Diencephalic sites from which calling can be evoked with small currents in Japanese quail.

A systematic stimulation survey f the diencephalon in Japanese quail, showed that calling could be evoked with currents as low as in the midbrain (less than 50 microA). These low threshold areas were located in the pre-optic area and posterior hypothalamus. Both are likely to influence output, but are not on a calling motor pathway from the forebrain. Putative pathways for calling had somewhat higher thresholds, than the preoptic area and posterior hypothalamus. Calling was evoked from much of the diencephalon with currents up to 200 microA, but positive sites tended to be located posteriorly. A few of the calls elicited resembled natural calls subjectively, but statistical analyses showed significant differences. Most elicited calls were unlike any spontaneous call and could be produced in both sexes.

Midbrain regions involved in call production in Java sparrows.

Calling has been evoked from the midbrain of Java sparrows by currents of less than 200 micro A. Minimum thresholds were found in the medial nucleus intercollicularis, higher threshold sites surrounded these. Additionally, more ventral sites were found. Calling evoked did not resemble natural calls, but was similar to that produced after bilateral denervation of the syrinx. These results indicate that the nucleus intercollicularis acts as a controller rather than an organizer of calling.

Effects of nicotine given into the brain of fowls.

1 The effects of nicotine, given into the IIIrd ventricle of adult conscious fowls (Gallus domesticus) or infused into various brain regions of conscious young chicks, were tested on behaviour, electrocortical activity, respiratory rate and body temperature. Its effects given intraventricularly or applied externally to the brain-stem of anaesthetized fowls were also examined.2 After intraventricular nicotine, fowls squatted for 3 to 5 min with eyes closed, electrocortical activity resembling that during sleep but with superimposed spike activity. Following this, fowls reawakened and tachypnoea developed, together with partial abduction of the wings from the trunk, the back becoming horizontal and the tail flexed. These effects were prevented by pempidine.3 Intraventricular nicotine suppressed or, less commonly, reduced operant key-pecking, an effect unrelated linearly to dose.4 Intraventricular nicotine given to fowls anaesthetized with chloralose produced brief apnoea, followed by increased amplitude of respiratory excursion for about 5 minutes. Respiratory rate accelerated slightly but tachypnoea did not develop. Nicotine applied directly to the ventral brain-stem increased respiratory amplitude in three out of seven fowls.5 In anaesthetized fowls, intraventricular nicotine raised blood pressure for 2 to 3 min, an effect prolonged up to 70 min by acute bilateral vagotomy, whereas pressor effects of intravenous nicotine were extended merely two to three fold. Dividing the spinal cord at C2 prevented pressor effects of intraventricular nicotine; those of intravenous nicotine were unaltered.6 In young chicks, nicotine infused into the diencephalon, telencephalon and myelencephalon induced effects similar to those observed immediately after intraventricular nicotine, i.e. chicks squatted with closed eyes but recovered within 3 to 5 minutes. Simultaneously, electrocortical activity changed from an alert to the sleep pattern, usually with superimposed ;spike' activity. Tachypnoea and associated postural changes did not develop. Pempidine prevented the behavioural and electrocortical effects of nicotine.

Effects of cholinomimetic agents given into the brain of fowls.

1 Effects of cholinomimetic agents, given into the IIIrd ventricle of adult fowls (Gallus domesticus) or infused into the hypothalamus of young chicks, were tested on behaviour, respiratory rate and body temperature.2 Carbachol evoked behavioural and electrocortical arousal but lacked postural and respiratory effects. Contrariwise, pilocarpine increased respiratory rate and induced postural changes, i.e. abduction of the wings, but lacked other behavioural effects and did not alter electrocortical activity. Benzoylcholine induced tachypnoea, postural changes and brief electrocortical arousal. Acetylcholine was ineffective unless given with physostigmine, when electrocortical arousal, postural changes and tachypnoea developed. Methacholine induced tachypnoea and postural changes.3 Effects of carbachol and pilocarpine were prevented by hyoscine and those of benzoylcholine by pempidine; hyoscine and pempidine were required together to prevent the effects of methacholine and to attenuate those of acetylcholine with physostigmine.

Effects of muscarine given into the brain of fowls.

1. The effects of muscarine, given intraventricularly, in adult conscious fowls (Gallus domesticus) or microinfused into various brain regions of conscious young chicks, were tested on behaviour, electrocortical activity and respiratory rate. Its effects given intraventricularly or intravenously to anaesthetized fowls were also examined.2. After intraventricular injection, muscarine elicited immediate behavioural and electrocortical arousal; body temperature was unaffected. After a delay of 30-40 min, tachypnoea developed together with postural changes which included partial abduction of the wings away from the trunk, the back and tail becoming horizontal. These effects were prevented by intravenous or intraperitoneal atropine or hyoscine, but not by pempidine or methylatropine, and were potentiated by physostigmine. Hyoscine given intraventricularly or intravenously did not affect electrocortical activity.3. Intraventricular muscarine given to anaesthetized adult fowls produced brief apnoea. On return of respiration, amplitude of respiratory excursion was diminished for about 5 min; tachypnoea did not develop. Blood pressure also rose briefly. With larger doses of intraventricular muscarine, large amplitude electromyographic potentials developed in the dorsal neck muscles followed later by side-to-side neck movements.4. Muscarine given intravenously to anaesthetized adult fowls, raised blood pressure and perfusion pressure in a perfused hind limb, an effect most likely due to secretion of adrenal medullary catecholamines; these pressor effects were prevented by pempidine and phenoxybenzamine. Given directly to the perfused hind limb, muscarine lowered perfusion pressure.5. In young chicks, muscarine microinfused into the diencephalon or myelencephalon elicited intense bilateral electrocortical alerting associated with periods of alternating violent motor activity and quiescence. Microinfusion of muscarine into the telencephalon induced ipsilateral electrocortical desynchronization without affecting behaviour. These effects of muscarine were prevented by intravenous, intraperitoneal or intracerebral hyoscine, but once its effects were established could be antagonized only with difficulty; pempidine did not prevent these effects. Microinfusions of muscarine into the brain did not affect posture, respiration or temperature.