The levator auris longus muscle of the mouse: A convenient preparation for studies of short- and long-term presynaptic effects of drugs or toxins

Angaut-Petit, D.; Molgó, Jordi; Connold, A.L.; Faille, Lucette

doi:10.1016/0304-3940(87)90175-3

Cited by 74 publications

(58 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, junctions with sprouts were restricted to the immediate vicinity of the injection sites, suggesting that exposure of LG junctions to CNTF was limited (see also Gurney et al, 1992). In contrast, consistent with the recognized advantages of LAL muscles for pharmacological studies (Angaut-Petit et al, 1987,Lanuza et al, 2002, we observed that CNTF injected between the subdermal connective tissue and the LAL fascia, but not CNTF injected subcutaneously into LG or other hindlimb muscles, formed a local subdermal swelling that persisted for at least one hour before vascular reabsorption (data not shown; cf., Lanuza et al, 2001). …”

Section: Discussionsupporting

confidence: 55%

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Wright

Son

2007

Experimental Neurology

View full text Add to dashboard Cite

Loss of synaptic activity or innervation induces sprouting of intact motor nerve terminals that adds or restores nerve-muscle connectivity. Ciliary neurotrophic factor (CNTF) and terminal Schwann cells (tSCs) have been implicated as molecular and cellular mediators of the compensatory process. We wondered if the previously reported lack of terminal sprouting in CNTF null mice was due to abnormal reactivity of tSCs. To this end, we examined nerve terminal and tSC responses in CNTF null mice using experimental systems that elicited extensive sprouting in wildtype mice. Contrary to the previous report, we found that motor nerve terminals in the null mice sprout extensively in response to major sprouting-stimuli such as exogenously applied CNTF per se, botulinum toxinelicited paralysis, and partial denervation by L4 spinal root transection. In addition, the number, length and growth patterns of terminal sprouts, and the extent of reinnervation by terminal or nodal sprouts, were similar in wildtype and null mice. tSCs in the null mice were also reactive to the sprouting-stimuli, elaborating cellular processes that accompanied terminal sprouts or guided reinnervation of denervated muscle fibers. Lastly, CNTF was absent in quiescent tSCs in intact, wildtype muscles and little if any was detected in reactive tSCs in denervated muscles. Thus, CNTF is not required for induction of nerve terminal sprouting, for reactivation of tSCs, and for compensatory reinnervation after nerve injury. We interpret these results to support the notion that compensatory sprouting in adult muscles is induced primarily by contact-mediated mechanisms, rather than by diffusible factors.

show abstract

Section: Discussionsupporting

confidence: 55%

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Wright

Son

2007

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…Increased EPP amplitude and quantal content at the NMJ of R6/1 mice We used the levator auris longus nerve-muscle preparation (Angaut-Petit et al, 1987) to characterize synaptic transmission at the NMJ of 5-to 6-month-old R6/1 transgenic mice. We found no significant changes in resting membrane potential (Ϫ61.5 Ϯ 1.6 mV, n ϭ 26 in WT vs Ϫ57.4 Ϯ 1.8 mV, n ϭ 26 in R6/1, p ϭ 0.11, Student's t test).…”

Section: Resultsmentioning

confidence: 99%

“…The levator auris longus (LAL) muscle was dissected as described previously (Angaut-Petit et al, 1987), stretched, and pinned in a Sylgard-coated perfusion chamber. glass microelectrodes filled with 3 mM KCl were placed close to the nerve terminal (10 -50 m) to minimize electrotonic filtering of postsynaptic potentials (Fatt and Katz, 1952).…”

Section: Methodsmentioning

confidence: 99%

Increased Neurotransmitter Release at the Neuromuscular Junction in a Mouse Model of Polyglutamine Disease

Rozas¹,

Gómez‐Sánchez²,

Tomás-Zapico³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

In Huntington's disease (HD), the expansion of polyglutamine (polyQ) repeats at the N terminus of the ubiquitous protein huntingtin (htt) leads to neurodegeneration in specific brain areas. Neurons degenerating in HD develop synaptic dysfunctions. However, it is unknown whether mutant htt impacts synaptic function in general. To investigate that, we have focused on the nerve terminals of motor neurons that typically do not degenerate in HD. Here, we have studied synaptic transmission at the neuromuscular junction of transgenic mice expressing a mutant form of htt (R6/1 mice). We have found that the size and frequency of miniature endplate potentials are similar in R6/1 and control mice. In contrast, the amplitude of evoked endplate potentials in R6/1 mice is increased compared to controls. Consistent with a presynaptic increase of release probability, synaptic depression under high-frequency stimulation is higher in R6/1 mice. In addition, no changes were detected in the size and dynamics of the recycling synaptic vesicle pool. Moreover, we have found increased amounts of the synaptic vesicle proteins synaptobrevin 1,2/VAMP 1,2 and cysteine string protein-␣, and the SNARE protein SNAP-25, concomitant with normal levels of other synaptic vesicle markers. Our results reveal that the transgenic expression of a mutant form of htt leads to an unexpected gain of synaptic function. That phenotype is likely not secondary to neurodegeneration and might be due to a primary deregulation in synaptic protein levels. Our findings could be relevant to understand synaptic toxic effects of proteins with abnormal polyQ repeats.

show abstract

“…C57BL/6 wild-type (WT) mice or synapsin TKO mice [kindly provided by Paul Greengard (Rockefeller University, New York, NY) and Hung-Teh Kao (Nathan Kline Institute, Orangeburg, NY) (Gitler et al, 2004a,b)] were housed and handled in accordance with the University of Colorado Institutional Animal Care and Use Committee. The levator auris longus muscle was dissected from adult mice as described previously (Angaut-Petit et al, 1987) and pinned in a Sylgard-lined chamber. For nerve stimulation, the nerve was drawn into a suction electrode.…”

Section: Methodsmentioning

confidence: 99%

Synaptic Vesicle Mobility in Mouse Motor Nerve Terminals with and without Synapsin

Gaffield¹,

Betz²

2007

J. Neurosci.

View full text Add to dashboard Cite

We measured synaptic vesicle mobility using fluorescence recovery after photobleaching of FM 1-43 [N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino)styryl) pyridinium dibromide] stained mouse motor nerve terminals obtained from wild-type (WT) and synapsin triple knock-out (TKO) mice at room temperature and physiological temperature. Vesicles were mobile in resting terminals at physiological temperature but virtually immobile at room temperature. Mobility was increased at both temperatures by blocking phosphatases with okadaic acid, decreased at physiological temperature by blocking kinases with staurosporine, and unaffected by disrupting actin filaments with latrunculin A or reducing intracellular calcium concentration with BAPTA-AM. Synapsin TKO mice showed reduced numbers of synaptic vesicles and reduced FM 1-43 staining intensity. Synaptic transmission, however, was indistinguishable from WT, as was synaptic vesicle mobility under all conditions tested. Thus, in TKO mice, and perhaps WT mice, a phospho-protein different from synapsin but otherwise of unknown identity is the primary regulator of synaptic vesicle mobility.

show abstract

The levator auris longus muscle of the mouse: A convenient preparation for studies of short- and long-term presynaptic effects of drugs or toxins

Cited by 74 publications

References 15 publications

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Increased Neurotransmitter Release at the Neuromuscular Junction in a Mouse Model of Polyglutamine Disease

Synaptic Vesicle Mobility in Mouse Motor Nerve Terminals with and without Synapsin

Contact Info

Product

Resources

About