摘要:

AbstractHow is the short‐term memory for a single form of learing distributed among the various elements of a neuronal circuit? To answer this question, we examined the short‐term memory for sensitization, using the siphon component of the defensive gill‐ and siphon‐withdrawal reflex. We found that the memory for short‐term sensitization is represented by at least four sites of circuit modification, each involving a different type of plasticity. These include (1) presynaptic facilitation of the sensory neuron connections onto both interneurons and motorneurons; (2) presynaptic inhibition at the connections of the L30 inhibitory neurons onto the excitatory interneuron L29; (3) posttetanic potentiation of the excitatory connections made by L29 onto a specific subclass of siphon motorneurons, the LFS cells; and (4) an increase in the tonic firing rate of the LFS siphon motor neurons, resulting in neuromuscular facilitation. Each of the heterosynaptic changes seems to involve a common modulatory transmitter and to utilize a common second messenger system. Moreover, each of these sites seems capable of encoding a different component of the short‐term memory. Facilitation of the connections of sensory neurons should contribute to the increase in amplitude of the response; the disinhibition of the L29 interneurons and the posttetanic potentiation at L29 synapses should contribute to an increase in the duration of the response; and the increase in tonic firing of the LFS subclass of siphon motor neurons seems capable of contributing both to an increase in response amplitude and to changes in response

ISSN:0022-3034    

DOI:10.1002/neu.480190402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractUsing tetranitroblue tetrazolium (TNBT) to stain neuromuscular synapses, we compared the development of the adult pattern of innervation in two fast‐twitch muscles in the rat: the androgen‐sensitive levator ani (LA) and the extensor digitorum longus (EDL), which is not thought to be androgen sensitive. We found that about 18% of adult LA muscle fibers, but only about 2% of adult EDL fibers, are multiply innervated. Moreover, synapse elimination occurs substantially later in the LA compared with the EDL. At 2 weeks after birth, the EDL is already predominantly singly innervated, whereas the LA is still predominantly multiply innervated. The apparent delay in the normal time course of synapse elimination in the LA corresponds to a similar delay in other aspects of neuromuscular development (the time course of appearance of axonal retraction bulbs, the growth of fibers, and the development of adult motor terminal morphology). Finally, motor terminals change during synapse elimination from morphologies resembling growth cones to the adult form of neuromuscular synapses. Because the period of synapse elimination is significantly different for muscles that differ in their androgen sensitivity, hormonal sensitivity may represent an important property of motoneurons or muscle fibers influencing the normal time course of neuromuscular synapse elimination in rats. Thus, androgen might regulate the normal ontogenetic process of synapse eliminat

ISSN:0022-3034    

DOI:10.1002/neu.480190403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractIn bullfrog B‐type sympathetic neurones axon injury produces substantial changes in somal membrane properties. These include a shortening of action potential afterhyperpolarization (AHP) and an increase in action potential (AP) duration. In the present experiments we compared two injury situations: nerve crush, which was followed by regeneration, and nerve cut, after which regeneration to the original target was prevented, to investigate whether these electrophysiological changes were related to axon regeneration. Both crush and cut injuries produced a similar maximum decrease in AHP duration (to 33 and 30%) by 14 days after axotomy. After nerve crush, AHP duration recovered to within control values by 42 days, while after cut it remained depressed. AHP amplitude decreased to the same extent after nerve crush or cut (to 62 and 58%), but the rate of decrease was slower following crush when compared with cut, and following both types of injury it still remained depressed at 42 and 49 days. Changes in AP duration also took longer to occur following nerve crush, reaching maximal values at 35–42 days, at which time AHP duration had returned to within the normal range. The early reduction in AHP duration and its rapid recovery in regenerating neurones suggests that the current underlying this membrane property is regulated by events associated with axon outgrowth and peripheral reconnection. In contrast, changes in AHP amplitude and AP repolarization appeared to be independent of the occurrence of axon regeneration and remained abnormal at 49 days despite the recovery of AHP duration. These results imply that the electrophysiological changes seen in B‐cells following injury are differentially regulated during subsequent regener

ISSN:0022-3034    

DOI:10.1002/neu.480190404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractPrevious work has demonstrated that the neurotoxin leptinotarsin elicits release of neurotransmitter from mammalian nerve terminals, and it has been suggested that the toxin may act either as a direct agonist of voltage‐sensitive calcium channels in these terminals (Crosland et al., 1984) or as a calcium ionophore (Madeddu et al., 1985a,b). Preliminary studies (Yeager et al., 1987) demonstrated that leptinotarsin also evokes transmitter release from isolated elasmobranch electric organ nerve terminals. We now report further investigations of the effects of leptinotarsin in this system. The action of the toxin is saturable, releasing about the same small fraction of total transmitter as that released by depolarization. An upper limit for the concentration for half maximal release is estimated to be 4 nM. Leptinotarsin‐evoked transmitter release exhibits behavior very similar to depolarization‐evoked release with respect to dependence on Ca2+, Ba2+, and Sr2+and blockade by Co2+, Cd2+, and trifluoperazine. Leptinotarsin also promotes the uptake of calcium into synaptosomes to a degree similar to that caused by depolarization by K+. The binding of leptinotarsin to nerve terminals is probably Ca2+dependent and receptor mediated. Taken together with the behavior of leptintoarsin‐evoked release in other preparations, these results are consistent with the hypothesis that this toxin acts by opening a presynaptic calcium channel. However, the possibility that leptinotarsin is a calcium ionophore cannot be e

ISSN:0022-3034    

DOI:10.1002/neu.480190405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480190406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480190407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480190401

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY