Disease relevance of Chrna7

• Intramuscular injection of botulinum toxin type A (BTX) is used to treat many disorders characterized by muscular spasms [1].
• A kinetic analysis of changes in BTX binding, performed 2 days following brain injury, indicated that the binding deficits are not due to significant changes in receptor affinity [2].
• Botulism is a generalized paralyzing disease caused by the toxin of Clostridium botulinum (BTX) [3].
• The clinical utility of using BTX to treat overactive bladder syndromes and bladder hypersensory states, especially those that may be caused by an augmentation of the purinergic pathway, should be studied further [4].
• Small quantities of botulinum toxin (BTX) are useful in the treatment of certain movement disorders, such as laryngeal spasmodic dysphonia, blepharospasm, and cervical dystonia [5].

High impact information on Chrna7

• The effect of extracellular Ca2+ concentration and myasthenic globulin on the distribution and appearance of acetylcholine receptor (AChR) clusters on rat myotubes was studied with tetramethyl-rhodamine-labeled alpha BTX [6].
• In competition binding experiments, alpha BTX, curare, nicotine, and quinacrine were the most potent competitors [7].
• Acetylcholine competed with 125I-alpha BTX binding at 2 sites with estimated affinities of 3.6 X 10(-8) and 7.4 X 10(-5) M [7].
• When binding of 125I-alpha bungarotoxin (125I-alpha BTX) to hypothalamic membranes is observed over a wide range of concentrations, 3 binding sites can be identified, with estimated equilibrium dissociation constants (Kds) of 4.1 X 10(-11) M, 6.2 X 10(-10) M, and 9.1 X 10(-7) M for high-, low-, and very-low-affinity interactions, respectively [7].
• In the rostral hypothalamus, high-affinity binding of 125I-alpha BTX was localized to the region of the supraoptic nucleus, paraventricular nucleus, suprachiasmatic nucleus, and the nucleus circularis complex [7].

Biological context of Chrna7

• There was no clear evidence that stimulation of sites in the medial part of disconnected vibrissa-cortex evoked eye movements during the first 6 days after BTX injection [8].
• The compound muscle action potential (MAP) of the vibrissae muscle began to reappear 4 weeks after the first BTX injection [9].

Anatomical context of Chrna7

• Various lines of evidence suggest that the high affinity agonist-binding sites in brain correspond to nicotinic cholinergic receptors similar to those found at autonomic ganglia; BTX-binding sites may also serve as receptors for nicotine and are possibly related to neuromuscular nicotinic cholinoceptors [10].
• Transcainide, a complex derivative of lidocaine, blocks the open state of BTX-activated sodium channels from bovine heart and rat skeletal muscle in two distinct ways [11].
• 6. At normal [Ca2+]o and [Mg2+]o, the depression of EPP amplitude during stimulation of the phrenic nerve at 30-50 Hz was somewhat larger at endplates from alpha BTX-treated rats than at control endplates [12].
• To this end a transitory flaccid paralysis of the vibrissae muscle was induced in adult rats that underwent two unilateral injections of 8 U of botulinum toxin (BTX) into a vibrissal pad, at a duration of 12 days from one another [9].
• Brain injury caused significant decreases in BTX binding in several regions of the hippocampus [13].

Associations of Chrna7 with chemical compounds

• 3. In vitro application of the Ca2+ channel blockers nifedipine (10 microM) or omega-conotoxin (40 nM) had no significant effect on the increased quantal content of endplates from alpha BTX-treated rats [12].
• 4. At control endplates, in vitro block of presynaptic K+ channels by 5 microM 3,4-diaminopyridine did increase the quantal content to a level which was similar to that found in endplates of alpha BTX-treated rats but also induced a broadening of EPPs, which was not found at endplates after alpha BTX treatment [12].
• Lifarizine displaced [3H]-batrachotoxinin-A 20-alpha-benzoate (BTX) binding with moderate affinity (pIC50 7.31 +/- 0.24) indicating an interaction with toxin site 2 [14].
• This hypothesis was tested by examining post mortem [3H]-nicotine and [125I]-alpha-bungarotoxin ([125I]-alpha BTX) binding following treatment in vivo with the quasi-irreversible and insurmountable CNS nicotinic blocker chlorisondamine, given either alone or in combination with chronic nicotine administration [15].
• In contrast, changes in the density of alpha3/alpha4 nAChr's, muscarinic AChr's, NMDA-type glutamate receptors, and L-type calcium channel expression were more regionally restricted and lower in magnitude, as compared to changes in BTX binding [16].

Analytical, diagnostic and therapeutic context of Chrna7

• In this study we have used alpha BTX conjugated to horseradish peroxidase (HRP) and quantitative electron microscopy to determine the intracellular pathway(s) of acetylcholine receptors during the internalization process [17].
• Binding of the muscarinic cholinergic receptor probe [3H]quinuclidinylbenzilate ([3H]QNB) and the putative nicotinic receptor probe [125I]alpha-bungarotoxin ([125I]alpha BTX) to vasopressin (VP) and oxytocin (OT) neuroendocrine cells was investigated with a combination of quantitative receptor binding, autoradiography and immunocytochemistry [18].
• OBJECTIVES: To assess the effects of intravesical injection of botulinum toxin type A (BTX) on a model of detrusor overactivity induced by intravesical infusions of adenosine triphosphate (ATP) and capsaicin [4].

References