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PubMed2004

Reversible disruption of tight junction complexes in the rat blood-brain barrier, following transitory focal astrocyte loss.

Breakdown of the blood-brain barrier is a feature of acute and chronic neurodegenerative changes, yet the relationship between astrocytes and the mature barrier remains unclear. We studied this role of astrocytes in vivo using a gliotoxin and evaluated changes in three vascular tight junction markers. Male Fisher F344 rats given systemic 3-chloropropanediol showed astrocytic loss in the inferior colliculus from 12-24 h until the lesion was repopulated 8-28 days later. Within 6 h of astrocyte loss, microvessels in this area began to demonstrate a loss of the normal paracellular localization of the transmembrane proteins occludin and claudin-5 and cytoplasmic zonula occludens-1, which correlated with focal vascular leak of dextran (10 kDa) and fibrinogen. Platelet endothelial adhesion molecule-1 staining revealed that there was no loss of the endothelial lining. Between 4-8 days, severe downregulation of tight junction protein expression was observed, which subsequently returned over the same time period as astrocytes repopulated the lesion. Unexpectedly, dextran and fibrinogen leak from vessels had ceased at 6 days, well before the return of occludin and claudin-5 to appropriate paracellular domains. Control nonvulnerable cortical tissue showed no change in astrocyte morphology and tight junction expression over the same time course. Our data supports a primary role for astrocytic contact in the expression of occludin, claudin-5, and zonula occludens-1 in the mature brain vasculature in vivo. However, barrier integrity to dextran (10 kDa) and fibrinogen can be restored in the absence of astrocytes and tight junction proteins (occludin, claudin-5, and zonula occludens-1).

Animals↗
PubMed1993

Transcellular retrograde labeling of radial glial cells with WGA-HRP and DiI in neonatal rat and hamster.

Topographically distinct populations of radial glial cells in the diencephalon and mesencephalon of neonatal rats and hamsters were transcellularly labeled with wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) and with the lipophilic tracer DiI. A comparison of the histological distribution of the two tracers is suggestive of two different mechanisms of transcellular labeling. Intraocular injections of WGA-HRP resulted in the uptake of exogenously applied WGA-HRP by retinal ganglion cells, followed by anterograde axonal transport and exocytosis within the optic target nuclei. In addition to the transneuronal labeling, which is typical of such injections, we observed the transcellular labeling of the processes and somata of radial glial cells that were topographically associated with the terminal fields of the labeled axons. Similar transcellular labeling of radial glial cells associated with the axon terminal fields of the colliculogeniculate projection to the medial geniculate nucleus was observed following injections of WGA-HRP in the inferior colliculus. The transcellular labeling within the radial glial cells was discontinuous and somatopetally concentrated, indicating the existence of a retrograde active transport mechanism within the radial glial processes subsequent to its uptake following release of tracer from axons. This type of labeling can be referred to as transcellular retrograde glioplasmic transport. In contrast, DiI was used as a tracer through its capacity to diffuse within the plasmalemma. Topographically distinct populations of radial glial cells were transcellularly labeled following placements of DiI in the retina, inferior colliculus, or dorsal thalamus of fixed brains. The radial processes of labeled radial glial cells consistently extended into regions that also contained labeled axons. It is likely that the transcellular radial glial labeling with DiI occurred via transmembranous diffusion. These data indicate that a close structural and functional relation exists between axons and glial cells in the developing brain.

Aging↗
PubMed1983

Morphology of neurons in the torus semicircularis of the northern leopard frog, Rana pipiens pipiens.

The neuronal morphology of the torus semicircularis of the northern leopard frog, Rana pipiens pipiens, was examined in Golgi-impregnated material. Neurons in each of the five subdivisions of the torus semicircularis (Potter, '65a) have distinct morphologies which are characteristic of the subdivision. Laminar nucleus neurons are mostly multipolar with spherical or ovoidal somata and smooth dendrites oriented primarily parallel and perpendicular to the cell laminae. Principal nucleus neurons have variable soma shapes with short dendrites (less than 100 micrometers) radiating in all directions. In the magnocellular nucleus, there are three major cell types: neurons characterized by small, spherical-shaped somata, with short, thin, radiating dendrites and many varicosities; bi- or tripolar neurons with ovoidal somata, and long (100-200 micrometers) and smooth dendrites orienting primarily dorsoventrally and mediolaterally; and multipolar neurons with triangular-shaped somata and very long (200-350 micrometers) dendrites, which are either smooth or highly spiny. Neurons in the commissural nucleus are mostly multipolar cells with ovoidal somata and beaded dendrites projecting mostly dorsally and ventrally. The subependymal midline nucleus contains mostly uni- or bipolar neurons with small ovoidal somata and straight, spiny dendrites. In addition to revealing the morphological features of neurons in the torus, the counterstained material shows further cytoarchitectural organization of the principal nucleus, i.e., the presence of a circular lamellar organization. The functional significance of these anatomical features is discussed.

Animals↗
PubMed2002

Single cell activity patterns of pedunculopontine tegmentum neurons across the sleep-wake cycle in the freely moving rats.

Microinjections of the excitatory amino acid, L-glutamate into the cholinergic cell compartment of the pedunculopontine tegmentum (PPT) of the rat induces both wakefulness and/or rapid eye movement (REM) sleep depending on the glutamate dosage. However, no studies have systematically recorded the electrical activity of these cells in the freely moving rat across the sleep-wake cycle. In this study, we have recorded the spontaneous activity patterns of single PPT cells (n = 70) in the freely moving rat across the sleep-wake cycle. PPT neurons were classified into three groups based on patterns in their spontaneous activity. The first group of cells (12.86%) was more active during REM sleep than they were during wakefulness or slow-wave sleep (SWS). The second group of cells (60.0%) was more active during REM and wakefulness than during SWS. The firing rate of the third group of cells (27.14%) did not change as a function of behavioral state. This study also demonstrated that the level of activity within the cholinergic cell compartment of the PPT during SWS drops to 7.4% of that observed during wakefulness and that during REM sleep it changes to 65.5% of wakefulness levels. These findings indicate that in the freely moving rat, the discharging of PPT neurons correlates with wakefulness and REM sleep. Additionally, these neurons may be an integral part of the brainstem wakefulness and REM sleep-generating mechanisms in the rat.

Action Potentials↗
PubMed2003

Mild carbon monoxide exposure impairs the developing auditory system of the rat.

The object of this study was to determine if chronic exposure to mild concentrations of CO in air caused changes in the integrity of the inferior colliculus during the most active period of synaptogenesis/auditory development. We examined all subregions of the inferior colliculus (IC) of rats by immunocytochemical approaches after pups were exposed chronically to CO concentrations of, 0, 12.5, 25, and 50 ppm in air starting at Day 8 through 20-22 days of age. Mother-reared pups were compared to the gastrostomy-reared pups with or without CO exposure for basal neural activity, using c-Fos immunoreactivity as a marker. Half the rats were examined at 27 days of age, 5 days after the end of CO exposure, and the other half were examined 50 days later at 75-77 days of age. In the central nucleus of the IC, the number of cells expressing a basal level of c-Fos was decreased significantly in the CO-exposed animals when compared to controls; however, there was little or no difference in the number of cells expressing c-Fos in the other subregions of the IC. We conclude that the central nucleus of the inferior colliculus is affected selectively by mild CO exposure (0.0012% in air) and that this reduction in neuronal activity persists into adulthood.

Animals↗
PubMed2005

Limiting iron availability confers neuroprotection from chronic mild carbon monoxide exposure in the developing auditory system of the rat.

Iron deficiency and chronic mild carbon monoxide (CO) exposure are nutritional and environmental problems that can be experienced simultaneously. We examined the effects of chronic mild CO exposure and iron availability on auditory development in the rat. We propose that chronic mild CO exposure creates an oxidative stress condition that impairs the spiral ganglion neurons. The CO-exposed rat pups had decreased neurofilament proteins and increased copper, zinc-superoxide dismutase (SOD1) in the spiral ganglion neurons. We conclude that the increased amount of SOD1 causes an increase in hydrogen peroxide production that allows the Fenton reaction to occur. This reaction uses both iron and hydrogen peroxide to generate hydroxyl radicals and leads to the development of oxidative stress that impairs neuronal integrity. However, rat pups with decreased iron and CO exposure (ARIDCO) exhibited in their cochlea an up-regulation of transferrin, whereas their expression of neurofilament proteins and SOD1 were similar to control. Consequently, reduced iron availability and the normal expression of SOD1 do not promote oxidative stress in the cochlea. By using basal c-Fos expression as a marker for cellular activation we found a significant reduction in c-Fos expression in the central nucleus of the inferior colliculus in iron-adequate rat pups exposed to CO. By contrast, rather than being reduced, c-Fos expression in the ARIDCO group is the same as for controls. We conclude that the cochlea of rat pups with normal iron availability is selectively affected by mild CO exposure, causing a chronic oxidative stress, whereas limiting iron availability ameliorates the effect caused by mild CO exposure by averting conditions that facilitate oxidative stress.

Animals↗
PubMed2006

Phosphorylated cAMP response element-binding protein levels in guinea pig brainstem auditory nuclei after unilateral cochlear ablation.

After left unilateral cochlear ablation (UCA) in young adult guinea pigs, the appearance of plasticities in auditory pathways suggested altered gene expression and modified phenotypic behaviors of auditory neurons. Because phosphorylated cyclic-AMP response element-binding protein (CREB-P) is a transcription factor that binds to certain genes to facilitate their expression, CREB-P levels were measured after UCA and correlated with postablation plasticities. After UCA, Western blotting was employed to quantify CREB-P levels and illustrate CREB levels in the anteroventral (AVCN), posteroventral (PVCN), and dorsal (DCN) cochlear nucleus; the lateral (LSO) and medial superior olive (MSO); the medial nucleus of the trapezoid body (MNTB); and the central nucleus of the inferior colliculus (ICc) for up to 145 days. We also quantified the levels of several protein synthesis regulators and synaptic markers in the AVCN at 60 days. Sucrose-based extraction buffer improved CREB-P recovery. CREB-P levels became depressed at 3 and 7 postablation days, except in the PVCN, where they were elevated at 7 days, and in the ICc, where they were elevated at both times. At 60 days, CREB-P levels in all the nuclei were elevated. In the AVCN, levels of the protein synthesis regulators and synaptic markers were also elevated at 60 days. By 145 days, CREB-P levels again declined, except in the AVCN, where elevations persisted and increased on the ablated side, and in the ICc, where CREB-P elevations remained. The changes in CREB-P levels coincided with several plasticities in glutamatergic and glycinergic transmitter release and receptor activities, and alterations in neurotrophic support, that developed after UCA. These findings suggest that UCA altered CREB-P levels, which in turn might have contributed to plasticities that appear after UCA.

Animals↗
PubMed1993

Metabolic activity of the central auditory structures following prolonged deafferentation.

The goal of this work was to evaluate, using autoradiographic techniques, the effects of variable periods of deafness on resting and evoked metabolic activity in central auditory structures elicited by direct electrical cochlear nucleus (CN) stimulation. Thirty-five pigmented guinea pigs, divided into five groups, underwent acute implantation of bipolar electrodes in the CN. One group was not deafened and served as hearing controls. The other four groups were deafened using an established protocol of sequential kanamycin/ethacrynic acid treatment and were tested at 4 weeks, 9 weeks, 16 weeks, and 15 months after deafening. Threshold currents for eliciting evoked middle latency responses (EMLRs) with direct CN stimulation were not significantly different between hearing and deafened groups. Autoradiographic data showed progressive reduction of the evoked metabolic response with incremental periods of deafferentation. Nevertheless, central auditory structures remained responsive to direct electrical stimulation of the CN. These data indicate that direct CN stimulation remains capable of activating the auditory tract despite prolonged periods of deafness.

Animals↗
PubMed2005

Aminoglycosides block the Kv3.1 potassium channel and reduce the ability of inferior colliculus neurons to fire at high frequencies.

The Kv3.1 potassium channel is expressed at high levels in auditory nuclei and contributes to the ability of auditory neurons to fire at high frequencies. We have tested the effects of streptomycin, an agent that produces progressive hearing loss, on the firing properties of inferior colliculus neurons and on Kv3.1 currents in transfected cells. We found that in inferior colliculus neurons, intracellular streptomycin decreased the current density of a high threshold, noninactivating outward current and reduced the rate of repolarization of action potentials and the ability of these neurons to fire at high frequencies. Furthermore, potassium current in CHO cells transfected with the Kv3.1 gene was reduced by 50% when cells were cultured in the presence of streptomycin or when streptomycin was introduced intracellularly in the pipette solution. In the presence of intracellular streptomycin, the activation rate of Kv3.1 current increased and inhibition by extracellular TEA become voltage-dependent. The data indicate that streptomycin inhibits Kv3.1 currents by inducing a conformational change in the Kv3.1 channel. The hearing loss caused by aminoglycoside antibiotics may be partially mediated by their inhibition of Kv3.1 current in auditory neurons.

Action Potentials↗
PubMed2005

Aversive stimulation of the inferior colliculus changes dopamine and serotonin extracellular levels in the frontal cortex: modulation by the basolateral nucleus of amygdala.

We have shown that stimulation of the neural substrates in the inferior colliculus (IC) causes a significant increase in the extracellular levels of dopamine (DA) in frontal cortex (FC). Also, it has been reported that the basolateral complex of the amygdala (BLA) serves as a filter for unconditioned and conditioned aversive information that ascend to higher structures from the brainstem. Linking these two kinds of information, this work examines whether inactivation of BLA interferes with the activation of cortical dopaminergic outputs produced by aversive stimulation of the IC. To this end, rats were implanted with an electrode in the IC for the determination of the threshold of escape responses. Each rat also bore a cannula implanted in the BLA for injections of lidocaine (10 microg/0.5 microL), muscimol (0.5 microg/0.5 microL), or its vehicle and a microdialysis probe in the FC for determination of the amount of DA and serotonin (5-HT). The data obtained show that IC electrical stimulation caused an increase in the DA release while it reduced the 5-HT release in the FC. BLA inactivation with both lidocaine or muscimol enhanced the aversiveness of the electrical stimulation of the IC and attenuated the increase in DA, while the reduction in 5-HT release in the FC remained unaffected. These findings suggest that ascending aversive information from IC on their way up to higher structures in the SNC courses with opposite modulation by DA/5-HT mechanisms in the FC. These processes are regulated by filters located in the BLA. It is proposed that the loss of these BLA regulatory mechanisms prevents the expression of these modulatory mechanisms in the FC that are adaptive responses in order to cope with unconditioned aversive stimulus triggered at the brainstem level.

Amygdala↗
PubMed1995

The P2Y purinoceptor-operated potassium channel is possibly regulated by the beta gamma subunits of a pertussis toxin-insensitive G-protein in cultured rat inferior colliculus neurons.

In whole-cell patches of inferior colliculus neurons, ADP evoked outwardly rectifying potassium currents with a latency of < 1 sec via P2Y purinoceptor. These currents were blocked by GDP beta S, while not by pertussis toxin (PTX). Additionally, a selective protein kinase C inhibitor, GF109203X, or a selective phospholipase A2 inhibitor, BPB, had no effect on the currents. In outside-out patches, ADP elicited single channel currents with same slope conductances as those obtained in cell-attached patches and the currents were again blocked by GDP beta S. The results presented here indicate that the P2Y purinoceptor-operated potassium channel in inferior colliculus neurons is activated only by a plasma membrane component, most likely by a direct coupling to the beta gamma subunits of a PTX-insensitive G-protein.

Adenosine Triphosphate↗
PubMed1994

Blockade of GABA uptake with tiagabine inhibits audiogenic seizures and reduces neuronal firing in the inferior colliculus of the genetically epilepsy-prone rat.

Tiagabine is a new anticonvulsant drug that blocks the uptake of GABA, prolonging the action of this inhibitory transmitter. In the present study the effects of systemically administered tiagabine [30 mg/kg, ip (ED50)] were examined on audiogenic seizure (AGS) severity and neuronal firing in the inferior colliculus (IC) in the freely moving genetically epilepsy-prone rat (GEPR-9). The IC is known to be critical to AGS initiation. The effects of focal microinjection of tiagabine into the IC were also examined. Bilateral focal microinjection of tiagabine into the IC significantly reduced seizure severity in the GEPR-9. Systemically administered tiagabine also produced a significant reduction in seizure severity in the GEPR-9. Tiagabine produced a reduction in IC (central nucleus) neuronal firing, which was significant only at high acoustic intensities (90-105 dB), concomitant with the considerable reduction in seizure severity. These data are consistent with enhancement by tiagabine of gamma-aminobutyric acid (GABA)-mediated inhibition in IC, which is most prominent at high acoustic intensities. The time course of the reduction in neuronal firing of IC neurons paralleled the reduction in seizure severity. Previous studies have shown that two forms of GABA-mediated inhibition (intensity-induced and offset inhibition) in IC neurons are most prominent at high stimulus intensities, which are required to induce AGS. The blockade of GABA uptake by tiagabine may act to inhibit audiogenic seizures, in part, by intensifying these naturally occurring forms of acoustically evoked inhibition in inferior colliculus neurons.

Acoustic Stimulation↗
PubMed1996

Increased responsiveness and failure of habituation in neurons of the external nucleus of inferior colliculus associated with audiogenic seizures of the genetically epilepsy-prone rat.

Initiation of audiogenic seizures (AGS) emanates from the inferior colliculus (IC) to other IC subnuclei in the genetically epilepsy-prone rat (GEPR). The external nucleus of IC (ICx) is a suggested site of convergence of the auditory output onto the sensorimotor integration network components for AGS in the brainstem. Neuronal firing was recorded from the ICx of the awake, freely moving GEPR and normal Sprague-Dawley rats using microwire electrodes in the present study. Auditory stimuli consisted of 12-kHz tones (100 ms, 5-ms rise-fall at rates of 1/4s, 1/2s, and 1/s). AGS incidence in the GEPR is highest at 12 kHz. In the GEPR, ICx neuronal responses to acoustic stimuli were significantly greater than those seen in normal rats. This increased ICx firing was observed at relatively high acoustic intensities (> 80 dB SPL), which are near the threshold for AGS induction. Repetition-induced response attenuation (habituation) is commonly observed in ICx neurons, which appears to be overcome in the GEPR during AGS initiation. Tonic, acoustically evoked ICx neuronal firing was observed just prior to wild running. ICx firing was suppressed during the tonic and postictal phases of AGS. Recovery of ICx responses occurred when the animal regained postural control. Abnormal, intense output has previously been observed in the GEPR IC central nucleus (ICc) neurons. The neuronal firing pattern changes observed in the ICx in the present study may result from this intense ICc output. Diminished efficacy of GABA, which has been observed in several regions of the GEPR brain, including the IC, in a number of previous studies, may be involved in the exaggerated ICx responses to acoustic stimuli in the GEPR. Participation of the ICx in the AGS neuronal network may be subserved by this acoustic hyperresponsiveness.

Acoustic Stimulation↗
PubMed1997

Effects of tectal grafts on sound localization deficits induced by inferior colliculus lesions in hooded rats.

The goals of this research were to examine the role of the inferior colliculus (IC) in mediating sound localization behavior and the ability of tectal grafts to restore function after IC ablation in the Long-Evans rat. Previous work has suggested that the IC is a major center for processing of information used in localizing sound sources in space. Adult rats were trained on a lick suppression paradigm to discriminate the location of the second pulse in a noise burst pair presented in the horizontal interaural plane. Following baseline testing, rats received bilateral IC lesions, bilateral lesions followed in 1 week by bilateral tectal grafts, or were sham operated. Sound localization ability was then tested 15 to 30 days and 40 to 50 days following surgical procedures. Performance across experimental groups was statistically the same during baseline testing. During the first operative test period lesion-only and grafted animals showed deficits in sound localization ability relative to controls. By the second postoperative test period control and grafted animals did not differ statistically in sound localization ability and performance of both groups was superior to that of lesion-only animals. Histology revealed a similar extent of IC damage in lesion-only and lesion-graft animals and revealed the presence of implanted tectal tissue in all grafted animals. There was significant neuron loss in the dorsal nucleus of lateral lemniscus (DNLL) in lesion-only animals relative to grafted rats and sham controls. Behavioral results suggest that the IC of pigmented rat is important for sound localization ability. The sparing of DNLL neurons in grafted animals suggests that the tectal grafts may directly integrate into or aid intrinsic recovery of the host auditory pathway.

Animals↗
PubMed1998

NMDA receptors in the inferior colliculus are critically involved in audiogenic seizures in the adult rats with neonatal hypothyroidism.

The effects of N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists were compared on audiogenic seizures in the rats neonatally exposed to propylthiouracil (PTU). The rats treated with 0.02% PTU through mother's milk during days 0-19 after delivery showed a high incidence of audiogenic seizures consisting of running fit (RF) followed by generalized tonic-clonic seizure (GTCS) after matured. The systemic administration with MK-801, a NMDA receptor antagonist dose-dependently inhibited both RF and GTCS. NBQX (6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione), a non-NMDA receptor antagonist, when systemically administered, failed to block audiogenic seizures. Audiogenic seizures caused a marked induction of c-fos messenger RNA (mRNA) in septal nucleus, bed nucleus of stria terminalis, amygdaloid nuclei, peripeduncular nucleus, and inferior colliculus, which was almost completely blocked by the pretreatment with MK-801. Bilateral microinjection of MK-801 into the inferior colliculus showed a tendency for inhibiting GTCS, but not RF, whereas CPP (3-(R)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid), a competitive NMDA receptor antagonist produced a significant inhibition against both RF and GTCS. These NMDA receptor antagonists administered into cisterna ambience, the floor of which is composed of inferior colliculus and neighboring structures, have shown potent blocking effects on both RF and GTCS. The present results suggest that NMDA receptors in the inferior colliculus, presumably in the subnucleus of external cortex may play the critical role in the initiation of audiogenic seizures in PTU-treated rats.

Acoustic Stimulation↗
PubMed1998

Glycine receptors in adult guinea pig brain stem auditory nuclei: regulation after unilateral cochlear ablation.

In young adult guinea pigs, the effects of unilateral cochlear ablation were determined on the specific binding of [3H]strychnine measured in subdivisions of the cochlear nucleus (CN), the superior olivary complex, and the auditory midbrain, after 2, 7, 31, 60, and 147 postlesion days. Changes in binding relative to that in age-matched controls were interpreted as altered activity and/or expression of synaptic glycine receptors. Postlesion binding declined ipsilaterally in most of the ventral CN and in the lateral superior olive (LSO). Binding was modestly deficient in the ipsilateral dorsal CN and in the anterior part of the contralateral anteroventral CN. Binding was elevated in the contralateral LSO. Transient changes also occurred. Binding was elevated transiently, between 2 and 31 days, contralaterally in parts of the anteroventral CN, bilaterally in the medial superior olive (MSO), and bilaterally in most of the midbrain nuclei. Binding was deficient transiently, at 60 days, in most of the contralateral CN and bilaterally in the midbrain nuclei. The present findings, together with previously reported postlesion changes in glycine release, were consistent with persistently weakened glycinergic inhibitory transmission ipsilaterally in the ventral CN and the LSO and bilaterally in the dorsal CN. Glycinergic inhibitory transmission was strengthened in the contralateral LSO and transiently strengthened in the MSO bilaterally. A hypothetical model of the findings suggested that glycine receptor regulation may depend on excitatory and glycinergic input to auditory neurons. The present changes in glycine receptor activity may contribute to altered auditory functions, which often accompany hearing loss.

Animals↗
PubMed1999

Differential roles in the neuronal network for audiogenic seizures are observed among the inferior colliculus subnuclei and the amygdala.

The inferior colliculus (IC) is established as the initiation site within the neuronal network for audiogenic seizures (AGS), but the relative importance of the IC subnuclei in AGS is controversial. The lateral and basolateral subdivisions of the amygdala are implicated in the expansion of the AGS network that occurs during AGS kindling. However, the role of the amygdala in the AGS network in nonkindled AGS is unknown. NMDA receptors are implicated in modulation of AGS and in neurotransmission in both the IC and amygdala. Therefore, changes in AGS severity in genetically epilepsy-prone rats (GEPR-9s) were examined after bilateral focal microinjection into IC subnuclei or lateral/basolateral subdivisions of the amygdala of a competitive NMDA receptor antagonist, 3-((+)-2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP). Blockade of AGS in IC central nucleus (ICc) and external cortex (ICx) was observed at identical doses of CPP, but these doses were ineffective in IC dorsal cortex (ICd). Microinjection of CPP into the amygdala did not produce significant changes in AGS severity except at doses 20 times those effective in IC. The latter data contrast with the anticonvulsant effects of amygdala microinjections on seizure severity in kindled AGS reported previously. The present data in concord with neuronal recording studies of these nuclei suggest that the ICc is the most critical site in AGS initiation, the ICx in propagation, and that the ICd plays a lesser role in the AGS network. The amygdala does not appear to play a requisite role in the neuronal network for AGS in animals that have not been subjected to AGS kindling.

Acoustic Stimulation↗