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J R Howe

Publications and source records attributed to J R Howe.

At least 73 records · Page 4Linked to original sources
PubMed1988

On the kinetics of large-conductance glutamate-receptor ion channels in rat cerebellar granule neurons.

Ion channels activated by glutamate, aspartate, and N-methyl-D-aspartate (NMDA) have been investigated in outside-out patches from cultured cerebellar granule neurons of the rat. Openings of these channels occur in bursts, within which the individual openings are separated by brief shuttings or gaps. The shut-time distributions obtained with each agonist were fitted with four exponential components. The briefest two components were considered as 'gaps within bursts'. Their mean time-constants were: glutamate, 58.0 microseconds and 592 microseconds; aspartate, 31.3 microseconds and 644 microseconds; NMDA, 40.5 microseconds and 903 microseconds. Distributions of burst durations were fitted with three exponential components. The mean time-constants obtained for the longest two components were: glutamate, 1.33 ms and 10.5 ms; aspartate, 2.15 ms and 10.3 ms; NMDA, 2.42 ms and 10.5 ms. Evidence is given that these two components of burst duration reflect the gating kinetics of 50 pS openings and not the fact that each agonist produces openings to more than one conductance level. Not only do openings occur in bursts, but these bursts were observed to occur in clusters, which can be hundreds of milliseconds long. We discuss the relation between the kinetics of single-channel openings observed in patches and the spectral components detected in whole-cell current noise.

Animals↗
PubMed1988

Noise and single channels activated by excitatory amino acids in rat cerebellar granule neurones.

1. Glutamate-receptor ion channels in rat cerebellar granule cells maintained in explant cultures have been investigated with patch-clamp methods. Properties of these channels were determined from noise analysis of whole-cell currents and from noise and single-channel currents recorded in outside-out membrane patches. 2. Glutamate (10-20 microM) evoked two types of response. Some granule cells gave small inward currents accompanied by clear increases in current noise ('large noise' responses), whereas other cells gave larger inward currents and small noise increases ('small noise' responses). 3. A mean single-channel conductance (gamma) of 46.6 pS was estimated for glutamate from four 'large noise' cells. A mean gamma value of 8.4 pS was estimated for seven other 'large noise' cells. The results suggest that in these latter cells glutamate activated both large (approximately equal to 50 pS) and small conductance (approximately equal to 140 fS) channels. 4. Applications of aspartate (10-30 microM) or N-methyl-D-aspartate (NMDA, 10-30 microM) produced small inward currents and large increases in noise; gamma noise = 48.5 pS (aspartate) and 46.7 pS (NMDA). 5. Large single-channel currents were evoked by glutamate, aspartate and NMDA in outside-out patches. The mean conductance values obtained for the largest amplitude openings were: gamma(glutamate) = 49.5 pS, gamma(aspartate) = 51.5 pS, and gamma(NMDA) = 53.0 pS. For each agonist, these 50 pS openings comprised 75-85% of the completely resolved currents in each patch. Openings to 40 and 30 pS conductance levels accounted for 10-15% and 3-7% of the total, and the presence of apparently direct transitions between these levels and the 50 pS level suggests they are sublevels of the same multi-conductance channels. 6. A mean channel conductance of 22.9 pS was estimated from noise evoked by quisqualate (10-30 microM). Single-channel currents were examined in four patches. In two, quisqualate evoked predominantly small currents of two amplitudes, gamma = 8.4 pS and 16.5 pS; some 50 pS openings were also present. In the other two patches, most openings were 50 pS events. 7. Granule cells gave inward currents to kainate (10-30 microM), and a mean conductance of 3.1 pS was estimated from kainate noise. In patches in which aspartate or NMDA produced mainly 50 pS openings, more than 74% of the single-channel currents evoked by kainate were of smaller amplitude, with mean conductances of gamma = 8.1 and 15.1 pS.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

Responses of rat dorsal horn neurons to natural stimulation and to iontophoretically applied norepinephrine.

Extracellular recordings were obtained of 177 neurons throughout the lumbar spinal dorsal horn of urethane- or halothane-anesthetized rats. These neurons all responded to iontophoretically applied L-glutamate and their responses to natural stimulation of the ipsilateral hindlimb were characterized. Iontophoretically applied norepinephrine was tested on 94 of these neurons. Fifty-one neurons were inhibited and 22 were excited. Norepinephrine produced a biphasic inhibitory/excitatory effect on nine neurons. Norepinephrine was exclusively inhibitory on superficial dorsal horn neurons that responded only to innocuous brush and touch and on neurons in the nucleus proprius that responded to brush, touch, and noxious skin pinch. Norepinephrine excited some superficial brush/touch/pinch neurons and produced short inhibitions that were followed by prolonged excitations of some nucleus proprius neurons that responded only to noxious skin pinch. Neurons in the base of the dorsal horn that responded to low-threshold proprioceptive stimulation were excited by norepinephrine. Both the inhibitory and excitatory effects of norepinephrine were stereoselective, but they were not blocked by receptor subtype-selective antagonists. Desensitization to norepinephrine occurred for 30% of the neurons. This study demonstrates that the inhibitory effects of norepinephrine on rat dorsal horn neurons are not restricted to neurons that are responsive to noxious stimuli and that some of these neurons are primarily excited by norepinephrine. The excitatory effects of norepinephrine on low-threshold proprioceptive neurons may contribute to norepinephrine's known enhancement of spinal flexor reflex activity.

Action Potentials↗
PubMed1987

Characteristics of long-duration inhibitory postsynaptic potentials in rat neocortical neurons in vitro.

The characteristics of long-duration inhibitory postsynaptic potentials (1-IPSPs) which are evoked in rat frontal neocortical neurons by local electrical stimulation were investigated with intracellular recordings from an in vitro slice preparation. Stimulation with suprathreshold intensities evoked 1-IPSPs with typical durations of 600-900 msec at resting membrane potential. Conductance increases of 15-60% were measured at the peak amplitude of 1-IPSPs (150-250 msec poststimulus). The duration of the conductance increases during 1-IPSPs displayed a significant voltage dependence, decreasing as the membrane potential was depolarized and increasing with hyperpolarization. The reversal potential of 1-IPSPs is significantly altered by reductions in the extracellular potassium concentration. Therefore it is concluded that 1-IPSPs in rat neocortical neurons are generated by the activation of a potassium conductance. 1-IPSPs exhibit stimulation fatigue. Stimulation with a frequency of 1 Hz produces a complete fatigue of the conductance increases during 1-IPSPs after approximately 20 consecutive stimuli. Recovery from this fatigue requires minutes. 1-IPSPs are not blocked by bicuculline but are blocked by baclofen.

Animals↗
PubMed1987

Intrathecal 6-hydroxydopamine or cervical spinal hemisection reduces norepinephrine content, but not the density of alpha 2-adrenoceptors, in the cat lumbar spinal enlargement.

The effect of the intrathecal administration of the catecholaminergic neurotoxin 6-hydroxydopamine, or of hemisection of the spinal cord at the Cl level, on the density of alpha 2-adrenoceptors and on the norepinephrine, dopamine, and serotonin content in the cat lumbar spinal enlargement was determined 2, 7 or 21 days after performance of each type of lesion. The intrathecal administration of 6-hydroxydopamine produced a time-dependent reduction of norepinephrine content in the cat lumbar spinal enlargement (95% reduction at 21 days) without significantly altering the serotonin content in this same tissue of the same cats. The dopamine content of the dorsal horn was not changed significantly, whereas ventral horn dopamine content was depleted after intrathecal 6-hydroxydopamine. alpha 2-Adrenoceptor binding site density was not significantly different from control either 2 or 21 days after 6-hydroxydopamine, but was increased significantly (50%) over the control density 7 days after 6-hydroxydopamine. Hemisection of the cervical spinal cord produced a bilateral 40-60% reduction of norepinephrine content in both the dorsal and ventral horns of the cat lumbar spinal enlargement 7 and 21 days later. Cervical hemisection did not significantly alter the alpha 2-adrenoceptor binding site density in these same cats either 2, 7, or 21 days after performance of the lesion. It is concluded that alpha 2-adrenoceptors located on the terminals of descending noradrenergic or other spinopetal fibers do not represent a significant fraction of the total population of alpha 2-adrenoceptors present in the dorsal or ventral cat lumbar enlargement.

Adrenergic Fibers↗
PubMed1987

The effect of unilateral dorsal root ganglionectomies or ventral rhizotomies on alpha 2-adrenoceptor binding to, and the substance P, enkephalin, and neurotensin content of, the cat lumbar spinal cord.

The density of alpha 2-adrenoceptor binding sites and the content of substance P, enkephalins, and neurotensin were determined in quadrants of the lumbar spinal enlargement of control cats and of cats upon which either unilateral dorsal root ganglionectomies or unilateral ventral rhizotomies had been performed. The performance of unilateral dorsal root ganglionectomies resulted in a significant decrease (45-55%) of substance P content in the ipsilateral dorsal horn 7 and 21 days postoperatively. The concentration of alpha 2-adrenoceptor binding sites ([3H]rauwolscine Bmax) in the ipsilateral dorsal horn was consistently and significantly decreased at these same postganglionectomy times (20% reduced relative to the contralateral dorsal horn). Enkephalin content 7 and 21 days after ganglionectomies was not significantly different from control, whereas the neurotensin content of the ipsilateral dorsal horn was significantly increased in the 21-day survival cats. The performance of unilateral ventral rhizotomies did not produce any statistically significant changes in the density of alpha 2-adrenoceptor binding sites or in the substance P or enkephalin content of any spinal quadrant. The neurotensin content of both the ipsilateral dorsal and ipsilateral ventral quadrants of the ventral rhizotomized cats was significantly increased. The significant decrease of alpha 2-adrenoceptor binding site concentration in the ipsilateral dorsal horn after unilateral dorsal root ganglionectomies suggests that approximately 20% of the alpha 2-adrenoceptors present within the cat lumbar spinal dorsal gray are located on the axons or terminals of primary sensory afferents. Consistent with this interpretation of the ganglionectomy results, we found significant levels of saturable [3H]rauwolscine binding to homogenates of the cat L4-Sl spinal dorsal root ganglia. Because alpha 2-adrenoceptor binding sites in the ipsilateral ventral lumbar spinal gray were not significantly reduced after unilateral ventral rhizotomies, our results provide no evidence for the location of alpha 2-adrenoceptor on lumbar spinal motoneurons.

Animals↗
PubMed1987

Baclofen reduces post-synaptic potentials of rat cortical neurones by an action other than its hyperpolarizing action.

1. Intracellular recordings were obtained from neurones in layers 2 and 3 of the rat frontal neocortex in an in vitro slice preparation. Three distinct types of stimulation-evoked post-synaptic potentials were recorded in these neurones: excitatory post-synaptic potentials (e.p.s.p.s); bicuculline-sensitive, chloride-dependent inhibitory post-synaptic potentials (i.p.s.p.s) with times to peak of 20-25 ms (fast(f)-i.p.s.p.s); bicuculline-insensitive, potassium-dependent i.p.s.p.s with bicuculline-insensitive, potassium-dependent i.p.s.p.s with times to peak of 150-250 ms (long(l)-i.p.s.p.s). 2. The effects of baclofen were investigated on seventy-one neurones. Baclofen was applied by ionophoresis or pressure ejection from micropipettes or was added to the superfusion medium. 3. Baclofen depressed stimulation-evoked e.p.s.p.s in fifty-seven of the sixty neurones tested. This effect was associated with an increase in the stimulation intensity required to produce a synaptically evoked action potential for thirty-nine of forty-four neurones. 4. Baclofen depressed f-i.p.s.p.s in thirty-seven of the thirty-nine neurones tested and l-i.p.s.p.s in each one of the seventeen neurones tested. Reversal potential values for each type of i.p.s.p. were not changed by baclofen and its depressions of each were independent of membrane potential (Em). Baclofen reduced the magnitude and the duration of the conductance increases that were associated with f- and l-i.p.s.p.s. 5. Baclofen hyperpolarized forty of seventy-one neurones and produced outward currents in three of four neurones recorded in voltage clamp at holding potentials between -55 and -65 mV. These actions were associated with 10-58% reductions of neuronal input resistance (RN) and 10-20% increases in neuronal input conductance (gN), respectively. Baclofen decreased the direct excitability of twenty-three of twenty-seven neurones tested. Determinations of the reversal potential for baclofen-induced changes of Em indicate that baclofen increases the conductance of rat neocortical neurones to potassium ions. 6. The EC50 for each action of DL-baclofen was approximately 1 microM. L-Baclofen was greater than 100 times more potent than D-baclofen. 7. Concentrations of bicuculline that blocked f-i.p.s.p.s and responses to ionophoretically applied gamma-aminobutyric acid (GABA) had no effect on the depressions of e.p.s.p.s or the hyperpolarizations and decreases in RN that baclofen produced. 8. Baclofen did not reduce the duration of action potentials that were prolonged with intracellular injections of caesium ions or by superfusions with medium that contained 10 mM-tetraethylammonium (TEA).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

D-baclofen does not antagonize the actions of L-baclofen on rat neocortical neurons in vitro.

The ability of D-baclofen to antagonize the actions of L-baclofen on rat neocortical neurons was investigated. Intracellular recordings were made from neurons in cortical layers 2 and 3 in an in vitro slice preparation. Baclofen stereoisomers were applied at known concentrations in the superfusion medium. At a concentration of 3 microM, L-baclofen produced approximately 70% depressions of excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) that were evoked by stimulation of superficial cortical layers. L-baclofen also hyperpolarized neocortical neurons. These hyperpolarizations were accompanied by decreases in neuronal input resistance and in direct excitability. We have shown previously that these latter effects are secondary to the action of baclofen to increase the potassium conductance of neocortical neurons. D-baclofen, at concentrations of 1-100 microM, did not antagonize depressions by L-baclofen of EPSPs and IPSPs nor the action of L-baclofen to increase the potassium conductance of neocortical neurons. At concentrations of 50-100 microM, D-baclofen produced 20-30% effects when applied alone, thus suggesting that these concentrations of D-baclofen produced a significant degree of receptor occupancy. Our results demonstrate that D-baclofen is not an antagonist or high affinity partial agonist at the receptors through which baclofen exerts its effects on single neurons in the rat neocortex.

Animals↗
PubMed1986

Characterization of [3H]rauwolscine binding to alpha 2-adrenoceptor sites in the lumbar spinal cord of the cat: comparison to such binding sites in the cat frontal cerebral cortex.

The binding of the selective alpha 2-adrenoceptor antagonist radioligand [3H]rauwolscine ([3H]RAUW) to homogenates of cat frontal cerebral cortex and cat lumbar spinal cord was investigated. Experiments were performed at 20 degrees C in 50 mM Tris HCl/l mM Na2EDTA buffer (pH 6.9 at 20 degrees C). At this temperature, specific [3H]RAUW binding, defined as the difference between the amount of [3H]RAUW bound in the absence and presence of 1 microM rauwolscine or 1 microM rauwolscine or 1 microM yohimbine, reaches equilibrium values by approximately 60 min and is reversible with a mean t1/2 of dissociation of 15 min in cortex and 20 min in spinal cord. The kinetically determined Kd of [3H]RAUW (mean K-1/mean K1) was 0.59 nM and 1.68 nM in cortex and spinal cord, respectively. The results of equilibrium saturation experiments, routinely performed at [3H]RAUW concentrations between 0.1 nM and 6.0 nM, indicate that [3H]RAUW binds to saturable sites in both CNS regions of the cat. Scatchard plots of saturation isotherm data were consistently linear and the mean Kd value determined from 10 such experiments was 0.72 nM in frontal cortex and 0.82 nM in lumbar spinal cord. A mean Bmax value of 230 fmol/mg protein was determined for saturable [3H]RAUW binding sites in the cat frontal cortex. In teh cat lumbar spinal gray, a mean Bmax value for saturable [3H]RAUW binding sites of 75 fmol/mg protein was obtained. Saturable [3H]RAUW binding sites in the cat lumbar spinal gray are present at apparently equal density in dorsal and ventral horns. Inhibition experiments, performed at 0.2 nM or 0.4 nM [3H]RAUW, indicate that the binding sites labeled by [3H] RAUW possess a pharmacology characteristic of alpha-adrenoceptors. Thus, rauwolscine, yohimbine, and phentolamine compete for specific [3H]RAUW binding with high affinity and are much more potent inhibitors than corynanthine, prazosin, and propranolol. Mean Hill coefficients, calculated from logit-log plots of competition data, were close to one for all antagonists examined. L-Epinephrine and L-norepinephrine were 15-20 times more potent inhibitors of specific [3H]RAUW binding than were their corresponding D-isomers. The agonist inhibitor potency series: p-aminoclonidine = clonidine = L-epinephrine greater than L-norepinephrine much greater than isoproterenol, is that expected of alpha 2-adrenoceptor sites. Mean Hill coefficients efficients for all agonists were considerably less than one.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

Radio-iodine in thyroid glands of swans, farm animals and humans, also in algae and river water from the Thames Valley, England.

A highly sensitive counting system has been used to measure radio-iodine in environmental samples from the Thames Valley. Iodine-125 and occasionally iodine-131 have been found in the thyroid glands of most of the swans that have died on the River Thames, the River Wey and the Grand Union Canal, and in algae and water samples from the Thames and many of its tributaries. The presence of this activity is ascribed to the waste discarded into the drainage system by hospitals and research laboratories, reaching the rivers via the effluent from sewage treatment works. The Thames is used as a source of drinking water, particularly in London and its western approaches. Weed and water samples collected from river water abstraction points, reservoirs, tap water supplies, and animal water troughs fed from this supply all contained low levels of iodine-125. The drinking water route can account for the iodine-125 found in the thyroids of farm animals from west Surrey and in a few people living in London. The amounts found constitute a trivial radiation dose to man and animals as they are far below the acceptable limit of exposure for man.

Animals↗
PubMed1984

[3H]p-Aminoclonidine binding to multiple alpha 2-adrenoceptor sites in homogenates of cat frontal cortex and cat spinal cord.

We have investigated the characteristics of [3H]p-aminoclonidine binding to homogenates of cat frontal cortex and of cat spinal cord. At 37 degrees C, saturable [3H]p-aminoclonidine binding displayed rapid association and dissociation kinetics. Scatchard plots of data obtained from either tissue were consistently biphasic. Computer-assisted nonlinear least squares regression analysis based upon a one ligand/two binding site model was employed to resolve these plots into two linear components. The results of this analysis indicate that, for homogenates of either tissue, the KD of [3H]p-aminoclonidine binding, to the high and low affinity binding sites respectively, is approximately 0.5 nM and 9 nM. Mean Bmax values (fmol/mg protein), for the high and low affinity binding sites respectively, of 28 and 149 for homogenates of cat frontal cortex and 7.1 and 56 for homogenates of cat spinal cord were obtained. The results of competitive inhibition experiments, where 0.13 nM [3H]p-aminoclonidine was used, indicate that catecholamines compete for [3H]p-aminoclonidine binding sites in a stereoselective fashion, and that these sites possess a pharmacology characteristic of alpha 2-adrenoceptors. The results of Hill analysis of the competition data suggest that alpha 2-adrenoceptor agonists and alpha 2-adrenoceptor antagonists possess selective affinity for these two alpha 2-adrenoceptor binding sites. The two populations of saturable [3H]p-aminoclonidine binding sites appear to correspond to those alpha 2-adrenoceptor ligand binding sites that have been referred to as the 'super high' and 'high' affinity state of the alpha 2-adrenoceptors.

Animals↗
PubMed1984

Swan thyroid glands and river algae as indicators of iodine-125 and iodine-131 in the River Trent and its tributaries.

Some mute swans have been found to have higher levels of radio-iodine in their thyroids than farm and wildlife animals. In the East Midlands of the U.K., elevated levels were confined to swans inhabiting major rivers like the Trent and Soar where the highest values occurred in thyroids collected downstream from sewage and water reclamation works. Comparing the concentrations of 125I and 131I in blanket weed, which is a food source of the swan, and river water samples collected from above, below and in such effluents, showed that radio-iodine enters the river via these routes. The environmental pathway is sewage effluent--(water reclamation)--river water--river weed--swan. The radioactivity originates from the widespread use of radio-iodine in hospitals and analytical laboratories where much of the liquid and soluble waste is discarded into the sewage drain system. With a simple counting assembly consisting of a heavily shielded thin NaI(Tl) crystal detector attached to a 2-channel scaler-timer it was possible to check large numbers of swan thyroid glands. Although relatively high count rates were frequently obtained the levels of radio-iodine in thyroids were too low to affect the health and well-being of the swan.

Animals↗
PubMed1984

Spinal peptidergic and catecholaminergic systems and nociception.

The authors review recent findings about the electrophysiology and anatomy of spinal peptidergic systems. The role of spinal catecholaminergic systems in nociception is also discussed. Recent data about the action of norepinephrine on dorsal horn neurons are presented.

Afferent Pathways↗
PubMed1983

Selective antagonism of the antinociceptive effect of intrathecally applied alpha adrenergic agonists by intrathecal prazosin and intrathecal yohimbine.

We have attempted to define the alpha adrenoceptor subtype(s) on which intrathecally applied alpha adrenergic agonists act to produce their antinociceptive effect. The potencies of intrathecal (i.t.) prazosin or i.t. yohimbine to antagonize the elevations of thermal nociceptive threshold induced by i.t. 2-[2,6-diethylphenylamino]-2-imidazoline (ST-91), methoxamine or norepinephrine (NE) were determined in the rat. Tail-flick and hot plate tests were used to determine thermal nociceptive threshold. At the ID50 level, the alpha-2 selective antagonist yohimbine was significantly more potent than the alpha-1 selective antagonist prazosin at blocking the analgesia produced by the alpha-2 selective agonist ST-91, whereas prazosin was significantly more potent than yohimbine at antagonizing the analgesia produced by the alpha-1 selective agonist methoxamine or by the nonselective alpha agonist NE. Analgesic doses of methoxamine evoked a readily observable disturbance of motor and autonomic function, whereas such effects were not observed after analgesic doses of ST-91 or NE. Both i.t. methoxamine and i.t. ST-91 elevated thermal nociceptive threshold in rats depleted of lumbar spinal cord NE by pretreatment 7 days before with i.t. 6-hydroxydopamine. Our results suggest that stimulation of either one of two separate populations of postsynaptic spinal alpha adrenoceptors will inhibit spinal nociceptive transmission. One of these populations appears to be composed of alpha-2 adrenoceptors. The subtype classification of the alpha adrenoceptors composing the other population remains unclear.

Adrenergic alpha-Agonists↗
PubMed1982

Changes in sensitivity to intrathecal norepinephrine and serotonin after 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine (5,6-DHT) or repeated monoamine administration.

The behaviorally defined analgesia evoked by direct application of norepinephrine (NE) or serotonin (5-HT) into the rat spinal subarachnoid space was assessed 1 to 28 days after respective intrathecal injection of 6-hydroxydopamine or 5,6-dihydroxytryptamine. These pretreatments effected supersensitivity to intrathecally administered NE and 5-HT, respectively, observable as early as 24 hr after neurotoxin-induced lesion. Dose-response curves for both NE or 5-HT, determined 7 days after pretreatment with their respective neurotoxins, were shifted significantly to the left as compared to controls. The onset of supersensitivity correlated well with the depletion of neurotransmitter levels in the spinal cord in the case of NE, but much correlation was not found for 5-HT. Whereas monoamine supersensitivity was undetectable 28 days postlesion, there was no significant recovery of spinal cord monoamine content at this time. Neurotoxin pretreatment was found to effect a significantly greater potentiation of NE- or 5-HT-induced analgesia than presynaptic reuptake blockade and elicited supersensitivity to agonists not readily taken up by presynaptic terminals, suggesting the involvement of postsynaptic components. Rats pretreated 7 days before with 5,6-dihydroxytryptamine exhibited some supersensitivity to intrathecal NE. Supersensitivity to 5-HT was not observed after 6-hydroxydopamine pretreatment. Rats made tachyphylactic to the antinociceptive effect of intrathecally injected NE displayed a complete lack of analgetic response to 5-HT. Similarly, rats tachyphylactic to 5-HT exhibited a subnormal analgetic response to NE. Combination pretreatment with both neurotoxins produced significant hyperalgesia as compared to yoked controls and to nociceptive thresholds determined before neurotoxin administration.

5,6-Dihydroxytryptamine↗
PubMed1975

Midbrain deafness following head injury.

A patient is described who became deaf following a head injury. Postmortem examination revealed bilateral lesions of the lateral lemnisci and inferior colliculi. The clinical pattern of midbrain deafness is examined and compared with syndromes of cortical and peripheral auditory impairment.

Audiometry↗