A histological study of kainic acid-induced lesions in the rat brain

Wuerthele, Suzanne M.; Lovell, Kathryn L.; Jones, M. Z.; Moore, Kenneth E.

doi:10.1016/0006-8993(78)90491-2

Cited by 167 publications

(28 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Honchar et al (1983) reported that administration of physostigmine or * pilocarpine to lithiun pretreated rats produced sustained limbic seizures and brain damage similar to which we observed with soman; this effect was also blocked by atropine. Similar damage to the piriform cortex also occurs with other agents which induce limbic motor seizures, such as kainic acid (Wuerthele et al, 1978;Schwob et al, 1981;Lothman and Collins, 1981;Sperk et al, 1983; our unpublished data) and folic acid derivatives . Distal damage to the piriform cortex caused by injection of kainic acid or folic acid into the substantia innominata was reduced by scopolamine and to even a greater extent by diazepam (McGeer et al, 1983).…”

Section: *Extensivesupporting

confidence: 60%

Proceedings of the Annual Chemical Defense Bioscience Review (4th) Held at Aberdeen Proving Ground, Maryland on 30 May-1 June 1984

Lindstrom¹

1984

View full text Add to dashboard Cite

Section: *Extensivesupporting

confidence: 60%

Proceedings of the Annual Chemical Defense Bioscience Review (4th) Held at Aberdeen Proving Ground, Maryland on 30 May-1 June 1984

Lindstrom¹

1984

View full text Add to dashboard Cite

“…3) and the resulting lesions surprisingly discrete, as evidenced by their confinement to subnuclei of the NTS. The boundaries of the lesions might have extended somewhat if the lesions had been studied after a longer post-injection period (Wuerthele, Lovell, Jones & Moore, 1978).…”

Section: Discussionmentioning

confidence: 99%

Localization by kainic acid lesions of neurones transmitting the carotid chemoreceptor stimulus for respiration in rat.

Housley

Sinclair

1988

The Journal of Physiology

124

View full text Add to dashboard Cite

SUMMARY1. An attempt has been made to test the hypothesis that in the nucleus of the tractus solitarius (NTS) in the rat, the most caudal region of synaptic terminals of the carotid sinus nerve, just caudal to the obex, represents mainly the site of synapse of chemoreceptor fibres from the carotid body.2. Under halothane anaesthesia, the neurotoxin kainic acid was used to lesion this region and a second region, immediately rostral to obex, where terminals are thought to arise mainly from baroreceptor fibres of the carotid sinus nerve.3. Measurements based on the distribution of fluorescent dye co-injected with the kainic acid showed that the two groups of 100 nl microinjections were centred 0-82 mm apart and that the injectate spread through mean distances of 0 57 mm (caudal microinjections) and 0-52 mm (rostral microinjections). Nissl staining was used to determine cellular degeneration. The caudal lesions mostly involved ventrolateral and commissural subnuclei of NTS and the rostral lesions involved lateral and dorsolateral subnuclei.4. Ventilatory sensitivity to hypoxia was tested under light halothane anaesthesia, 1 day after lesioning. To enhance the responses, the contralateral carotid sinus nerve was sectioned prior to experiments. Caudal lesions reduced the ventilatory response to inspired oxygen (20-9-9-6 % 02) by a mean of 67 % and rostral lesions by 18 % of the effect produced by carotid sinus nerve section on that side. Subsequent section of the carotid sinus nerve on the side of the NTS lesion confirmed that caudal lesions produced effects comparable to those of carotid body denervation; rostral lesions did not.5. These results strongly support the hypothesis that chemoreceptor and baroreceptor afferent fibres in the carotid sinus nerve synapse at substantially separable sites in the nucleus of the tractus solitarius. The identification of the site in NTS caudal to the obex as the principal site of carotid chemoreceptor synapses places them close to but not upon respiratory premotor neurones of the same nucleus.4-2

show abstract

“…Three studies have reported that severing the stria terminalis did not result in excessive weight gain in rats, but this may have been due to the use of males (6,7,73). Although electrolytic lesions have obvious shortcomings, excitotoxic lesions also have limitations: 1) damage to axons occurs at some sites, 2) lesions sometimes occur at distant sites (presumably by transynaptic activation), and 3) incomplete cell loss sometimes occurs (15,16,28,42,85,87,113). There is also the problem of widespread diffusion when ibotenic acid is injected into the amygdala (114), often necessitating high dosages to get effects.…”

Section: Anterograde Degeneration and Retrograde Tracing Experimentsmentioning

confidence: 99%

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport

King

Cook

Rossiter

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

King, Bruce M., Jack T. Cook, Kirk N. Rossiter, and Bethany L. Rollins. Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport. Am J Physiol Regul Integr Comp Physiol 284: R965-R982, 2003. First published November 14, 2002 10.1152/ajpregu.00249.2002.-Small lesions centered in the posterodorsal region of the medial amygdala resulted in excessive weight gains in female rats. Unilateral lesions were nearly as effective as bilateral lesions in the first 48 h after surgery (ϩ21 to ϩ32 g). Assessment of lesion damage was done by both qualitative evaluation and by a quantitative grid-point counting method. The critical sites for weight gain were the intra-amygdaloid bed nucleus of the stria terminalis and the posterodorsal medial amygdaloid nucleus. Incidental damage to the overlying globus pallidus was negatively related to weight gain. The cupric silver method for demonstrating axonal degeneration was applied to brains with obesity-inducing lesions. A dense pattern of degenerating terminals was found in the lateral septum, amygdala, ventral striatum, and ventromedial hypothalamus. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intra-amygdaloid bed nucleus of the stria terminalis or in the posterodorsal medial amygdaloid nucleus labeled cells in the amygdala, lateral septum, and hypothalamus, reciprocating the anterograde projections from the amygdala to these areas. The data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is similar to the better-known role of this part of the brain in mediating reproductive behavior. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these two sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel. nucleus accumbens; hypothalamus; stria terminalis SEVERAL RECENT STUDIES have demonstrated that bilateral electrolytic lesions of the amygdala in female rats can result in marked hyperphagia and excessive weight gains. Daily food intake nearly doubles, and weight gains of 20-30 g during the first 3 days after lesions are not unusual (e.g., 45, 50-53, 84). Weight gains of Ն100 g in 20-25 days have been observed (50, 51). The lesions result in a marked preference for carbohydrates (53). Although food intake eventually returns to normal, the excessive weight gain is maintained indefinitely, with a marked increase in adipose tissue (50).These results are similar to those reported many years ago for cats, dogs, and primates (including humans) given amygdaloid lesions or temporal lobectomies (e.g., 9, 32, 37, 70, 103). In the rat, the effective lesion site for hyperphagia and obesity has recently been identified as the posterodorsal part of the medial amygdaloid nucleus (MePD) and the intra-amygdaloid bed nucleus of the stria terminalis (BSTIA), together ...

show abstract

A histological study of kainic acid-induced lesions in the rat brain

Cited by 167 publications

References 13 publications

Proceedings of the Annual Chemical Defense Bioscience Review (4th) Held at Aberdeen Proving Ground, Maryland on 30 May-1 June 1984

Proceedings of the Annual Chemical Defense Bioscience Review (4th) Held at Aberdeen Proving Ground, Maryland on 30 May-1 June 1984

Localization by kainic acid lesions of neurones transmitting the carotid chemoreceptor stimulus for respiration in rat.

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport

Contact Info

Product

Resources

About