Muneaki Mizote

Rapid recovery of structure and function of the cholinergic synapses in the cat superior cervical ganglionin vivo following stimulation-induced exhaustion

SummaryCat superior cervical ganglia (SCG) were tetanically stimulatedin vivo at 30–100 Hz until neural transmission was exhausted, and then were allowed to rest and recover. Changes in their cholinergic synapses were examined electrophysiologically and morphologically during the time of tetanic stimulation and during recovery. For morphometric analysis the presynaptic terminal was subdivided into two areas: an area directly over the active zone, termed zone-I, (bounded by a hemicircle with a diameter equivalent to the active zone length), and the remaining preterminal area, termed zone-II. In control ganglia before stimulation synaptic vesicle density in zone-I (SVD-I) averaged 90 μm−2 and the number of vesicles actually attached to the active zone (SVA) averaged about 2.5 per single profile of nerve terminal. Upon stimulation, the postganglionic potential immediately began to decline in amplitude and disappeared after 1 min of stimulation. Simultaneously, SVD-I declined to less than 35 μm−2 and SVA declined to less than 1 per section. Thereafter, stimulation was terminated and the ganglion was allowed to rest. Recovery of the postganglionic potential was monitored by stimulation at 1 Hz. The postganglionic potential reached control levels after only 1 min of rest. Likewise, the structural parameters, SVD-I and SVA, also rapidly recovered, reaching control levels after only 30 sec of rest, slightly faster than the postganglionic potential. This illustrates that stimulation-induced fatigue of transmitter output and depletion of synaptic vesicles recover to the control level at a high rate in synapses of the cat SCG with a normal supply of blood. In fact, morphological recovery may be slightly faster than electrophysiological recovery. Mechanisms of vesicle formation and migration to the presynaptic area are discussed in light of these observations.

Poststimulation Increase of Synaptic Vesicle Number in the Preganglionic Nerve Terminals of the Cat Sympathetic Ganglion InVivo

Vesicular release of neurotransmitter has been suggested in a variety of nerve endings by morphological reports in which tetanic stimulation is shown to cause the reduction of synaptic vesicles (SVs) in number and simultaneously to depress the postsynaptic response (Ceccarelli et al., 1973; Heuser and Reese, 1973; Pysh and Wiley, 1974; Zimmerman and Whittaker, 1974a, b). Vesicular release of transmitter via exocytosis is supposed to be followed by the subsequent reformation of vesicles by endocytotic retrieval of terminal plasmamembrane by coated vesicles (recycling hypothesis of synaptic-vesicle membrane) (Heuser and Reese, 1973). Questions remains, however, concerning the vesicle hypothesis of the release of quanta of neurotransmitter (Zimmerman, 1979; Ceccarelli and Hurlbut, 1980; Tauc, 1979; Israel and Manarche, 1985). In addition, recent articles have shown the low rate of coated vesicles in the SV reformation, having implied the necessities of examinations for other mechanisms for supplying SVs during transmitter release (Kadota and Kadota, 1982; Meshul and Pappas, 1984; Parducz, 1986; Torri-Tarelli et al., 1987). The purpose of this study is to examine the ultrastructural changes in an neuro-neuronal synapse under normal supply of blood. The preganglionic nerve terminal of the cat superior cervical ganglion (SCG) was employed as the experimental material in the present experiment. It was simple to maintain this ganglion under intact blood sypply and to fix rapidly by perfusion via the lingual artery (Kadota and Kadota, 1982).

1329 Correlation between post-tetanic potentiation and synaptic spinule

Takanori Hashimoto, Yasushi Kajii, Toru Nishikawa Psychostimulants elicit a progressive and persistent enhancement of behavioral responses to these drugs (behavioral sensitization). To get an insight into the possible involvement of neuronal plasticit,y in the behavioral sensitization, we studied the effects of single administration of MAP and cocaine on the expression of a plasticity-related molecule, tissue plasminogen activator (TPA) mRNA. An acute injection of MAP and cocaine induced TPA mRNA in a subpopulation of neurons in the mediodorsal frontal cortex, agranular insular cortex and piriform cortex. Similar distribution and time course of TPA mRNA expression was seen after systemic application of nomifensine and phencyclidine which are also capable to produce sensitization. Pretreatment with dopamine receptor antagonists, haloperidol and SCH23390, inhibited MAP-induced TPA mRNA expression. Retrograde tracer study combined with in situ hybridization revealed majority of TPA mRNA expressing cells project to the medial striatum.

1411 The synaptic spinule formation attendant on the post-tetanic potentiation in the cat superior cervical ganglion in vivo

Following peripheral nerve injury, pathological states such as allodynia and/or hyperalgesia have been reported to develop in a subpopulation of patients. Although peripheral neural mechanisms are likely to contribute to the pathological state, persistence of pain after healing of the damaged tissue suggests that plastic changes in the CNS, including the spinal cord, may also play a important role in processing the pathological pain transmission. To investigate plastic changes in synaptic transmission at the spinal level, whole cell recordings were made from substantia gelatinosa (SC) and laminae IV/V neurons in the spinal cord slice with attached dorsal root dissected from rats with or without sciatic nerve transection (SNT) No significant changes in passive and active membrane characteristics, including resting membrane potential, input resistance and configuration of action potential and spike after potentials, were detected between normal and SNT rats. In the control rats, primary afferent stimulation with intensity sufficient to activate Ad afferents elicited a monosynaptic fast EPSC in the majority of SC neurons. In the SNT rats, however, a polysynaptic EPSC with a long latency was evoked by activation of afferent fibers. The stimulus intensity for eliciting the polysynaptic EPSCs was much lower than that for activation of A6 afferents, suggesting that AB afferents are responsible for generation of this response. In addition, the conduction velocity and threshold of these afferents were not significantly altered. These observations suggest that synaptic plasticity occuned in a subset of deep dorsal horn neurons, which begin to transmit sensory information’to SG. This plastic change may.