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Biomedical subjects

F G Graeff

Publications and source records attributed to F G Graeff.

126 records · Page 7Linked to original sources
PubMed1973

Nondiscriminated avoidance of shock by pigeons pecking a key.

Four pigeons were trained to avoid shock by pecking a key on a free-operant avoidance schedule in which no exteroceptive stimulus signalled impending shock. Response rate was an inverse function of response-shock interval when shock-shock interval was held constant at 2 sec and response-shock intervals varied from 5 to 40 sec. Amphetamine increased response rates in two subjects and reserpine markedly reduced responding in one.

Journal Article↗
PubMed1969

Behavioural and somatic effects of bradykinin injected into the cerebral ventricles of unanaesthetized rabbits.

1. The effects of bradykinin (1-5 mug) injected into the cannulated lateral cerebral ventricles were studied in unanaesthetized rabbits before and after intravenous atropine, diphemanil and morphine.2. The intraventricular injections of bradykinin produced a short-lasting phase of behavioural excitation with vocalization followed by sedation. The behavioural excitation was associated with desynchronization in the electrocorticogram (e.co.g.), bradycardia and hypotension followed by tachycardia and hypertension. Tachypnoea was also observed. The subsequent phase of sedation was more prolonged and associated with synchronization of the e.co.g. and signs of catalepsy. Intense miosis was present during both phases.3. With repeated intraventricular injections of bradykinin, excitation, miosis, cardiovascular responses and tachypnoea diminished and eventually disappeared but the sedation did not exhibit tachyphylaxis.4. Atropine abolished the e.co.g. desynchronization, vocalization and bradycardia, reduced the duration of the excitatory and sedatory phase, diminished the tachycardia and hypotension, enhanced the hypertension, but did not affect the miosis and tachypnoea.5. Diphemanil affected only the cardiovascular effects produced by intraventricular bradykinin. They were affected in the same way as by atropine.6. Morphine did not affect the excitatory phase, but enhanced the cardiovascular effects produced by intraventricular bradykinin.7. The intraventricular injection of bradykinin (50 mug) caused a reduction in the amount of noradrenaline but not of 5-hydroxytryptamine (5-HT) in the brain stem; the amount of dopamine in the caudate nuclei was not affected.8. It is suggested that central cholinergic and adrenergic systems are activated by intraventricular bradykinin.

Animals↗
PubMedDate not supplied

Lesion of the ventral periaqueductal gray reduces conditioned fear but does not change freezing induced by stimulation of the dorsal periaqueductal gray.

Previously-reported evidence showed that freezing to a context previously associated with footshock is impaired by lesion of the ventral periaqueductal gray (vPAG). It has also been shown that stepwise increase in the intensity of the electrical stimulation of the dorsal periaqueductal gray (dPAG) produces alertness, then freezing, and finally escape. These aversive responses are mimicked by microinjections of GABA receptor antagonists, such as bicuculline, or blockers of the glutamic acid decarboxylase (GAD), such as semicarbazide, into the dPAG. In this work, we examined whether the expression of these defensive responses could be the result of activation of ventral portion of the periaqueductal gray. Sham- or vPAG electrolytic-lesioned rats were implanted with an electrode in the dPAG for the determination of the thresholds of freezing and escape responses. The vPAG electrolytic lesions were behaviorally verified through a context-conditioned fear paradigm. Results indicated that lesion of the vPAG disrupted conditioned freezing response to contextual cues associated with footshocks but did not change the dPAG electrical stimulation for freezing and escape responses. In a second experiment, lesion of the vPAG also did not change the amount of freezing and escape behavior produced by microinjections of semicarbazide into the dPAG. These findings indicate that freezing and escape defensive responses induced by dPAG stimulation do not depend on the integrity of the vPAG. A discussion on different neural circuitries that might underlie different inhibitory and active defensive behavioral patterns that animals display during threatening situations is presented.

Animals↗