Eberhardt K. Sauerland

The role of the lower brain stem in cortically induced inhibition of somatic reflexes in the cat.

Abstract The role of the lower brain stem in cortically induced alteration of somatic reflexes was investigated in the cat. The anterior portion of the orbital gyrus, previously implicated in the inhibition of monosynaptic and polysynaptic reflexes at all levels of the neuraxis, was shown to project directly to the ventromedial bulbar reticular formation (chiefly to the nucleus reticularis gigantocellularis) and to the pontine tegmentum (mainly to the nucleus reticularis pontis oralis). As a result of single pulse application to the anterior portion of the orbital gyrus, short latency (0.4–0.5 msec), direct responses were obtained in the ipsilateral and contralateral pontine and medullary reticular regions. The amplitude of these responses was approximately equal in the medullary inhibitory area, whereas, in the pontine facilitatory region, the size of contralaterally evoked responses was 40–65 % less than that of the ipsilaterally evoked potentials. The fact that the ventromedial bulbar reticular formation participates in the mechanism of orbital-cortically induced inhibition of the monosynaptic masseteric reflex, has been demonstrated in transection experiments. Transections of the medulla oblongata 2 mm caudal to the obex (P17) and lower had no effect on the efficiency of cortically induced reflex inhibition. More rostral transections (P15-P10) led to ineffectiveness and abolition of the cortically induced inhibitory influence. Moreover, transections at even more rostral levels (P8-P5) caused facilitation of the masseteric reflex following orbital-cortical stimulation. It is assumed that the descending orbito-medullary and orbito-pontine fibers synapse with neurons of the reticulo-spinal tract, and that axon collaterals of these neurons or axons of other reticular cells in the medullary or pontine reticular formation mediate inhibitory or excitatory influences, respectively, to the trigeminal and possibly also to other cranial nerve motor nuclei. A simple schematic drawing illustrates the role of the lower brain stem in orbital-cortically induced reflex alteration.

Inhibition of monosynaptic and polysynaptic reflexes and muscle tone by electrical stimulation of the cerebral cortex

Abstract Electrical stimulation of the rostral end of a forebrain inhibitory and EEG synchronizing system has resulted in suppression of motor behavior, induction of sleep, and inhibition of the monosynaptic masseteric reflex in cats and monkeys. The experiments reported here are concerned with a closer examination of the inhibitory effects exerted by the cortical end of this system on somatic reflexes at different levels of the neuraxis and in various stages of vigilance in the adult cat. Electrical stimulation, consisting of a short train of pulses, was applied to the rostral portion of the orbital gyrus. Following the train of impulses to the cortex, test reflexes were electrically elicited, and the effects of cortical stimulation on reflex discharges were studied. Electrical stimulation of the cortical inhibitory area resulted in immediate and consistent inhibition of a variety of monosynaptic and polysynaptic reflexes at different levels of the neuraxis. This inhibition was diffuse and nonreciprocal when the concurrently recorded EEG was synchronized. On the other hand, reflexes for antigravity muscles were inhibited and those for their antagonists facilitated, when the EEG was desynchronized. Additionally, diffuse inhibition of spontaneous muscle tone and synchronization of the EEG were obtained by electrical stimulation of this same cortical area. These findings provide some neurophysiological basis for an understanding of forebrain inhibitory mechanisms.

Fiber projections from rostral basal forebrain structures in the cat

Abstract Rostral basal forebrain structures, such as preoptic and rhinencephalic regions, are known to receive direct projections from the orbital cortex, and thus may participate in descending influences on brain stem and spinal structures. Projections from these preoptic and rhinencephalic sites were traced in the present study by means of the Nauta method. The medial forebrain bundle was followed from the olfactory tubercle to the mamillary body, and from the preoptic area to the subthalamus, the central gray matter of rostral midbrain and the midbrain tegmentum. Projections to the amygdaloid complex were chiefly confined to the anterior amygdaloid region. Three projection pathways to the thalamus were observed. The first coursed in the stria medullaris via the inferior thalamic peduncle to terminate in nuclei reticularis, ventralis anterior, anterior ventralis, anterior dorsalis, parataenialis, medialis dorsalis, and habenularis lateralis. The second pathway entered the internal medullary lamina via the inferior thalamic peduncle to distribute in nucleus medialis dorsalis and in the intralaminar nuclei. The third pathway to the thalamus ascended through medial hypothalamic areas to distribute fibers to nucleus ventralis medialis and the midline nuclei. Ascending fibers from the preoptic area were traced to the olfactory tubercle and the septal region. Based on these findings, possible modulating influences exerted by the orbital cortex through the medial forebrain bundle on thalamocortical and brain stem-hippocampal systems might be envisioned.

Cortically induced presynaptic inhibition of trigeminal proprioceptive afferents.

Abstract 1. Using a modification of Walls technique 30 , cortically induced primary afferent depolarization (CPAD) in trigeminal proprioceptive fibers was investigated in the cat. Increased excitability of central processes of mesencephalic tract neurons was observed in the trigeminal motor and the hypoglossal nucleus. 2. The time course of CPAD in trigeminal proprioceptive fibers was characterized by the following parameters: Latency of onset 10–15 msec; peak 37 msec; declining phase 100–120 msec; total duration approximately 150 msec. 3. The time course of cortically induced changes of the monosynaptic masseteric reflex was examined. There were two phases of cortically evoked reflex suppression: The first one had its peak at a conditioning interval of about 10 msec; it was complete and relatively short-lasting. The second suppressive phase had its peak at a conditioning interval of approximately 40 msec; it was substantially weaker than the first phase and was very prolonged. There was a close resemblance between the time course of the second phase and that of CPAD in trigeminal proprioceptive fibers. 4. Neurophysiological data were supported by pharmacological studies. Picrotoxin strongly reduced CPAD in trigeminal proprioceptive fibers and abolished the second phase of masseteric reflex suppression. Strychnine affected only the first phase. 5. CPAD in trigeminal proprioceptive fibers was induced by a conditioning stimulus consisting of 3 pulses. The most effective cortical area included the anterior portions of the orbital and coronal gyri. Contralateral stimulation of the cerebral cortex was slightly more effective than that of the ipsilateral side. 6. It is concluded that the two phases of cortically induced masseteric reflex inhibition are due to two different inhibitory mechanisms: The first phase is produced by postsynaptic inhibition; the second phase is due to presynaptic inhibition. Thus, cortically evoked influences on the masseteric monosynaptic reflex of the brain stem are manifested at the postsynaptic as well as at the presynaptic level.

Effects of ethanol on EEG spectra of the intact brain and isolated forebrain.

Abstract The effects of ethanol on the frontoparietal EEG were studied in acutely prepared immobilized cats. Animals with intact brains as well as isolated forebrain preparations (telencephalon and diencephalon intact; brain stem detached by means of a precollicular transection) were investigated. Taped EEG samples of 17 sec duration selected and digitized by a Classic LINC computer. Frequency spectra were computed for frequencies from 0–29 Hz, using the Cooley-Tukey algorithm. In animals with intact brains, intravenous ethanol injections (0.08 g/kg/min) consistently induced a decrease in higher EEG frequencies and an increase of energy in the lower frequency band. The shift toward lower EEG frequencies was also observed in precollicular preparations under the influence of ethanol. Whereas the effect of ethanol on the EEG in the intact brain could be sufficiently explained by its depressant action on the reticular activating system of the brain stem, the profound ethanol-induced changes of the EEG in precollicular preparations provide a basis for the assumption that ethanol also exerts a direct influence upon certain structures of the forebrain.

Presynaptic depolarization of lingual and glossopharyngeal nerve afferents induced by stimulation of trigeminal proprioceptive fibers.

Abstract The effect of trigeminal proprioceptive input from masticatory muscles on the level of polarization of lingual and glossopharyngeal nerve afferents was studied in cats with complete precollicular transection of the brain. A modification of Walls technique was utilized to determine excitability changes of the central terminals of lingual and glossopharyngeal fibers in nucleus oralis and nucleus parasolitarius, respectively. Primary afferent depolarization of these sensory nerves could be induced by electrical stimulation of the masseteric nerve, anterior digastric nerve, or the trigeminal mesencephalic nucleus. Primary afferent depolarization of lingual and glossopharyngeal fibers was also produced by brisk tension of jaw elevator muscles as well as of jaw openers, whereas moderate sustained tension of these muscles had no effect on the level of terminal polarization. It was concluded that masticatory proprioceptive activities, excluding those mediated in group IA fibers from spindle organs, are responsible for the observed primary afferent depolarization. It appears that the depolarization of presynaptic terminals of lingual and glossopharyngeal fibers plays an important role in the control of reflexly induced tongue movements.

Presynaptic depolarization of trigeminal cutaneous afferent fibers induced by ethanol

Abstract The effect of ethyl alcohol (ethanol) on the level of polarization of trigeminal cutaneous afferents was studied in cats. A modification of Walls technique was utilized to determine excitability changes of trigeminal cutaneous neurons at two different structural levels: at the central terminals located in the spinal trigeminal nucleus; and at the level of the cell bodies contained within the trigeminal ganglion. The excitability of these neuronal structures was expressed in the form of stimulus-response curves. In addition, the effect of ethanol on cerebral cortically conditioned stimulus-response curves and on time courses of cortically induced excitability changes was determined. Intravenous ethanol injections (0.08 g/kg/min) consistently produced primary afferent depolarization (PAD) of central terminals of trigeminal fibers, whereas ganglion cells and fiber processes, contained in the trigeminal ganglion, were not significantly altered in their level of polarization. Ethanol-induced changes in PAD were greater in cortically conditioned than in nonconditioned states. In preparations with complete precollicular transection, ethanol failed to induce consistent and significant PAD. The observed changes in PAD of presynaptic (central) terminals were discussed with respect to the concept of presynaptic inhibition. It was concluded that at least part of the depressant action of ethanol on the trigeminal somesthetic system is due to an enhancement of presynaptic depolarization. It appears that descending cerebral-cortical influences play an important role in this inhibitory mechanism.

THE ROLE OF THE BRAIN STEM IN ORBITAL CORTEX INDUCED INHIBITION OF SOMATIC REFLEXES

Publisher Summary The orbital surface of the frontal lobe appears to be unique in its capacity for inhibiting both somatomotor and visceromotor activities. Electrical stimulation of the orbital surface of the frontal lobe can induce states of behavioral inhibition and the onset of sleep. Electrical stimulation of the orbital-frontal cortex inhibits a brain-stem monosynaptic reflex as well as spinal reflexes. Both pre- and postsynaptic inhibitory processes play a role in cortically produced reflex inhibition. This chapter illustrates the role of the brain stem in orbital cortically evoked changes of somatic reflexes in the cat. Orbital cortically induced inhibition of the monosynaptic masseteric reflex depends upon the integrity of the ventromedial bulbar reticular formation.

Cortically induced changes of presynaptic excitability in higher-order auditory afferents

Abstract The influence of various cerebral cortical areas on the excitability level of higher-order auditory afferents was studied in cats under general anesthesia. A modification of Walls technique was utilized to determine excitability changes of third-order or fourth-order auditory sensory neurons (or both) terminating in the medial geniculate body. Conditioning stimulation to certain areas of the ipsilateral cerebral cortex induced a substantial increase in presynaptic excitability of these auditory afferents. The time course of presynaptic excitability was characterized by a long duration (up to 240 msec) and showed its maximum at 45–60 msec. Two separate cortical areas were most effective in inducing these excitability changes: the auditory cortex and the orbital gyrus. The findings are discussed with special consideration of the concept of presynaptic inhibition and the well-known inhibitory capacity of the orbital cortex.