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Patterns of convergence in the central nucleus of the inferior colliculus of the Mongolian gerbil: organization of inputs from the superior olivary complex in the low frequency representation.

Projections to the inferior colliculus (IC) from the lateral and medial superior olivary nuclei (LSO and MSO) were studied in the gerbil (Meriones unguiculatus) with neuroanatomical tract-tracing methods. The terminal fields of projecting axons were labeled via anterograde transport of biotinylated dextran amine (BDA) and were localized on series of horizontal sections through the IC. In addition, to make the results easier to visualize in three dimensions and to facilitate comparisons among cases, the data were also reconstructed into the transverse plane. The results show that the terminal f

Neuroanatomical basis for acupuncture point PC8 in the rat: neural tracing study with cholera toxin subunit B.

OBJECTIVES: This study was performed to investigate the innervations related to acupuncture point PC8 in rats using a neural tracing technique. METHODS: After 6 μL of 1% cholera toxin subunit B (CTB) was injected into the site between the second and third metacarpal bone in rats, a corresponding site to acupuncture point PC8 in the human body, CTB labelling was examined with immunofluorescence and immunohistochemistry in the dorsal root ganglia (DRG), spinal cord and brainstem. RESULTS: All CTB labelling appeared on the ipsilateral side of the injection. The labelled sensory neurons distribu

Parkinson's disease: a dual-hit hypothesis.

Accumulating evidence suggests that sporadic Parkinson's disease has a long prodromal period during which several non-motor features develop, in particular, impairment of olfaction, vagal dysfunction and sleep disorder. Early sites of Lewy pathology are the olfactory bulb and enteric plexus of the stomach. We propose that a neurotropic pathogen, probably viral, enters the brain via two routes: (i) nasal, with anterograde progression into the temporal lobe; and (ii) gastric, secondary to swallowing of nasal secretions in saliva. These secretions might contain a neurotropic pathogen that, after

Neurogenic inflammation in nasal allergy: histochemical and pharmacological studies in guinea pigs. A review.

The role of neuropeptides in nasal allergy was examined in guinea pigs by histochemical and pharmacological study. Intranasal application of … e to TDI enhanced the biosynthesis of both SP and CGRP in the trigeminal ganglion neurons and their axonal transportation to the terminals in the nasal mucosa. In animals pretreated with capsaicin before sensitization, TDI did not induce nasal allergy-like behaviors and histamine release in the nasal mucosa. Since capsaicin depletes SP and CGRP in the sensory nerv …

Chromogranin A in the olfactory system of the rat.

The olfactory bulb of the rat contains chromogranin A at a similar level as the adrenal gland or the hypophysis as revealed by immunoblots. Olfactory chromogranin A also displays the same size as chromogranin A of endocrine cells. In the hippocampus and other brain regions, we could not detect chromogranin A by immunoblotting. In contrast, chromogranin A messenger ribonucleic acid (using S1 nuclease protection assays) was observed in all brain regions examined, including the olfactory bulb. By in situ hybridization histochemistry with a complementary ribonucleic acid probe (280 nucleotides), a

Claustroneocortical projections studied in the cat by means of multiple retrograde fluorescent tracing.

The topographical interrelations of claustroneocortical cells and their degree of divergent collateralization were investigated in cat by means of retrograde fluorescent double labeling. The tracers Fast Blue (FB) and Nuclear Yellow (NY) were injected in several combinations in two different cortical fields. FB-labeled and NY-labeled cells were found in all cases in the insular portion of the ipsilateral claustrum (CII). The distributions of labeled cells confirmed the organization reported in previous studies. In some cases the two labeled cell populations were segregated in different parts o

Serotonin transporter in the temporal lobe, hippocampus and amygdala in SUDEP.

Several lines of evidence link deficient serotonin function and SUDEP. Chronic treatment with serotonin reuptake inhibitors (SRIs) reduces ictal central apnoea, a risk factor for SUDEP. Reduced medullary serotonergic neurones, modulators of respiration in response to hypercapnia, were reported in a SUDEP post-mortem series. The amygdala and hippocampus have high serotonergic innervation and are functionally implicated in seizure-related respiratory dysregulation. We explored serotonergic networks in mesial temporal lobe structures in a surgical and post-mortem epilepsy series in relation to SU

Ocular Hypertension Results in Hypoxia within Glia and Neurons throughout the Visual Projection.

The magnitude and duration of hypoxia after ocular hypertension (OHT) has been a matter of debate due to the lack of tools to accurately report hypoxia. In this study, we established a topography of hypoxia in the visual pathway by inducing OHT in mice that express a fusion protein comprised of the oxygen-dependent degradation (ODD) domain of HIF-1α and a tamoxifen-inducible Cre recombinase (CreERT2) driven by a ubiquitous CAG promoter. After tamoxifen administration, tdTomato expression would be driven in cells that contain stabilized HIF-1α. Intraocular pressure (IOP) and visual evoked poten

Cytotoxic effects of adriamycin on the central nervous system of the mouse--cytofluorescence and electron-microscopic observations after various modes of administration.

Adriamycin (doxorubicin) is commonly used in the treatment of malignant tumours. Adverse effects on the CNS have not been described so far, … uscularly or/and intradermally and letting it pass into the spinal cord or brain-stem by retrograde axonal transport. In model experiments, adriamycin was injected into the tongue and six hours later its fluorescence could be detected in the hypoglossal neurons. Animals allowed to survive for a longer period, showed selective damage to these neurons as evidenced b …

Upregulation of RIN3 induces endosomal dysfunction in Alzheimer's disease.

BACKGROUND: In Alzheimer's Disease (AD), about one-third of the risk genes identified by GWAS encode proteins that function predominantly in … immunofluorescence and yeast two hybrid assays. Live imaging of primary neurons was used to examine axonal transport of amyloid precursor protein (APP) and β-secretase 1 (BACE1). Immunoblotting was used to detect protein expression, processing of APP and phosphorylated forms of Tau. RESULTS: We have shown that RIN3 mRNA level was significantly increased in the hi …

A serial study of retinal changes following optic neuritis with sample size estimates for acute neuroprotection trials.

Following an episode of optic neuritis, thinning of the retinal nerve fibre layer, which indicates axonal loss, is observed using optical co … nerve fibre layer thickness of the affected eye alone. Inflammation in the optic nerve and impaired axonal transport (implied by retinal nerve fibre layer swelling) are associated with visual dysfunction and demyelination (long visual evoked potential latency) during acute optic neuritis. Retinal nerve fibre layer thinning is usually evident within 3 months. Optic …

Pathogenesis of diabetic neuropathy: role of altered phosphoinositide metabolism.

A unifying metabolic hypothesis completely accounting for the development of one or more of the chronic complications of diabetes on the bas … oire of responses to a variety of insults, so that Wallerian degeneration, axonal atrophy, impaired axonal transport, and dystrophic changes in diabetic neuropathy may represent multiple factors. On the other hand, the increasingly recognized importance of the phosphoinositide cascade in neuromodulation may attribute a progressively wider range of disturbances in …

Exosome-based therapeutic approach for spinal cord injury: A review.

Spinal cord injury (SCI) is a devastating neurological condition associated with high rates of disability and mortality, placing substantial burdens on patients, families, and healthcare systems. Current treatment strategies, including surgical decompression, pharmacological intervention, and rehabilitation, offer only limited functional recovery. Exosomes, extracellular vesicles with a double-membrane structure, range in diameter from 30 to 150 nm and play a key role in intercellular communication by transporting proteins, lipids, and nucleic acids. Recent studies have highlighted their poten

Vesicular trafficking and cell-cell communication in neurodevelopment and neurodegeneration.

Regulation of vesicle biology and trafficking plays a critical role in cell viability. Vesicular trafficking is a process that entails vesicle biogenesis, transport, and sorting of materials such as proteins, enzymes, hormones, and neurotransmitters to different cellular compartments. This phenomenon is especially important in cells of the central nervous system, including neural progenitors, neurons, and glial cell populations, because of their highly polarized architecture. In line with that, disruption in vesicular trafficking during cortical development affects progenitor proliferation and

Loss of synaptic Munc13-1 underlies neurotransmission abnormalities in spinal muscular atrophy.

Spinal muscular atrophy (SMA) is a devastating neurodegenerative disease characterized by degeneration of spinal motoneurons, leading to muscle atrophy and synaptic loss. SMN functions in mRNA splicing, transport, and local translation are crucial for maintaining synaptic integrity. Within the presynaptic membrane, the active zone orchestrates the docking and priming of synaptic vesicles. The Munc13 family proteins are key active zone components that operate precise neurotransmitter release in conjunction with voltage-gated Ca2+ channels (VGCCs). However, the role of Munc13s in synaptic dysfun

Defective neurite elongation and branching in Nibp/Trappc9 deficient zebrafish and mice.

Loss of function in transport protein particles (TRAPP) links a new set of emerging genetic disorders called "TRAPPopathies". One such disorder is NIBP syndrome, characterized by microcephaly and intellectual disability, and caused by mutations of NIBP/TRAPPC9, a crucial and unique member of TRAPPII. To investigate the neural cellular/molecular mechanisms underlying microcephaly, we developed Nibp/Trappc9-deficient animal models using different techniques, including morpholino knockdown and CRISPR/Cas mutation in zebrafish and Cre/LoxP-mediated gene targeting in mice. Nibp/Trappc9 deficiency i

Амиотропический латеральный склероз и лобовое дегенерация: сходства в генетическом фоне

Амиотрофический боковой склероз (ALS) — это разрушительное, равномерно смертоносное прогрессивное дегенеративное расстройство моторных нейронов, которое перекликается с клиническим, морфологическим и генетическим дегенерацией лобар (FTLD). Хотя известно, что многие различные мутации в различных генах вызывают амиотрофный боковой склероз, по-прежнему мало что известно о том, как они избирательно влияют на биологию моторных нейронов и сходятся ли они на общих путях, чтобы вызвать нейронное дегенерацию. Многие генные мутации содержатся в белках, которые имеют схожие функции. Их можно сгруппироват

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… Axonal Transport Defects Axonal transport defects are a common observation in various neurodegenerative diseases, and mutations in components of the axonal transport machinery have unequivocally shown that impaired axonal transport can cause neurodegeneration [ 77 ]. … There is evidence that TDP-43 may also be involved in the axonal transport defects seen in ALS [ 27 ]; axonal transport defects are commonly seen in neurodegenerative diseases [ 78 ]. …

Tetanus toxin C-fragment protects against excitotoxic spinal motoneuron degeneration in vivo.

The tetanus toxin C-fragment is a non-toxic peptide that can be transported from peripheral axons into spinal motoneurons. In in vitro experiments it has been shown that this peptide activates signaling pathways associated with Trk receptors, leading to cellular survival. Because motoneuron degeneration is the main pathological hallmark in motoneuron diseases, and excitotoxicity is an important mechanism of neuronal death in this type of disorders, in this work we tested whether the tetanus toxin C-fragment is able to protect MN in the spinal cord in vivo. For this purpose, we administered the

Ni(2+) affects dopamine uptake which limits suitability as inhibitor of T-type voltage-gated Ca(2+) channels.

Neuronal T-type voltage-gated Ca(2+) channels are reported to have physiological roles that include regulation of burst firing, Ca(2+) oscillations, and neurotransmitter release. These roles are often exposed experimentally by blocking T-type channels with micromolar Ni(2+). We used Ni(2+) to explore the role of axonal T-type channels in dopamine (DA) release in mouse striatum, but identified significant off-target effects on DA uptake. Ni(2+) (100 μM) reversibly increased electrically evoked DA release and markedly extended its extracellular lifetime, detected using fast-scan cyclic voltammet

Neuronal autophagy and neurodegenerative diseases.

Autophagy is a dynamic cellular pathway involved in the turnover of proteins, protein complexes, and organelles through lysosomal degradation. The integrity of postmitotic neurons is heavily dependent on high basal autophagy compared to non-neuronal cells as misfolded proteins and damaged organelles cannot be diluted through cell division. Moreover, neurons contain the specialized structures for intercellular communication, such as axons, dendrites and synapses, which require the reciprocal transport of proteins, organelles and autophagosomes over significant distances from the soma. Defects i