Disease relevance of Nerve Endings

• Histamine plays a role as a neurotransmitter in the mammalian brain, and histamine release from nerve endings is enhanced in ischemia by facilitation of histaminergic activity [1].
• Clostridium botulinum neurotoxins (BoNTs) act on nerve endings to block acetylcholine release [2].
• We previously reported that histamine H(3) receptors (H(3)Rs) are present in cardiac sympathetic nerve endings (cSNE) of animals and humans, where they attenuate norepinephrine (NE) release in normal and hyperadrenergic states, such as myocardial ischemia [3].
• Under these conditions both excitatory and inhibitory terminals are enriched with aspartate, which may be released from these nerve endings and thus contribute to the pattern of neuronal death characteristic of hypoglycemia [4].
• Mild myasthenia gravis patients were compared with normals with respect to the capacity of their motor nerve endings (MNEs) to generate a neostigmine-induced postactivation repetition (PAR) [5].

Psychiatry related information on Nerve Endings

• These results support the hypothesis that persistent elevations of Abeta, which normally operates as a modulator of N-type voltage gated calcium channels, could increase internal nerve ending Ca2+ and excitatory neurotransmitter release to produce the early neurotoxic effects that eventually lead to Alzheimer's disease [6].

High impact information on Nerve Endings

• The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1 receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II [7].
• Immunohistochemical studies in the human brain using two of these antibodies detects the huntingtin in perikarya of some neurons, neuropiles, varicosities and as punctate staining likely to be nerve endings [8].
• Consistent with this function, we found BNC1 in the lanceolate nerve endings that lie adjacent to and surround the hair follicle [9].
• The mechanisms whereby hormones and neurotransmitters such as adrenaline, galanin and somatostatin, which are released by intraislet nerve endings and the pancreatic D cells, produce inhibition of insulin secretion are not clear [10].
• Under basal conditions, vasopressin and oxytocin release was inhibited by relaxin but, when the nerve endings were depolarized, vasopressin and oxytocin secretion was potentiated [11].

Chemical compound and disease context of Nerve Endings

• The efficacy of sumatriptan in migraine relief has been attributed to its interaction with 5-hydroxytryptamine1D (5-HT1D) receptors in cerebral blood vessels and/or on nerve endings of the trigeminovascular system in the dura mater [12].
• In addition, it mediates cardiac hypertrophy indirectly by stimulating release of norepinephrine from cardiac nerve endings and endothelin from endothelial cells [13].
• Binding of [3H]GBR 12935 to dopamine uptake sites was lost in the nucleus caudatus ipsilateral to ventral midbrain infarctions, confirming their location on nigrostriatal nerve endings [14].
• Effect of tetanus toxin on oxytocin and vasopressin release from nerve endings of the neurohypophysis [15].
• This study localizes changes in arachidonic acid metabolism and lipoxygenase activity resulting from bicuculline-induced status epilepticus in the brain subcellular fraction enriched in nerve endings [16].

Biological context of Nerve Endings

• Thus, it suggests that PAMP and adrenomedullin, which are derived from the same gene, exhibit different hypotensive mechanisms: PAMP inhibits neural transmission at peripheral sympathetic nerve ending, although adrenomedullin directly dilates vascular smooth muscle, possibly through CGRP-like receptor [17].
• In brain tissue from HD heterozygotes with adult onset and more clinically severe juvenile onset, where the largest expansions occur, a mutant protein of equivalent intensity to wild-type huntingtin was detected in cortical synaptosomes, indicating that a mutant species is synthesized and transported with the normal protein to nerve endings [18].
• Bradykinin B2-receptor activation augments norepinephrine exocytosis from cardiac sympathetic nerve endings. Mediation by autocrine/paracrine mechanisms [19].
• On the basis of the selectivity of these effects, we propose that there is a specific population of nerve endings in the cerebral cortex that contains both a proline-transport system and binding sites for Leu- and Met-enkephalin and furthermore, that these binding sites may be related to the putative delta receptor [20].
• Cyclic AMP-dependent phosphorylation of the alpha subunit of the sodium channel in synaptic nerve ending particles [21].

Anatomical context of Nerve Endings

• Here we describe an extracellular matrix glycoprotein of the elasmobranch electric organ that is localized near the nerve endings [22].
• Immunohistochemical studies have shown the existence of synapses between nerve endings containing dopamine and gonadotropin releasing hormone (LH-RH) respectively in the hypothalamic median eminence [23].
• This report describes studies with nerve endings isolated from the rat hypothalamus in which dopamine at higher concentrations than those used previously has been found to stimulate the degradation of LH-RH but not thyrotropin releasing hormone (TRH) [23].
• High amounts are present in axons and nerve endings in the rat neostriatum (caudate-putamen) and a role for cholecystokinin as a neurotransmitter in this functionally important area is possible [24].
• An electron micrographic morphometric analysis of nerve endings in substantia nigra of rats repeatedly treated with haloperidol was performed [25].

Associations of Nerve Endings with chemical compounds

• Evidence for extramitochondrial pyruvate dehydrogenase involved in acetylcholine synthesis in nerve endings [26].
• The dopa analogue 6-fluorodopa (6-FD) used with positron emission tomography (PET) allows in vivo visualization of dopamine and its metabolites in nigrostriatal nerve endings [27].
• The supply of glutamate from the afferent nerve endings has been suggested to be a necessary factor [28].
• Release of substance P from isolated nerve endings [29].
• Acetylcholine (ACh), the major parasympathetic neurotransmitter, is released by intrapancreatic nerve endings during the preabsorptive and absorptive phases of feeding [30].

Gene context of Nerve Endings

• VAMP-1 was not present in the acinar cell but was found in the nerve endings innervating the acini [31].
• We report that isolated nerve endings contain immunoreactive endothelin, the level of which is regulated by homeostatic mechanisms involved in control of water balance [32].
• In addition, aFGF, released from the traumatized nerve endings, may be one of the first signals initiating protective recovery and repair processes following damaging auditory stimuli [33].
• In the vestibular organs, KCNQ4 is restricted to the type I hair cells and the afferent calyx-like nerve endings ensheathing these sensory cells [34].
• NPY nerve endings makes synaptic contact with the POMC/Y1-R-positive neurons [35].

Analytical, diagnostic and therapeutic context of Nerve Endings

• Immunogold electron microscopy of subcellular particles revealed that synaptobrevin is localized in nerve endings where it is concentrated in the membranes of virtually all small synaptic vesicles [36].
• To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs [37].
• 3. The constrictor response to electrical stimulation of PAN was markedly reduced by the alpha-adrenergic antagonist phentolamine (10(-5) M, the alpha 1-blocker prazosin (10(-5) M), and guanethidine (10(-5) M) which inhibits the release of noradrenaline, ATP, and neuropeptide Y from sympathetic nerve endings [38].
• Both amines were virtually absent from all organs except the adrenals following chemical sympathectomy with 6-hydroxydopamine, thereby establishing that m- and p-octopamine are localized within sympathetic nerve endings [39].
• The diminished response of cocultures to OT is probably due to desensitization of lactotrophs by the residual amounts of this peptide present in the disrupted nerve endings [40].

References