke. The present review summarized recent evidences on the function and the therapeutic potential of galanin in post-ischemic stroke to provide a further understanding of galanin's role. Hence, we suggest that galanin needs to be considered as a therapeutic factor in the alleviation of post-stroke pathologies.
Depression ; Galanin ; Inflammation ; Learning ; Memory ; Neurons ; Neuropeptides ; Pathology ; Stroke

Female ; Humans ; Male ; Nervous System Neoplasms ; pathology ; Neuroglia ; pathology ; Neurons ; pathology

Itch is an unpleasant sensation that provokes the desire to scratch. While acute itch serves as a protective system to warn the body of external irritating agents, chronic itch is a debilitating but poorly-treated clinical disease leading to repetitive scratching and skin lesions. However, the neural mechanisms underlying the pathophysiology of chronic itch remain mysterious. Here, we identified a cell type-dependent role of the anterior cingulate cortex (ACC) in controlling chronic itch-related excessive scratching behaviors in mice. Moreover, we delineated a neural circuit originating from excitatory neurons of the ACC to the ventral tegmental area (VTA) that was critically involved in chronic itch. Furthermore, we demonstrate that the ACC→VTA circuit also selectively modulated histaminergic acute itch. Finally, the ACC neurons were shown to predominantly innervate the non-dopaminergic neurons of the VTA. Taken together, our findings uncover a cortex-midbrain circuit for chronic itch-evoked scratching behaviors and shed novel insights on therapeutic intervention.
Mice ; Animals ; Gyrus Cinguli/physiology* ; Pruritus/pathology* ; Mesencephalon ; Cerebral Cortex/pathology* ; Neurons/pathology*

Parkinson's disease (PD) is the second most common neurodegenerative disease, characterized by loss of dopaminergic (DA) neurons in the dense part of the substantia nigra (SNpc). Postmortem analysis of PD patients and experimental animal studies found that microglial cell activation and increased levels of pro-inflammatory factors were common features of PD brain tissue. At the same time, the invasion and accumulation of peripheric immune cells were detected in the brain of PD patients. In this paper, peripheral inflammation across the blood-brain barrier (BBB), the misfolded α-synuclein (α-syn)-induced microglial cell activation and intracerebral inflammation in PD are summarized, providing potential therapeutic measures for delaying the onset of PD.
Animals ; Blood-Brain Barrier ; Dopaminergic Neurons ; pathology ; Humans ; Inflammation ; pathology ; Microglia ; Parkinson Disease ; pathology ; Substantia Nigra ; pathology ; alpha-Synuclein

The damage degree of neurons in perilesion at different time points was observed in order to explore the optimal operation occasion. Piglet lobar hematomas were produced by pressure-controlled infusions of 2.5 mL autonomous blood into the right frontal hemispheric white matter over 15 min, and the metabolic changes were ambulatorily detected with MRS at 3rd, 12th, 24th and 48th h after hematoma induction. Brain tissues of perihematoma were also obtained at different time points. The transcription level of Bax gene was detected by in situ hybridization and apoptosis by TUNEL technique, and the pathologic change of neurons was observed under an electron microscope. The results showed that the number of Bax positive cells reached the peak at 24 h (79.00 +/- 4.243/5 fields). There was no significant difference in A values between 3 h and 6 h, 12 h (P > 0.05), but there significant difference between 24 h and 3 h, 6 h, 12 h (P < 0.05). The number of apoptotic cells reached the peak at 24 h (P < 0.001), and there was no significant difference between 3 h and 6 h (P = 0.999). The area of the apoptotic cells showed no significant difference between 3 h and 6 h or among 3 h, 6 h and 6 h (P > 0.05). Lac peak mainly occurred at 24 h and 48 h, while on the healthy side, no Lac peak was detectable. The ratio of NAA/Cr presented a descent tendency, but there was no significant difference among the groups before 12 h (P > 0.05), there was very significant difference between 3, 6 and 24, 48 h (P < 0.01). Under electronic microscopy, the neuronal damage surrounding hematoma in 3 to 6 h was milder than in 24 h to 48 h. It was concluded that the secondary apoptosis, damage and metabolic disturbance of the neurons surrounding hematoma was milder in 3-6 h in acute intracerebral hemorrhage, while obviously aggravated in 24-48 h. An effective intervention is needed to reduce secondary damage as soon as possible.
Brain/*pathology ; Cerebral Hemorrhage/*pathology ; Hematoma/*pathology ; Magnetic Resonance Imaging ; Neurons/pathology ; Random Allocation ; Swine ; Swine, Miniature ; Time Factors

Alzheimer Disease ; Diabetic Neuropathies ; pathology ; Glaucoma ; pathology ; Humans ; Multiple Sclerosis ; pathology ; Nerve Fibers ; pathology ; Ophthalmoscopy ; Optic Nerve ; pathology ; Parkinson Disease ; pathology ; Retinal Neurons ; pathology ; Tomography, Optical Coherence

OBJECTIVETo evaluate the efficacy and the mechanism of application of selective head cooling on neuronal morphological damage during postischemic reperfusion in a rabbit model.

METHODS168 New Zealand rabbits were randomized into three groups. Group I [n = 24, (38 +/- 0.5) degrees C, non-ischemic control]; Group II [n = 72, (38 +/- 0.5) degrees C, normothermic reperfusion]; Group III [n = 72, (28 +/- 0.5) degrees C, selective head cooling, initiated at the beginning of reperfusion). Animals in three subgroups (n = 24, each) of Group II and Group III had reperfused lasting for 30, 180 and 360 min respectively. Using computerized image analysis technique on morphological changes of nucleus, the degree of neuronal damage in 12 regions were differentiated into type A (normal), type B (mild damaged), type C (severely damaged) and type D (necrotic). Fourteen biochemical parameters in brain tissues were measured.

RESULTSAs compared with Group I, the counts of type A neuron decreased progressively, and those of type B, C and D increased significantly in Group II during reperfusion (P < 0.01). In Group II, vasoactive intestinal peptide, b-endorphine, prostacyclin, T3 and Na+, K(+)-ATPase were correlated with the changes of type A; b-endorphine and thromboxane with type B; glucose and vasopressin with type C; Na+, K(+)-ATPase, glutamic acid, T3 and vasoactive intestinal peptide with type D (P < 0.05). As compared with Group II, the counts of type A increased, and those of type C and D significantly decreased in Group III (P < 0.01). In Group III, Ca2+, Mg(2+)-ATPase were correlated with the changes of type A, C and D (P < 0.01).

CONCLUSIONSelective head cooling for sex hours during postischemic reperfusion does improve neuronal morphological outcomes in terms of morphological changes.

Animals ; Brain Ischemia ; pathology ; Cold Temperature ; Neurons ; pathology ; Rabbits ; Reperfusion Injury ; prevention & control ; Resuscitation ; methods