Amygdaloid Complex In Rats Research Articles

Kindling-induced changes in morphine analgesia and catalepsy: Evidence for independent opioid systems

Repeated stimulation of the amygdaloid complex in rats results in the kindling of epileptic seizures. During the process of kindling and prior to the appearance of full behavioral convulsions, naloxone-sensitive changes in responsiveness to noxious stimulation occur, which disappear with repeated stimulation. When full behavioral convulsions appear, a short period of post-ictal behavioral depression (PID) can be seen immediately following convulsions. Naloxone either attenuates or completely blocks the occurrence of the PID. In order to test further the opioid nature of these phenomena, the development of tolerance to PD with repeated stimulation and the development of cross-tolerance to the analgesic and motor depressant effects of morphine were tested in kindled animals. Repeated elicitation of full behavioral convulsions resulted in a progressive decrease of PID duration across days. PID was also decreased in morphine tolerant animals. Repeated convulsions also induced cross-tolerance with both morphine analgesia and morphine-induced catalepsy. In contrast, animals tested following 10 days of amygdaloid stimulation which did not cause full behavioral convulsions to develop, showed cross-tolerance to the analgesic but not the motor depressant effect of morphine. The possibility that two different opioid systems, which are independent of one another are activated during different phases of kindling is discussed.

Depletion in amygdaloid 5-hydroxytryptamine concentration and changes in social and aggressive behaviour.

5,7-Dihydroxytryptamine (10 and 20 microgram) was microinjected bilaterally into the amygdaloid complex of rats and resulted in 55% and 80% depletion in 5-hydroxytryptamine concentration, respectively. The lesioned animals exhibited fewer dominance behaviours and submitted more often to an intruder into their home-cages than did the vehicle-injected controls. The lesioned rats were also more submissive than were the controls when they were intruding into another rat's territory. Only the higher dose of toxin altered social investigatory behaviour when this was measured in an arena in which neither rat had established territory. The lesioned rats displayed less social interaction and had reduced levels of motor activity. The results are compared with those of other studies in which there has been regional or general depletion of brain 5-hydroxytryptamine concentration.

Injections of kainic acid into the amygdaloid complex of the rat: An electrographic, clinical and histological study in relation to the pathology of epilepsy

Kainic acid has been injected unilaterally into the amygdaloid complex of rats. Electro-encephalographic and clinical changes have been studied in relation to subsequently demonstrated neuropathology using Fink-Heimer and Nissl stainings. Epileptiform electroencephalographic activity began (after 5–60 min) at the site of the injection and spread to the ipsilateral hippocampus, contralaterally and to the cortex. Motor signs of epilepsy occurred repetitively for 2–6 h; subsequently, irregular or regular spikes occurred continuously (for 4–30 h) without positive motor signs. Neuronal loss and gliosis was invariably noted at the injection site. In addition, neuronal loss and degenerative changes were present at other sites where lesions are found after status epilepticus; these included various hippocampal fields, the contralateral amygdala and claustrum and, bilaterally, the midline thalamic nuclei, lateral septum and various cortical areas. The first damage to appear (after 2 h of epileptiform activity) was in the ipsilateral CA3a hippocampal subfield. A correlation was found between the severity of the epileptiform activity in the ipsilateral hippocampus and the severity of pathological alterations. This, as well as other observations suggest that the distant brain damage is not a consequence of the diffusion (or intra-axonal transport) of kainic acid but is causally related to the epileptiform activity induced by the toxin. Intra-amygdaloid injections of kainic acid thus provide a particularly suitable model for investigating the relationship between seizure activity and epileptic brain damage.

Avoidance learning: long-lasting deficits after temporal lobe seizure.

Microinjections of carbachol (carbamylcholine chloride) into the amygdaloid complex of rats produced behavioral and electrophysiological seizures which subsided within 24 hours. A persisting functional change caused a deficit in avoidance learning 1 to 3 weeks after the seizure. A cholinergic system is implicated by the fact that cholinergic blockade (scopolamine) of the amygdala during training reversed the effects of the seizures induced by carbachol.

Aphagia and adipsia following lesions of the amygdala

Lesions of the medial nucleus of the amygdaloid complex in rats produces aphagia and adipsia.

Release of gonadotropins induced by amygdaloid stimulation in the rat.

The amygdaloid nuclei were stimulated by iron deposits or by implanting crystalline carbachol in rats in persistent estrus induced by continuous illumination. Both electrochemical and chemical stimulation produced ovulatory response from the medial nucleus or the basolateral complex of the amygdala. Also, chemical stimulation of the bed nucleus of the stria terminalis was effective in inducing ovulation. Negative responses were observed by stimulating other areas or when the stria terminalis was found to be damaged by the electrode tract. The ovulatory response was blocked by transection of the stria terminalis but not by interruption of the ventral amygdalofugal fibers. Injection of atropine, reserpine or urethane was not effective in blocking ovulation inducedby amygdaloid stimulation. Plasma LH was found significantly higher 5 hr after chemical stimulation of the basolateral amygdaloid complex in ovariectomized rats primed with estradiol benzoate as compared to controls. Also, electrochemical amygdaloi...

Formation of a Conditioned Emotional Response (CER) Following Lesions of the Amygdaloid Complex in Rats

Formation of a conditioned emotional response (CER), using suppression of food-reinforced bar-pressing as an index, was studied in a group of rats with amygdaloid lesions ( N = 5) and in a sham-operate control group ( N = 5). In contrast to control animals, which typically suppressed in two to three sessions, none of the amygdaloid operates met criterion within the set limit of 15 sessions or showed signs of suppression. Increasing the intensity and duration of shock also proved ineffective in these animals. Only by punishing each bar-press during the CS period could their responding be suppressed. Further tests on generalization of conditioned suppression, performed on two of the control animals, revealed relatively flat generalization gradients, consistent with other findings. Results were discussed in terms of amygdaloid effects on non-reinforced behavior in discrimination situations. “Inhibition” of responding associated with nonreinforcement appears to involve some of the same processes that operate in shock-motivated behavior.