Showing papers on "Cuneate nucleus published in 1976"

Effects of two benzodiazepines, phenobarbitone, and baclofen on synaptic transmission in the cat cuneate nucleus.

Abstract: The effects of diazepam, flunitrazepam, phenobarbitone and baclofen on excitatory as well as on pre- and postsynaptic inhibitory processes in the cuneate nucleus were studied in decerebrate cats. Afferent presynaptic inhibition in the cuneate nucleus, evoked by volleys in the median nerve, and assessed by the size of the positive cuneate surface potential (P wave), the dorsal column reflex (DCR), and the increased excitability of primary afferent terminals of the ulnar nerve, was markedly enhanced by diazepam (0.1–3.0 mg/kg i.v.) and flunitrazepam (0.01–0.3 mg/kg i.v.), slightly enhanced by lower doses of phenobarbitone (3–20 mg/kg i.v.), but depressed by baclofen (1–10 mg/kg i.v.). Diazepam, flunitrazepam and phenobarbitone also increased postsynaptic inhibition in the cuneate nucleus which was measured by the decrease after conditioning volleys in the median nerve of the short-latency lemniscal response to cuneate stimulation. The GABA receptor blocking agent, picrotoxin, antagonized the effects of diazepam on pre- and postsynaptic inhibition in a surmountable way. After thiosemicarbazide (TSC), an inhibitor of GABA synthesis, both pre-and postsynaptic inhibition were greatly reduced and the augmenting effect of diazepam on both types of inhibition was nearly abolished. Aminooxyacetic acid (AOAA), an inhibitor of GABA degradation, slightly enhanced pre- and postsynaptic inhibition; the effects of diazepam were unaffected by AOAA. Diazepam, flunitrazepam and phenobarbitone did not alter the resting excitability of primary afferent endings or of cuneo-thalamic relay (CTR) cells in the cuneate nucleus. After higher doses (30 mg/kg i.v.) of phenobarbitone pre- and postsynaptic inhibition, which were enhanced by 10 mg/kg of this drug, tended to return to pre-drug values or below. Phenobarbitone, in contrast to benzodiazepines, also depressed in a dose-dependent way the N wave, which is an index of the orthodromic excitation of the CTR cells. Baclofen strongly depressed the cuneate N wave, decreased the excitability of CTR cells, reduced pre- and postsynaptic inhibition, but had no effect on the resting excitability of primary afferent endings. Our findings suggest the following modes of action of the above mentioned drugs: 1. benzodiazepines enhance selectively the GABA-mediated pre- and postsynaptic inhibition in the cuneate nucleus; 2. phenobarbitone slightly enhances pre- and postsynaptic inhibition only in a narrow dose range, and in addition reduces the excitatory processes in the cuneate nucleus; 3. baclofen seems to depress the excitation of cuneate relay cells and interneurones postsynaptically; the depression of relay cells is probably non-specific.

Blockade by amino acid antagonists of neuronal excitation mediated by the pyramidal tract.

Abstract: 1. The responses to glutamate and amino acid antagonists of cells in the cuneate nucleus of anaesthetized rats have been examined.2. 1-hydroxy-3-amino-pyrrolidone-2 (HA-966) and glutamic acid diethylester applied by micro-iontophoresis reduced glutamate excitation of the neurons. HA-966 WAS EFFECTIVE ON MORE CELLS THAN GLUTAMIC ACID DIETHYLESTER AND WAS MORE POTENT. HA-966 DID NOT AFFECT EXCITATORY RESPONSES TO ACETYLCHOLINE.3. Spike activity of cuneate cells was evoked by stimulating the cerebral cortex. Spikeswhich could be attributed to monosynaptic activation of the cells were studied. The pyramidal tract is the only corticofugal pathway known to be capable of short latency activation of dorsal column nucleus neurones.4. HA-966 reversibly blocked the evoked activity in twenty-eight (70%) of forty units in which monosynaptically evoked spikes were induced.5. The results raise the possibility that the neurotransmitter released by neurones of the pyramidal tract may be an excitatory amino acid.

Input-output relation of transmission through cuneate nucleus.

Abstract: 1. In decerebrate cats, micro-electrodes were inserted into the cuneate nucleus to stimulate afferent terminals with single shocks of varying intensities. Estimates of the input and output of the nucleus were obtained by integrating antidromic responses in forelimb cutaneous nerves and orthodromic responses in the medial lemniscus. 2. Input-output curves were normally very non-linear, reflecting the high synaptic potency of small inputs. They were fitted readily by power functions, with exponents averaging 0-50. 3. The normal input-output relation rapidly disappeared after interruption of the blood supply. A loss of synaptic efficiency of small inputs was indicated by curves with exponents of greater than or equal to 1; this was associated with a sharp increase in terminal excitability. 4. Within the range of surface temperature 30-40 degrees C, warming made the input-output curves steeper but reduced terminal excitability, whereas cooling had the opposite effect. The efficiency of transmission was thus inversely correlated with terminal excitability. 5. The non-linear shape of cuneate input-output curves is probably not determined by inhibitory control, since picrotoxin depressed rather than enhanced outputs. 6. On the other hand, pentobarbitone made the input-output curves markedly steeper and tended to lower terminal excitability.

The negative potential wave evoked in cuneate nucleus by stimulation of afferent pathways: its origins and susceptibility to inhibition.

Abstract: 1. The negative (N)-wave evoked at various depths in the cuneate nucleus by stimulation of afferents in the ipsilateral forepaw or dorsal column has been studied in the rat. 2. Micro-iontophoretic applications of gamma-aminobutyric acid (GABA) into the vicinity of the recording electrode markedly reduced the amplitude of the negative wave, but only when recordings were made near the base of the cuneate nucleus. Nearer the surface of the medulla, GABA was much less effective. 3. A similar depth distribution obtained for the depression of the negative wave by micro-iontophoretic Mg2+ and enhancement by Ca2+. 4. Depression of the negative wave by conditioning stimulation of the afferent pathway also showed a similar depth distribution. The conditioned depression of the negative wave was most marked during the first 30 ms after the conditioning stimulus and this early depression could be antagonized by iontophoretic (+)-bicuculline methochloride. A lesser degree of conditioned inhibition of the negative wave persisted up to 80-200 ms but this was resistant to (+)-bicuculline methochloride. Thus, conditioned depression of the negative wave appeared to be mediated only in part by a GABA-like transmitter. 5. It is concluded that the negative wave recorded near the base of the cuneate nucleus has some of the predicted properties of a post-synaptic potential. These properties are not seen when the negative wave is recorded more superficially, near the surface of the medulla.

Concerning the ionic basis of presynaptic inhibition.

Abstract: The superfused rat cuneate nucleus has been used to investigate the sensitivity of primary afferent terminals and of evoked primary afferent depolarization (PAD) to alterations in extracellular K+ and Cl- ions levels. Results indicate that PAD is caused by an efflux of Cl- from primary afferent terminals rather than by an increase in extracellular K+.

Is glutamic acid the pyramidal tract neurotransmitter

Abstract: Applied by microiontophoresis, 1-hydroxy-3-amino-pyrrolidone-2 (HA-966) antagonized excitation by glutamic acid but not by acetylcholine of neurones in the rat cuneate nucleus. HA-966 blocked the short latency excitation of cuneate neurones following stimulation of the pyramidal tract on 28 of 40 cells (70%). Thus, glutamate or a related amino-acid may be the neurotransmitter released by pyramidal tract neurones.

Some effects of picrotoxin on afferent terminals in the cuneate nucleus of the cat

Abstract: The slow potentials recorded from dorsal roots or from the dorsal region of the spinal cord have been explained as the result of the operation of two very different mechanisms. The first was suggested by Barron and Matthews (1938), who pointed out that any depolarising agent released by activity of the profuse unmyelinated fibres and terminals in the dorsal horn would tend to depolarise both the active and adjacent inactive fibres. The most obvious possible agent of such a depolarisation is K+. Unmyelinated fibres in the vagus nerve indeed release substantial amounts of K+ during activity (Keynes and Ritchie, 1965; Rang and Ritchie, 1968), and more recent studies with K+ -sensitive micro­electrodes have shown significant increases in extracellular K+ concentration after the arrival of afferent volleys, both in the cuneate nucleus and the dorsal horn (Krnjevic and Morris, 1972, 1974; Vyklický, Sykova, Křiž and Ujec 1972; Křiž Sykova, Ujec and Vyklický, 1974).

Caudate influence on transmission in the cuneate nucleus - Jubran A. Hush

Abstract: The caudate nucleus, part of the "extrapyramidal motor system" has been considered to be almost exclusively involved in motor function. In 1942, however, Mettler and Mettler n described abnormal responses to sensory stimulation following bilateral striatal lesions in cats. More recently, Ungerstedt 12 has shown that unilateral degeneration of the nigrostriatal dopamine system in rats produces a severe 'sensory neglect' in addition to the well known asymmetries in movement and posture. These animals failed to orient themselves toward tactile, auditory, visual and olfactory stimuli applied contralateral to the lesioned side. Sensory modalities gradually recovered but normal reactions to tactile stimuli failed to return 3 months after the lesion 12. Electrical stimulation of the nigrostriatal system has been shown to produce both facilitatory and/or inhibitory influences on cortical and thalamic activity evoked by visual, auditory or somatic stimuliS, 8,9. Results of sensory interactions at the thalamocortical level are often difficult to interpret but this can be minimized if one studies the first relay along the sensory pathway. The purpose of the report is to demonstrate the effects of electrical stimulation of the caudate nucleus on afferent somatic transmission in the cuneate nucleus. Cats were anesthetized with a-chloralose (50 mg/kg) or pentobarbital sodium (36 mg/kg), paralyzed with gaUamine triethiode, and artificially respired. End-tidal CO~, femoral blood pressure and rectal temperature were maintained within physiological range. The dorsal column nuclei were exposed and most of the recordings were made from one of the cuneate nuclei. Bipolar needle stimulating electrodes were inserted into the central pad of the ipsilateral forepaw (IFP). The cutaneous stimulus consisted of a single square pulse of 0.1 msec duration and an amplitude not exceeding 6 V. Small (O.D., 0.6 mm), coaxial electrodes were placed stereotaxically in the medial lemniscus (contralateral to the cuneate nucleus recorded from) at the caudal end of the thalamus and in each head of the caudate nuclei (at AP coordinate of q18.5 mm). The medial lemniscal electrode was used for recording the lemniscal response to contralateral forepaw (CFP) stimulation and for bipolar antidromic stimulation of the cuneate neurons. Conditioning electrical stimulation of the caudate nuclei consisted of single (0.01-0.03 msec) pulses or a train of 2-4 such pulses at 312 Hz. Four types of

Differences in timing of corticocuneate and corticogracile actions

Abstract: Publisher Summary This chapter focuses on a study analyzing differences in timing of corticocuneate and corticogracile actions. In all experiments, the animals were anesthetized with sodium pentobarbitone; some were also given gallamine triethiodide intermittently to improve mechanical stability by inducing paralysis during single unit recording. In the experiments, transmission through each nucleus was studied by recording the monophasic mass potential in the crossed medial lemniscus generated by a single shock to either the superficial radial nerve or the medial plantar nerve. These are both cutaneous nerves. The twice-threshold shocks that were used activated the large A fibers maximally without exciting A delta fibers. Time courses of inhibition of transmission by the cortical conditioning stimuli were obtained. The results showed that the latency of the corticofugal inhibition of the cuneate nucleus is less than half that for the gracile nucleus, which agrees with the prediction from the earlier antidromic studies.