Fred Ramade

Thalamic-Hypothalamic Interrelationships and Stress-Induced Rebounding Adrenocortical Response in the Pigeon

Plasma corticosterone levels were determined by protein-binding assay at 2- and 5-min intervals after systemic or neurogenic stress. The same corticosterone (B) profile was observed after hemispherectomy as in intact pigeons, exhibiting episodic increase including several successive peaks after stress application. Hypothalamic stimulation of ACTH injection resulted in a simpler adrenocortical response, analogous to the first peak of the response to stress. Postero-lateral deafferentation of the hypothalamus unabled neurogenic stress to promote any plasma B increase and significantly altered the response to systemic stress since only the first peak of B occurred. Such a single peak response to both systemic and neurogenic stresses was observed after surgical interruption of neural connections between hypothalamic and thalamic structures without interferring with posterior afferents to the basal hypothalamus. The role of thalamic-hypothalamic interrelationships in modulating the stress-induced adrenocorticotropic activity is discussed.

Adaptation of the Adrenocortical Response during Repeated Stress in Thalamic Pigeons

Chronic vascular catheterization allowed to obtain serial blood samples before and after stress application to thalamic pigeons. Daily repetition of the same stress, at the same hour, for 5 weeks led to drastic changes in the stress-induced adrenocortical reaction. The rebounding, long-lasting rise in plasma corticosterone occurring after initial presentation of electrical footshocks was replaced by a single peak of corticosterone, lower and shorter than the initial response. Moreover, an anticipatory conditioned rise in corticosterone appeared before stress. Random distribution of stressful stimuli, thrice a day, for 5 weeks resulted in the single peak pattern of post-stress adrenocortical reaction, without any anticipatory component. When electrical footshocks were omitted after 5 weeks of daily regular presentation of stress, only the anticipatory peak in plasma corticosterone occurred. Shifting the daily lighting from the usual 06.00 a.m. to 04.00 a.m. led to a shift in the anticipatory conditioned endocrine response which appeared 2 h sooner than usual. Thalamic involvement in the process of adaptation to chronic stress is discussed.

Adrenocortical Responses to Systemic or Neurogenic Stress and to Hypothalamic Stimulation in Chronically Catheterized Thalamic Pigeons

Thalamic and intact pigeons were equipped with a chronic arterial catheter and with a miniature electronic device for hypothalamic telestimulation. Chronic catheterization allowed for repetitive blood sampling in freely moving birds subjected to either systemic (ether inhalation) or neurogenic (electrical foot shocks) stress and to electrical stimulation of the hypothalamic corticotropic area. Corticosterone levels were determined by protein binding assay at 2-, then 5- and 10-min intervals, for 100 min. Basal and experimentally modified plasma corticosterone concentrations were not different in thalamic and intact pigeons. Corticosterone profile exhibited episodic increase including three peaks at 12, 35 and 60 min after stress application. Only the first peak of plasma corticosterone appeared after hypothalamic stimulation. It is suggested that extrahypothalamic neuronal networks are responsible for the long-lasting repetitive adrenocorticotropic response to stress, which are not involved in the single response to hypothalamic stimulation itself. Furthermore, such extrahypothalamic neuronal networks shoudl be located at the diencephalic or rhombencephalic level since hemispherectomized pigeons exhibited the same profile of stress-induced episodic hypercorticosteronemia as seen in intact birds.

Effect of short exposure to cold on plasma thyroxine in Coturnix quail: Role of the infundibular complex and its neural afferents

Exposure of control quail to low ambient temperature (4 degrees) for a short duration (15 min) led to a rapid increase in plasma thyroxine (T4) levels. A peak appeared 40 min after the cold began and was followed by a progressive and slow decline. T4 levels were elevated in birds maintained for up to 3 hr at 4 degrees. Restraint stress could be accompanied by a slight and late decrease in thyroxine concentration, indicating that glucocorticoids could partly inhibit thyroid function. Both cold and restraint stresses elicited sustained adrenocortical activation. No thyroid response to cold appeared after complete or partial neural deafferentation of the hypothalamus, indicating that cold signals were conveyed to the thyrotropic centers from peripheral and/or deep thermoreceptors through neural posterior-lateral afferents to the hypothalamus. No thalamic relay appeared to be necessary since normal thyroidal stimulation was observed after thalamic-hypothalamic disconnection. Such a response persisted in hemispherectomized quail.

Effects of Chronic Intracerebroventricular GABAergic Treatment on Basal and Chronic or Acute Stress-Induced Adrenocortical Activities in the Thalamic Pigeon

Muscimol was chronically administrated to the third ventricle of thalamic pigeons by means of osmotic minipumps at the rate of 0.25 microgram X h-1 for 28 days. No abnormal behavioural sign was noted. The animals were subjected daily to chronic intermittent stress for the same 28-day period. Basal and stress-induced adrenocortical activities were evaluated by recording serial plasma corticosterone levels at the end of the experimental session. Untreated controls exhibited both components of the adaptation of the adrenocortical response to chronic stress: attenuation, i.e., a decrease in magnitude and disappearance of the late rebounding phenomenon, and anticipation, i.e., the occurrence of a conditioned component before stress itself. The adaptation to chronic stress was partly impaired by GABAergic treatment. The anticipatory conditioned peak subsisted but the magnitude of the post-stress peak was found not to be reduced whereas rebounding events were suppressed after chronic as well as acute stress. The basal resting levels of corticosterone were significantly lowered in muscimol-treated animals. A lesion placement in the anterior dorsomedial thalamus (ADMT) resulted in the same profile of stress-induced plasma corticosterone levels as seen after muscimol administration. Adaptation did not develop in ADMT animals and GABAergic stimulation, either acute or chronic, had no effect on their response to stress.

Adaptation of the Adrenocorticotropic Response to Chronic Intermittent Stress Was Altered by Intracerebroventricular Infusion of Hemicholinium-3

The role of diencephalic cholinergic neurotransmission in regulating hypothalamic-pituitary-adrenocortical (HPA) axis was investigated by means of administration of hemicholinium-3 (HC-3), a blocker of acetylcholine synthesis, in the third ventricle of hemispherectomized pigeons. Except for an early increase in ACTH and corticosterone levels following injection as a bolus of HC-3 that was ascribed to some stress-like situation, all data indicated that hypothalamic acetylcholine depletion resulted in inhibiting effects on the HPA axis. Twenty-four hours after injection of 6 micrograms of HC-3, the response to acute stress was markedly reduced in both magnitude and duration. Permanent instillation of HC-3 in the third ventricle at the rate of 0.25 microgram/h for 9 days led to lowered basal resting HPA activity and severely affected the development of adaptation to chronic intermittent stress. The anticipatory conditioned, endocrine response did not appear whereas attenuation of the poststress component was amplified. It is suggested that cholinergic mechanisms are involved in modulating the HPA function and particularly the conditioning process that takes place in the course of adaptation of the HPA response to chronic intermittent application of the same stressor.

Hypothalamic multiunit activity correlates of the adrenocortical response to stress.

The corticotropic response to stress was studied by means of multiple unit activity (MUA) recording from the adrenocorticotropic region of the hypothalamus, and plasma corticosterone (B) determination. MUA was permanently obtained and B was measured at 2, then 5 and 10 min intervals before and after neurogenic (electrical shocks) or systemic (ether inhalation) stress was applied. Experiments were made on steady unanesthetized, unrestrained thalamic pigeons. Post-stress alterations of MUA and B were closely in parallel, exhibiting a rapid and sustained increase in firing rate and shifting by 5-10 min, in corticosteronemia. Three successive and progressively decreasing peaks of MUA and B could be observed. Basal resting values were restored by approximately 90 min. Adrenocorticotropic responses to stress appear to be modulated through neural thalamic and/or rhombencephalic mechanisms.

The adrenocortical response to stress from the pre-hatching period to the adult state in the pigeon: Thalamic participation

The stress‐induced adrenocortical response was kinetically evaluated for 100 min after ether vapor exposure in late embryos (30 h before hatching) and in 1, 2, 3 and 6‐wk‐old squabs. An‐adult‐pattern of corticosterone profile was seen in intact 6‐wk‐old pigeons, i.e. a polyphasic increase of corticosterone including successive peaks at 12–15, 35, 60 and 90 min after stress application. In 1‐wk‐old squabs, a small adrenocortical response to stress included only a single peak of corticosterone at 12–15 min. The early peak was found again, with the same magnitude, 2 wk after hatching but it was followed by two later and smaller peaks 35 and 60 min after stress. The adult pattern was visible in 3‐wk‐old stressed pigeons, although the magnitude of the response was still smaller than in adult controls. A single, high peak of corticosterone occurred 12–15 min after stress application, without any later peak, in embryos and a similar monophasic response was seen in thalamic lesioned adult birds. Therefore, it can be suggested that the polyphasic reverberating adrenocortical response to stress depends upon relationships between the adrenocorticotrophic hypothalamus and the anterior mediodorsal thalamus. Such thalamic‐hypothalamic interrelations appear to mature during the early post‐hatching weeks.

Effect of GABAergic treatment on resting and stress-induced adrenocortical activities in the thalamic pigeon

Muscimol was injected (0.5 mg kg-1) intravenously to either intact or thalamic-lesioned animals through a chronic catheter. Plasma samples were obtained at 7-min intervals and exhibited a moderate and transient increase in corticosterone levels in both groups, together with some symptoms of light discomfort (e.g., ptiloerection or panting). All these signs disappeared within 45 to 60 min. Intraventricular injection of bicuculline (3.5 micrograms) provoked a corticosterone profile quite similar to a stress-induced polyphasic pattern. Acute stress (electrical footshocks for 30 sec) was applied 2 hr after drug treatment. In controls, the stress-induced adrenocortical response appeared to be markedly modified after muscimol injection. The usual polyphasic rebounding profile was replaced by a monophasic one. This effect of muscimol did not occur when bicuculline had been injected in the 3rd ventricle. Bicuculline alone did not alter the stress-induced profile. GABAergic treatment had no effect on the monophasic response of thalamic-lesioned birds.