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Removal of the labyrinthine organs on one side is followed by a number of severe postural and dynamic reflex deficits. Some of these deficits, in particular the posture of head and body, are normalized again over a period that varies strongly between species. Other, more persistent motor deficits are substituted, e.g. by the saccadic system. This partial normalization of the function is accompanied by changes in response properties of the central vestibular neurons on the operated side. Available evidence suggests the occurrence of reactive synaptogenesis in cat and frog. In the latter species the synaptic efficacy of commissural vestibular connections increases and the metabolic activity of central vestibular neurons on the operated side recovers post-operatively. The onset of both changes, however, is delayed by about 30 days, which is too late to be causally related with the initial, rapid period of postural recovery in frog and cat. In frogs additional, early (7-15 days p.o.) and late (45-60 p.o.) synaptic changes were detected in the branchial spinal cord. These multiple changes survive the isolation of the spinal cord and must be propriospinal in origin. Selective lesions of individual vestibular nerve branches indicate that inactivation of utricular inputs is a sufficient and necessary condition to provoke postural deficits and early spinal changes similar to those after hemilabyrinthectomy. Therefore, a close correlation between spinal plasticity and postural recovery is indicated. In essence, the elimination of vestibular afferent inputs results in a series of behavioral distortions that are partially normalized by a multitude of synaptic mechanisms at distributed anatomical sites over different periods of time.

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1. The release of ink from the ink gland of Aplysia californica in response to noxious stimuli is mediated by three electrically coupled motor neurons, L14A, L14B, L14C, whose cell bodies are located in the abdominal ganglion. The initial synaptic input to the ink motor neurons is relatively ineffective in firing the cells. As a result, a pause of 1--3 s often occurs before the cells attain their maximum firing frequency and cause the release of ink. Using current and voltage-clamp techniques we have analyzed the mechanisms underlying the firing pattern of these cells. 2. The presence of a fast transient K+ current appears to play an important role in mediating the firing pattern of the ink motor neurons. Their high resting potential (-75 mV) ensures that the steady-state level of inactivation of the conductance channels for the fast K+ current will normally be low. Thus a train of EPSPs or a depolarizing current pulse can activate this current maximally, thereby reducing the initial effectiveness of the excitatory input. 3. In addition to the fast transient K+ current, four other currents were identified: 1) a fast transient tetrodotoxin-sensitive inward current, presumed to be carried by Na+; 2) a slower tetrodotoxin-insensitive inward current, presumed to be carried by Ca2+; 3) a slow transient outward tetraethylammonium- (TEA) sensitive current; and 4) a very slow TEA-insensitive outward current. 4. A decreased conductance EPSP, which turns on over a several-second period, contributes to a late acceleration of spike discharge in the L14 cells. 5. The results suggest that a unique combination of biophysical properties of the L14 cells and the features of the synaptic input cause them to act as a low-pass filter in the reflex pathway for inking. Their high resting potential, which ensures minimal inactivation of the fast transient K+ current channel, makes these cells preferentially responsive to strong and long-lasting stimuli. The delayed recruitment of a decreased conductance EPSP augments the tendency of the L14 cells to fire in an accelerating burst pattern.