Journal of neurophysiology
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Comparative Study
Differential effects of morphine on corneal-responsive neurons in rostral versus caudal regions of spinal trigeminal nucleus in the rat.
The initial processing of corneal sensory input in the rat occurs in two distinct regions of the spinal trigeminal nucleus, at the subnucleus interpolaris/caudalis transition (Vi/Vc) and in laminae I-II at the subnucleus caudalis/spinal cord transition (Vc/C1). Extracellular recording was used to compare the effects of morphine on the evoked activity of corneal-responsive neurons located in these two regions. Neurons also were characterized by cutaneous receptive field properties and parabrachial area (PBA) projection status. ⋯ To determine if the Vc/C1 transition acted as a relay for the effect of intravenous morphine on corneal stimulation-evoked activity of Vi/Vc units, morphine was applied topically to the dorsal brain stem surface overlying the Vc/C1 transition. Local microinjection of morphine at the Vc/C1 transition increased the evoked activity of 4 Vi/Vc neurons, inhibited that of 2 neurons, and did not affect the remaining 12 corneal neurons tested. In conclusion, the distinctive effects of morphine on Vi/Vc and Vc/C1 neurons support the hypothesis that these two neuronal groups contribute to different aspects of corneal sensory processing such as pain sensation, autonomic reflex responses, and recruitment of descending controls.
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Comparative Study
Forms of forward quadrupedal locomotion. II. A comparison of posture, hindlimb kinematics, and motor patterns for upslope and level walking.
To gain insight into the neural mechanisms controlling different forms of quadrupedal walking of normal cats, data on postural orientation, hindlimb kinematics, and motor patterns of selected hindlimb muscles were assessed for four grades of upslope walking, from 25 to 100% (45 degrees incline), and compared with similar data for level treadmill walking (0.6 m/s). Kinematic data for the hip, knee, ankle, and metatarsophalangeal joints were obtained from digitizing ciné film that was synchronized with electromyographic (EMG) records from 13 different hindlimb muscles. Cycle periods, the structure of the step cycle, and paw-contact sequences were similar at all grades and typical of lateral-sequence walking. ⋯ The EMG activity of stance-related muscles also increased in amplitude with grade, and three muscles not active during the stance phase of level walking had stance activity that increased in amplitude and duration at the steepest grades; these muscles were the ST, FDL, and extensor digitorum brevis. Overall the changes in posture, hindlimb kinematics, and the activity patterns of hindlimb muscles during upslope walking reflected the need to continually move the body mass forward and upward during stance and to ensure that the paw cleared the inclined slope during swing. The implications of these changes for the neural control of walking and expected changes in hindlimb kinetics for slope walking are discussed.
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Mechanisms of blockade of tetrodotoxin-resistant (TTXr) Na+ channels by local anesthetics in comparison with the sensitivity of tetrodotoxin-sensitive (TTXs) Na+ channels were studied by means of the patch-clamp technique in neurons of dorsal root ganglions (DRG) of rat. Half-maximum inhibitory concentration (IC50) for the tonic block of TTXr Na+ currents by lidocaine was 210 micromol/l, whereas TTXs Na+ currents showed five times lower IC50 of 42 micromol/l. Bupivacaine blocked TTXr and TTXs Na+ currents more potently with IC50 of 32 and 13 micromol/l, respectively. ⋯ Because it was found that TTXr Na+ channels predominantly occur in smaller sensory neurons, their blockade might underlie the suppression of the sensation of pain. Different sensitivities and varying proportions of TTXr and TTXs Na+ channels could explain the known differential block in spinal anesthesia. We suggest that the frequency reduction at low local anesthetic concentrations may explain the phenomenon of paresthesia where sensory information are suppressed gradually during spinal anesthesia.
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Spinal neurons processing information from the ureter have been characterized in rats 1-4 days after the implantation of an experimental ureteric stone and compared with those of normal rats. The effects of a conditioning noxious stimulation of the ureter in the presence of the hyperalgesia evoked by the calculosis also were examined. Extracellular recordings were performed at the T12-L1 segments of the spinal cord. ⋯ A noxious ureteric distention applied to neurons with ureter input evoked a complex mixture of increases and decreases in somatic receptive field size and/or somatic input properties markedly different from the generalized increases in excitability seen when such a stimulus was applied to normal animals. We conclude that the presence of a ureteric stone evokes excitability changes of spinal neurons (enhanced background activity, greater number of ureter-driven cells, decreased threshold of convergent somatic receptive fields), which likely account for the referred hyperalgesia seen in rats with calculosis. However, further noxious visceral input occurring in the presence of persistent hyperalgesia produces selective changes that cannot be explained by a generalized excitability increase and suggest that the mechanisms underlying maintenance of hyperalgesia include alteration of both central inhibitory and excitatory systems.
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Most retinal amacrine (ACs) and ganglion cells (GCs) express temporal contrast by generating action potentials at only the onset and offset of the light stimulus. This study investigated the neural mechanisms that underlie this temporal contrast enhancement. Whole cell patch recordings were made from bipolar cells (BCs), ACs, and GCs in the retinal slice preparation. ⋯ This suggests that a voltage-dependent conductance converts the relatively transient current responses to more sustained voltage responses. Our results imply a synaptically driven local GABAergic feedback at bipolar terminals, mediated by GABAC receptors. This feedback appears to be a significant component of the mechanism underlying temporal contrast enhancement in - ACs and GCs.