Article Figures & Data
Figures
- Fig. 1.
Schematic drawing representing eye movements under normal and altered conditions. Eye position (position) in spontaneous eye movements (left) and eye velocity (velocity) during VOR induction (right) are schematically represented in a control situation and under hypothetical alterations of velocity processing (velocity imbalance), integration (integrator failure), or both. On theright, the solid line represents eye velocity, and the dotted line represents head velocity. Because eyes move in a direction opposite to the head during the reflex response, the head velocity curve has been inverted to facilitate comparison with the eye velocity curve. The horizontal dashed line corresponds to the mean head velocity, which by definition is zero. The horizontal dashed and dotted line represents the mean eye velocity, which is also zero in the absence of velocity imbalance. The vertical dotted lines indicate the head and eye phase peaks.Left, During spontaneous movements, alterations in the processing of velocity signals produce nystagmic eye movements with ramp-like slow phases, whereas a failure of oculomotor integration produces gaze-holding impairment, causing exponential drifts toward a central position. When integration is absent, the drift time constant is estimated to be 0.16 sec (Goldberg, 1980). If both velocity and integration deficits occur at the same time, a nystagmus with curved slow phases will appear. Right, During VOR induction, the velocity imbalance appears as a positive or negative value of the mean slow eye velocity, whereas the integration deficit results in a decreased reflex gain and increased phase lead. A velocity imbalance with gain reduction and enhanced phase lead should be expected when both alterations are present.
- Fig. 2.
Effects of unilateral injections of drugs affecting the NO–cGMP pathway in the PH nucleus of an alert cat during spontaneous eye movements. Recordings of right eye position in the horizontal plane (HEP) under control conditions and after injections of the indicated drugs in the left PH nucleus, in either darkness (D) or light (L). Doses and times after injection were as follows: l-NAME, 50 nmol, 19 (D) and 20 (L) min; l-arginine (L-Arg), 100 nmol, 8 (D) and 11 (L) min; SNAP, 20 nmol, 5 (D) and 4 (L) min; and 8-Br-cGMP, 4 nmol, 6 (D) and 8 (L) min. Eye position is plotted as degrees (deg). Vertical arrows indicate movement direction: l, left; r, right.Straight and curved arrows indicate linear and exponential slow phases, respectively. Slow phases forl-NAME and l-arginine were best fit to a linear equation, whereas slow phases for SNAP and 8-Br-cGMP were best fit to an exponential equation.
- Fig. 3.
Effects of unilateral injections of drugs affecting the NO–cGMP pathway in the PH nucleus of an alert cat during sinusoidal vestibular stimulation in darkness. Representative recordings of eye (solid line) and head (dotted line) velocity (V) during VOR induction by turntable rotation at 0.1 (A) and 1 Hz (B) under control conditions and after injections of the indicated drugs in the PH nucleus. The head velocity curve has been inverted to facilitate comparison with the eye velocity curve. Movement direction as indicated in Figure 2.
- Fig. 4.
Velocity imbalance, gain, and phase lead of the vestibulo-ocular reflex after local administration in the PH nucleus of drugs affecting the NO–cGMP pathway. A, Velocity imbalance (VI) produced by the different drugs during VOR induction by rotation of the head at 0.1 and 1 Hz. Positive values represent velocity imbalance toward the injected side and negative values toward the contralateral side. B, Gain of the VOR induced by rotation of the head at 0.1 and 1 Hz after injection of the different drugs. Gain is expressed as a percentage of the control value for each experiment. Gray bar, 100% ± SD of control values. C, Changes in phase lead during the VOR induced by rotation of the head at 0.1 and 1 Hz produced by injection of the different drugs. Values are expressed in degrees (deg). Gray bar, 0 ± SD of control values. n = 2 for d-NAME;n = 3 for SNAP and l-arginine;n = 4 for 8-Br-cGMP; and n = 5 for l-NAME.
- Fig. 5.
Distribution of nitrergic neurons and neurons containing NO-sensitive guanylyl cyclase in the PH nucleus and adjacent areas. A, Photomicrograph of a coronal brainstem section (posterior 8, according to Berman, 1968) through the PH and MV nuclei stained with a polyclonal antibody recognizing neuronal NOS. A dense group of nitrergic neurons is observed in the PH (arrows). B, Photomicrograph of a coronal brainstem section at a similar rostrocaudal level stained with a polyclonal antibody raised against cGMP. The neuropil is densely stained in the dorsal part of the PH nucleus (arrows), and a cluster of labeled cell bodies (boxed area) appears in an intermediate location between the PH and MV nuclei.C, Higher magnification of the area indicated inB, showing the morphology of NO-sensitive cGMP-producing neurons. Scale bars: A, B, 250 μm;C, 100 μm.
Tables
- Table 1.
Effect of individual drug injections on VOR gain, phase lead, and postsaccadic drift time constant
Drug VOR (0.1 Hz) VOR (1 Hz) Spontaneous eye movements ΔGaina ΔPhase lead (deg)b ΔGaina ΔPhase lead (deg)b Time constant (sec)c SNAP −0.01 −2.0 −0.03 2.0 0.90 ± 0.40 0.02 0.9 −0.12 4.6 0.57 ± 0.12 −0.06 8.9* 0.07 −0.5 0.73 ± 0.26 8-Br-cGMP −0.03 7.0 0.00 2.6 1.78 ± 0.44 −0.01 6.5 −0.03 −0.8 1.45 ± 0.76 −0.03 1.1 0.03 −0.1 1.70 ± 0.24 −0.07 −0.8 −0.02 0.3 0.84 ± 0.37 a Values represent changes in VOR gain after drug injection. Absolute gain values in control conditions were 0.83 ± 0.08 for 0.1 Hz and 0.94 ± 0.12 for 1 Hz. n = 7.
b Values represent changes in VOR phase lead after drug injection. Absolute phase lead values in control conditions were 10.2 ± 2.8 for 0.1 Hz and 6.9 ± 2.6 for 1 Hz. n = 7.
c Mean ± SD of time constants calculated immediately before VOR induction.
* p < 0.05 when phase leads before and after injection were compared.
