Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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The amplitude of the acoustic startle response (ASR) is markedly reduced when the startle eliciting pulse is preceded by a weak, non-startling stimulus at an appropriate lead time, usually about 100 ms. This phenomenon is termed prepulse inhibition (PPI) and has received considerable attention in recent years as a model of sensorimotor gating. We report here on experiments which were undertaken in order to investigate some of the neural mechanisms of PPI. ⋯ Neurotoxic lesions of the cholinergic neurons of the PPTg significantly reduced PPI without affecting the ASR amplitude in the absence of prepulses. No effect on long-term habituation of the ASR was observed. The present data indicate that the pathway mediating PPI impinges upon the primary acoustic startle circuit through an inhibitory cholinergic projection from the PPTg to the PnC.
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To assess speed- and gait-related changes in semitendinosus (ST) activity, EMG was recorded from three cats during treadmill locomotion. Selected step cycles were filmed, and hip and knee joint kinematics were synchronized with EMG records. Swing-phase kinetics for trot and gallop steps at 2.25 m/s were compared for gait-related differences. ⋯ Rotatory and transverse gallops at 4.0 m/s had similar swing phase kinetics and ST-EMG. Gait-related changes in ST-EMG, particularly at the trot-gallop transition, are not congruent with neural models assuming that details of the ST motor pattern are produced by a spinal CPG. We suggest that motor patterns programmed by the spinal CPG are modulated by input from supraspinal centers and/or motion-related feedback from the hindlimbs to provide appropriate gait-specific activation of the ST.
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Evidence is presented suggesting that the neural correlate of the eye-blink reflex can be evoked in an in vitro brainstem-cerebellum preparation from the turtle by using electrical rather than natural stimulation of cranial nerve inputs. Abducens nerve discharge is triggered by brief electrical stimulation of the ipsilateral trigeminal nerve. This discharge corresponds behaviorally to EMG recordings of extraocular muscles and eye retraction recorded in situ, in a reduced preparation. ⋯ Sustained reflex activity is further postulated to originate from recurrent excitation in pathways within the caudal brainstem, particularly the reticular formation. This interpretation is consistent with the observed patterns of sulforhodamine label, the effects of local microinjections of APV, and the elimination of sustained activity when the caudal brainstem is transected. These data have implications for pathways that may underlie conditioning of the eye-blink response.
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Recordings of the activity of 2705 single neurones were made in entorhinal and perirhinal cortex, area TG of the temporal lobe, and the inferior temporal cortex both during monkeys' performance of a serial recognition memory task using complex pictures and when monkeys were shown objects. Responses of 120 (9.7%) of the visually responsive neurons recorded were significantly smaller to the second than to the first presentations of unfamiliar stimuli. The incidence of such responses was highest in perirhinal cortex plus areas TE1 and TE2 of the temporal lobe, intermediate in lateral entorhinal cortex and areas TE3 and TG, and lowest in other parts of entorhinal and inferior temporal cortex. ⋯ Neurones signalling information of use for recognition memory are found in cortex close to the rhinal sulcus where lesions result in major deficits in the performance of recognition memory tasks. The conjunction of these findings provides strong evidence for the importance of these neurones and this cortex for processes (recency and familiarity discrimination) necessary for recognition and working memory. The possible relation of the neuronal responses to priming memory is also discussed.
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The redistribution of neurotransmitter amino acids resulting from 20 min of ischaemia was studied in the rat hippocampus by quantitative, electron microscopic immunocytochemistry and by in vivo microdialysis. Changes in the distribution of glutamate, glutamine, aspartate and GABA in various cell compartments of CA1 were analysed immediately after ischaemia or after 60 min of reperfusion, by incubating ultrathin sections with antisera raised against protein glutaraldehyde conjugates of the respective amino acids and subsequently with a secondary antibody coupled to colloidal gold particles. Transverse microdialysis probes coupled with HPLC and implanted in the same animals were used to determine the extracellular concentration of amino acids in the left hippocampus and to apply a drug (BW1003C87) believed to modify the extracellular release of amino acids induced by ischaemia. ⋯ The glutamate-glutamine ratio in glial cells was greatly increased after ischaemia, but recovered to a normal level within 1 h of reperfusion. Aspartate-like immunoreactivity was substantially reduced in pyramidal cell somata both immediately and 60 min after ischaemia, while profiles that were immunopositive for GABA in control brains showed increased GABA immunolabelling. These results suggest that postsynaptic neuronal elements as well as glial cells contribute to the extracellular overflow of excitatory amino acids during an ischaemic event: post-synaptic elements by leaking or releasing glutamate and aspartate, and glial cells by losing their ability to convert glutamate to glutamine effectively.(ABSTRACT TRUNCATED AT 400 WORDS)