Journal of neurophysiology
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1. Primary afferent depolarization (PAD) can be evoked by sensory volleys, supraspinal commands, or the activity of spinal locomotor networks (locomotor-related PAD). In this study we investigated the effect of locomotor-related PAD and of sensory-evoked PAD on the monosynaptic transmission between the group IA muscle afferents and motoneurons in the lumbosacral spinal cord. 2. ⋯ We conclude from these results that the locomotor-related PAD did not contribute significantly to the modulation of transmission in the monosynaptic reflex pathway of the cat during fictive locomotion. On the other hand, the results confirmed that PAD evoked by sensory input decreases group IA afferent transmission efficiently most probably by presynaptic inhibition. The results suggest therefore that, during real locomotion, sensory feedback induced by the moving limbs or perturbations will evoke an important presynaptic inhibition of the release from group IA primary afferent terminals.
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1. The introduction of a period of darkness between the disappearance of an initial fixation target and the appearance of a peripheral saccade target produces a general reduction in saccadic reaction time (SRT)-known as the gap effect- and often very short latency express saccades. To account for these phenomena, premotor processes may be facilitated by release of visual fixation and advanced preparation of saccadic programs. ⋯ These findings indicate that training-dependent express saccades are restricted to a specific spatial location dictated by the training target, and their incidence is facilitated by high predictability of target presentation, long-duration foreperiod, absence of visual fixation, eccentric initial eye position opposite to the saccade direction, and express saccade occurrence in the previous trial. The release of fixation afforded by the gap accounts for the general gap effect, but has only a modulatory influence on express saccade generation. We conclude that advanced motor preparation of saccadic programs generally reduces SRT and is primarily responsible for the occurrence of express saccades, which therefore may be caused mainly by neuronal changes restricted to a specific locus-coding for the trained movemen
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1. During alertness, lemniscal thalamocortical neurons in the ventral medial geniculate body (MGBv) encode sound signals by firing action potentials in a tonic mode. When they are in a burst firing mode, characteristic of thalamic neurons during some sleep states, the same stimuli may have an alerting function, leading to conscious perception of sound. ⋯ Also, K+ conductances may contribute to spike repolarization, because 4-AP (100 microM) or tetraethylammonium (2 mM) application led to prolonged action potentials and the generation of plateau potentials. A fast afterhyperpolarization, likely mediated by a Ca(2+)-dependent K+ conductance, limited the tonic firing. Such conductances, therefore, may regulate the re
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1. The present study addresses the involvement of voltage-dependent calcium channels of the N and L type in the spinal processing of innocuous and noxious input from the knee joint, both under normal conditions and under inflammatory conditions in which spinal cord neurons become hyperexcitable. In 30 anesthetized rats, extracellular recordings were performed from single dorsal horn neurons in segments 1-4 of the lumbar spinal cord. ⋯ The data suggest, therefore, that voltage-dependent calcium calcium channels of both the N and the L type are important for the sensory functions of the spinal cord. They are involved in the spinal processing of nonnociceptive as well as nociceptive mechanosensory input from the joint, both under normal and inflammatory conditions. The present results show in particular that N- and L-type channels are likely to be involved in the generation of pain evoked by noxious mechanical stimulation in normal tissue as well as in the mechanical hyperalgesia that is usually pres
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1. The main purposes of this study are to characterize the intracellular and extracellular responses of cells in superficial layers of entorhinal cortex (EC) in chronically epileptic animals, determine whether their altered physiology is dependent on being connected to hippocampus, and investigate whether there is evidence of augmented excitation and inhibitory interneuron disconnection. 2. Functional connectivity was maintained between the hippocampal area and the EC in vitro in a combined rat hippocampal-parahippocampal slice preparation by slicing with a vibratome at a 30-deg angle to the base of the brain. ⋯ IPSPs were not seen or markedly reduced at all stimulus intensities. These intracellular responses never resembled control responses. Intracellur responss correlated precisely in morphology and duration with extracellular field potentials. (ABSTRACT TRUNCATED)