Auditory Evoked Potentials from the primary auditory cortex of the cat: topographic and pharmacological studies

Authors:

• Robert T. Knight

• Simon Brailowsky

Date: 1989

PubMed: 1691975

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Abstract:

Wave VI (8.4 msec) of the brain-stem auditory evoked potential (BAEP) was maximal in a discrete region of primary auditory cortex (AI) of the anesthetized cat. Wave VI underwent rapid amplitude decrease over millimeter distances in the AI region and followed high stimulation rates. Wave VI did not show intracortical polarity inversion nor was it abolished by epicortical or intracortical GABA administration. The data are compatible with a wave VI source in the terminal axons of the thalamo-cortical radiations. Middle latency auditory responses (MAEPs) generated 10-40 msec after auditory stimulation were also recorded in a circumscribed area of AI. In contrast to wave VI, these primary auditory cortex potentials (Pa 18.3 msec; Nb 31.9 msec) underwent transcortical polarity inversion, correlated with intracortical multi-unit activity in the AI region and were reversibly altered or abolished by epicortical or intracortical GABA administration to the AI region. The data suggest that the Pa and Nb components of the cat MAEP are intracortically generated by neuronal elements in the AI region.

Recovery From GABA-Mediated Hemiplegia in Young and Aged Rats: Effects of Catecholaminergic Manipulations

Authors:

• Simon Brailowsky

• Robert T. Knight

Date: 1987

PubMed: 3683725

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Abstract:

We investigated the participation of catecholaminergic mechanisms in the functional recovery from motor cortex lesions in young (9 months) and aged (26 months) rats. The animals were studied during the recovery period from an hemiplegic syndrome secondary to small motor cortex lesions potentiated by the localized, chronic (7 days) infusion of GABA into the lesion site. Acute administration of haloperidol (0.1 mg/kg IP) to these recovered animals induced a re-emergence of the contralateral motor syndrome in both groups. In the young group, the haloperidol-induced hemiplegia lasted one day whereas in the aged animals the deficit was significantly prolonged lasting three days. Apomorphine administration (0.5 mg/kg IP) prior to or immediately after haloperidol injection failed to prevent or reverse the reappearance of the motor deficit. Adult animals recovered from motor cortex aspirations performed 7 to 12 months prior were refractory to haloperidol effects. Amphetamine administration to young rats treated chronically with saline or GABA infusion into the somatomotor region also failed to alter the clinical evolution of the motor deficit. The evidence suggests that dopaminergic mechanisms are involved in the functional recovery from brain lesions and that these mechanisms are most susceptible to neuroleptic blockade during the early post-lesional period. The deleterious effects of dopaminergic blockade are heightened in aged populations. The use of dopaminergic antagonists in brain-lesioned subjects, and particularly in geriatric populations, is considered potentially harmful, particularly in the early stages of the recovery process.

Phenytoin Increases the Severity of Cortical Hemiplegia in Rats

Authors:

• Simon Brailowsky

• Robert T. Knight

• Robert Efron

Date: 1986

PubMed: 3719374

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Abstract:

The effects of systemic phenytoin administration on the motor deficit resulting from a cortical lesion were studied in rats trained to walk coordinately on a narrow beam. The somatomotor cortex lesion was produced by an indwelling cannula through which saline or GABA were infused chronically via an osmotic minipump. Phenytoin (50 mg/kg i.p.) administered between days 3 and 5 after the intracortical catheter implantation produced a significant increase in the severity of the resulting hemiplegic syndrome. This DPH effect was more noticeable in those animals also receiving intracortical GABA infusions. The anticonvulsant at the dose used had no effect on motor performance when administered preoperatively or when given to the animals 14 days after surgical intervention when their hemiplegic syndrome had cleared. These findings suggest that phenytoin administration to brain-damaged individuals in the initial postlesion stage may be deleterious.

Gamma-Aminobutyric Acid-Induced Potentiation of Cortical Hemiplegia

Authors:

• Simon Brailowsky

• Robert T. Knight

• Katherine Blood

• Donatella Scabini

Date: 1986

PubMed: 3942881

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Abstract:

A novel model of hemiplegia in young and aged rats is described. Osmotic minipumps were used to deliver a chronic (7 days), localized application of gamma-aminobutyric acid (GABA) (100 micrograms/microliter/h), to the somatomotor cortex of unrestrained rats. This resulted in an easily quantifiable, contralateral and reversible motor syndrome in both young and aged animals. In the young group, the motor deficit cleared over 5-day period, while in the aged animals it persisted for at least a 2-week period. Control animals treated with saline-filled minipumps did not develop a long-lasting motor deficit. The GABA-induced facilitation of hemiplegia due to small motor cortex lesions and the age effects on behavioral recovery of function are discussed. Cortical inhibitory mechanisms may play a role in debilitating syndromes such as stroke or post-epileptic paralysis.

Altered Peripheral and Brainstem Auditory Function in Aged Rats

Authors:

• Gregory V. Simpson

• Robert T. Knight

• Simon Brailowsky

• Oscar Prospero-Garcia

Date: 1985

PubMed: 4063825

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Abstract:

A technique for conducting free-field brainstem auditory evoked potential (BAEP) audiometry in unanesthetized, unrestrained rats revealed a non-recruiting 18 dB elevation of click threshold in aged rats. BAEPs were first recorded in young and aged rats to clicks of equal intensity (80 dB SPL). Compared to the young group, aged animals exhibited longer wave I and wave IV latencies with no difference seen in the I-IV central conduction time. The prominent negative wave (No) following wave IV was also delayed and the I-No and IV-No conduction times increased in the aged group. When BAEPs were recorded to clicks with intensities adjusted to 35 dB above individual threshold, no differences in wave I or wave IV latencies or in the I-IV central conduction time were found between groups. However, the No component was delayed and the I-No and IV-No conduction times remained prolonged in the aged group. The results suggest that in addition to changes in peripheral auditory structures, changes in the rostral auditory brainstem accompany age-related hearing loss in rats.

Surface auditory evoked potentials in the unrestrained rat: component definition

Authors:

• Robert T. Knight

• Simon Brailowsky

• Gregory V. Simpson

Date: 1985

PubMed: 2412796

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Abstract:

Auditory evoked potentials (AEPs) to click and pure tone stimuli were recorded in unrestrained, unanesthetized rats. The middle latency rat AEPs (N17, P23, N38) had midline scalp distributions similar to human MAEPs and were recorded to within 15 dB above BAEP threshold. In contrast to human MAEPs, rat MAEPs were decreased in amplitude at high stimulation rates and only the N17 component was unaltered by slow wave sleep. The longer latency N50, N80 and P130 components had several response properties comparable to human N100-P200 vertex potentials. These included restricted midline fronto-central scalp distributions, progressive increases in amplitude at ISIs up to 4-8 sec and marked attenuation during slow wave sleep. The frequency sensitivity of the rat AEP revealed a decreased response to pure tones below 4 kHz but robust responses for stimuli up to at least 45 kHz. There was a notch in the rat audiogram with decremented component amplitudes to pure tone stimuli centered at 35 kHz. When equated for intensity, click and pure tone stimuli in the range of the rats maximal audiometric sensitivity (8-20 kHz) generated comparable AEP components. These results provide normative data on rat surface recorded AEPs. It is suggested that these surface recorded rat AEPs are generated by subcortical neural systems involved in the detection of auditory transients.

Inhibitory modulation of cat somatosensory cortex: a pharmacological study

Abstract:

In anesthetized preparations, GABA and taurine produced rapid, reversible inhibition of the negative component (N20) of the primary somatosensory evoked potential (SEP) without effect on the earlier positivity (P11). This effect was also produced by low doses of 4-aminopyridine. Neither bicuculline or picrotoxin antagonized these drug effects. A predominance of type B GABA receptors in the superficial layers of the somatosensory cortex is proposed.

Authors:

• Simon Brailowsky

• Robert T. Knight

Date: 1984

PubMed: 6509318

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Pa component of cat auditory evoked potential originates in primary auditory cortex

Authors:

• Robert T. Knight

• Simon Brailowsky

Date: 1983