Properties of conditioned abducens nerve responses in a highly reduced in vitro brain stem preparation from the turtle.
Previous work suggested that the cerebellum and red nucleus are not necessary for the acquisition, extinction, and reacquistion of the in vitro classically conditioned abducens nerve response in the turtle. These findings are extended in the present study by obtaining conditioned responses (CRs) in preparations that received a partial ablation of the brain stem circuitry. In addition to removing all tissue rostral to and including the midbrain and cerebellum, a transection was made just caudal to the emergence of the IXth nerve. Such ablations result in a 4-mm-thick section of brain stem tissue that functionally eliminates the sustained component of the unconditioned response (UR) while leaving only a phasic component. We refer to this region of brain stem tissue caudal to the IXth nerve as the "caudal premotor blink region." Neural discharge was recorded from the abducens nerve following a single shock unconditioned stimulus (US) applied to the ipsilateral trigeminal nerve. When the US was paired with a conditioned stimulus (CS) applied to the posterior eighth, or auditory, nerve using a delay conditioning paradigm, a positive slope of CR acquisition was recorded in the abducens nerve, and CR extinction was recorded when the stimuli were alternated. Resumption of paired stimuli resulted in reacquisition. Quantitative analysis of the CRs in preparations in which the caudal premotor blink region had been removed and those with cerebellar/red nucleus lesions showed that both types of preparations had abnormally short latency CR onsets compared with preparations in which these regions were intact. Preparations with brain stem transections had significantly earlier CR offsets as more CRs terminated as short bursts when compared with intact or cerebellar lesioned preparations. These data suggest that a highly reduced in vitro brain stem preparation from the turtle can be classically conditioned. Furthermore, the caudal brain stem is not a site of acquisition in this reduced preparation, but it contributes to the sustained activity of both the UR and CR. Finally, the unusually short CR onset latencies following lesions to the cerebellum are not further exacerbated by removal of the caudal brain stem. These studies suggest that convergence of CS and US synaptic inputs onto the abducens nerve reflex circuitry may underlie acquisition in this reduced preparation, but that mechanisms that control learned CR timing arise from the cerebellorubral system. (+info)
Discharge profiles of abducens, accessory abducens, and orbicularis oculi motoneurons during reflex and conditioned blinks in alert cats.
The discharge profiles of identified abducens, accessory abducens, and orbicularis oculi motoneurons have been recorded extra- and intracellularly in alert behaving cats during spontaneous, reflexively evoked, and classically conditioned eyelid responses. The movement of the upper lid and the electromyographic activity of the orbicularis oculi muscle also were recorded. Animals were conditioned by short, weak air puffs or 350-ms tones as conditioned stimuli (CS) and long, strong air puffs as unconditioned stimulus (US) using both trace and delayed conditioning paradigms. Motoneurons were identified by antidromic activation from their respective cranial nerves. Orbicularis oculi and accessory abducens motoneurons fired an early, double burst of action potentials (at 4-6 and 10-16 ms) in response to air puffs or to the electrical stimulation of the supraorbital nerve. Orbicularis oculi, but not accessory abducens, motoneurons fired in response to flash and tone presentations. Only 10-15% of recorded abducens motoneurons fired a late, weak burst after air puff, supraorbital nerve, and flash stimulations. Spontaneous fasciculations of the orbicularis oculi muscle and the activity of single orbicularis oculi motoneurons that generated them also were recorded. The activation of orbicularis oculi motoneurons during the acquisition of classically conditioned eyelid responses happened in a gradual, sequential manner. Initially, some putative excitatory synaptic potentials were observed in the time window corresponding to the CS-US interval; by the second to the fourth conditioning session, some isolated action potentials appeared that increased in number until some small movements were noticed in eyelid position traces. No accessory abducens motoneuron fired and no abducens motoneuron modified their discharge rate for conditioned eyelid responses. The firing of orbicularis oculi motoneurons was related linearly to lid velocity during reflex blinks but to lid position during conditioned responses, a fact indicating the different neural origin and coding of both types of motor commands. The power spectra of both reflex and conditioned lid responses showed a dominant peak at approximately 20 Hz. The wavy appearance of both reflex and conditioned eyelid responses was clearly the result of the high phasic activity of orbicularis oculi motor units. Orbicularis oculi motoneuron membrane potentials oscillated at approximately 20 Hz after supraorbital nerve stimulation and during other reflex and conditioned eyelid movements. The oscillation seemed to be the result of both intrinsic (spike afterhyperpolarization lasting approximately 50 ms, and late depolarizations) and extrinsic properties of the motoneuronal pool and of the circuits involved in eye blinks. (+info)
Stereotactic radiosurgery for cavernous sinus cavernous hemangioma--case report.
A 40-year-old female presented with cavernous sinus cavernous hemangioma manifesting as left abducens and trigeminal nerve pareses. Magnetic resonance imaging revealed a left cavernous sinus tumor. The tumor was partially removed. Histological examination of the specimen confirmed cavernous hemangioma. Radiosurgery was performed using the gamma knife. The tumor markedly decreased in size after radiosurgery and morbidity was avoided. Cavernous sinus cavernous hemangiomas may be difficult to treat surgically due to intraoperative bleeding and cranial nerve injury. Stereotactic radiosurgery can be used either as an adjunct treatment to craniotomy, or as the primary treatment for small cavernous sinus cavernous hemangioma. (+info)
The authors present the clinical findings of a 30-year-old female and a 29-year-old male who both had isolated unilateral lateral rectus muscle palsy in neuro-Behcet's disease. The clinical feature related to isolated abduscens nerve palsy was identified by CT, systemic assessment and extraocular examination. These patients' constellation of findings appear to be unique: it does not follow any previously reported pattern of ocular manifestations of neuro-Behcet's disease. (+info)
Quantitative analysis of abducens neuron discharge dynamics during saccadic and slow eye movements.
The mechanics of the eyeball and its surrounding tissues, which together form the oculomotor plant, have been shown to be the same for smooth pursuit and saccadic eye movements. Hence it was postulated that similar signals would be carried by motoneurons during slow and rapid eye movements. In the present study, we directly addressed this proposal by determining which eye movement-based models best describe the discharge dynamics of primate abducens neurons during a variety of eye movement behaviors. We first characterized abducens neuron spike trains, as has been classically done, during fixation and sinusoidal smooth pursuit. We then systematically analyzed the discharge dynamics of abducens neurons during and following saccades, during step-ramp pursuit and during high velocity slow-phase vestibular nystagmus. We found that the commonly utilized first-order description of abducens neuron firing rates (FR = b + kE + r, where FR is firing rate, E and are eye position and velocity, respectively, and b, k, and r are constants) provided an adequate model of neuronal activity during saccades, smooth pursuit, and slow phase vestibular nystagmus. However, the use of a second-order model, which included an exponentially decaying term or "slide" (FR = b + kE + r + uE - c), notably improved our ability to describe neuronal activity when the eye was moving and also enabled us to model abducens neuron discharges during the postsaccadic interval. We also found that, for a given model, a single set of parameters could not be used to describe neuronal firing rates during both slow and rapid eye movements. Specifically, the eye velocity and position coefficients (r and k in the above models, respectively) consistently decreased as a function of the mean (and peak) eye velocity that was generated. In contrast, the bias (b, firing rate when looking straight ahead) invariably increased with eye velocity. Although these trends are likely to reflect, in part, nonlinearities that are intrinsic to the extraocular muscles, we propose that these results can also be explained by considering the time-varying resistance to movement that is generated by the antagonist muscle. We conclude that to create realistic and meaningful models of the neural control of horizontal eye movements, it is essential to consider the activation of the antagonist, as well as agonist motoneuron pools. (+info)
Apparent dissociation between saccadic eye movements and the firing patterns of premotor neurons and motoneurons.
Saccadic eye movements result from high-frequency bursts of activity in ocular motoneurons. This phasic activity originates in premotor burst neurons. When the head is restrained, the number of action potentials in the bursts of burst neurons and motoneurons increases linearly with eye movement amplitude. However, when the head is unrestrained, the number of action potentials now increase as a function of the change in the direction of the line of sight during eye movements of relatively similar amplitudes. These data suggest an apparent uncoupling of premotor neuron and motoneuron activity from the resultant eye movement. (+info)
Early components of the human vestibulo-ocular response to head rotation: latency and gain.
To characterize vestibulo-ocular reflex (VOR) properties in the time window in which contributions by other systems are minimal, eye movements during the first 50-100 ms after the start of transient angular head accelerations ( approximately 1000 degrees /s(2)) imposed by a torque helmet were analyzed in normal human subjects. Orientations of the head and both eyes were recorded with magnetic search coils (resolution, approximately 1 min arc; 1000 samples/s). Typically, the first response to a head perturbation was an anti-compensatory eye movement with zero latency, peak-velocity of several degrees per second, and peak excursion of several tenths of a degree. This was interpreted as a passive mechanical response to linear acceleration of the orbital tissues caused by eccentric rotation of the eye. The response was modeled as a damped oscillation (approximately 13 Hz) of the orbital contents, approaching a constant eye deviation for a sustained linear acceleration. The subsequent compensatory eye movements showed (like the head movements) a linear increase in velocity, which allowed estimates of latency and gain with linear regressions. After appropriate accounting for the preceding passive eye movements, average VOR latency (for pooled eyes, directions, and subjects) was calculated as 8.6 ms. Paired comparisons between the two eyes revealed that the latency for the eye contralateral to the direction of head rotation was, on average, 1.3 ms shorter than for the ipsilateral eye. This highly significant average inter-ocular difference was attributed to the additional internuclear abducens neuron in the pathway to the ipsilateral eye. Average acceleration gain (ratio between slopes of eye and head velocities) over the first 40-50 ms was approximately 1.1. Instantaneous velocity gain, calculated as Veye(t)/Vhead(t-latency), showed a gradual build-up converging toward unity (often after a slight overshoot). Instantaneous acceleration gain also converged toward unity but showed a much steeper build-up and larger oscillations. This behavior of acceleration and velocity gain could be accounted for by modeling the eye movements as the sum of the passive response to the linear acceleration and the active rotational VOR. Due to the latency and the anticompensatory component, gaze stabilization was never complete. The influence of visual targets was limited. The initial VOR was identical with a distant target (continuously visible or interrupted) and in complete darkness. A near visual target caused VOR gain to rise to a higher level, but the time after which the difference between far and near targets emerged varied between individuals. (+info)
Expansion of afferent vestibular signals after the section of one of the vestibular nerve branches.
The anterior branch of N. VIII was sectioned in adult frogs. Two months later the brain was isolated to record in vitro responses in the vestibular nuclei and from the abducens nerves following electric stimulation of the anterior branch of N. VIII or of the posterior canal nerve. Extra- and intracellularly recorded responses from the intact and operated side were compared with responses from controls. Major changes were detected on the operated side: the amplitudes of posterior canal nerve evoked field potentials were enlarged, the number of vestibular neurons with a monosynaptic input from the posterior canal nerve had increased, and posterior canal nerve stimulation recruited stronger abducens nerve responses on the intact side than vice versa. Changes in the convergence pattern of vestibular nerve afferent inputs on the operated side strongly suggest the expansion of posterior canal-related afferent inputs onto part of those vestibular neurons that were deprived of their afferent vestibular input. As a mechanism we suggest reactive synaptogenesis between intact posterior canal afferent fibers and vestibularly deprived second-order vestibular neurons. (+info)