Search PubMed⌕ Search

Biomedical subjects

A G Phillips

Publications and source records attributed to A G Phillips.

At least 145 records · Page 8Linked to original sources
PubMed1980

Disruption of conditioned taste aversion in the rat by stimulation of amygdale: a conditioning effect, not amnesia.

Two experiments were conducted to determine whether the disruption of conditioned taste aversion by delivery of amygdaloid brain stimulation during conditioning could be attributed to the stimulus properties of the brain stimulation. In Experiment 1, animals receiving brain stimulation (a) while drinking saccharin, (b) during the onset of LiCl toxicosis, or (c) in the interval between taste exposure and toxicosis drank significantly more saccharin solution during a 48 hr retest than implanted or unoperated controls receiving similar taste-toxicosis pairings. In contrast, a group receiving brain stimulation during both conditioning and retention trials developed a strong conditioned aversion. Experiment 2 confirmed that amygdaloid stimulation can form a compound with the taste of the saccharin solution. A small but significant aversion was displayed by groups exposed to brain stimulation plus taste during conditioning and to either taste alone or brain stimulation alone during the retest. Again, the group presented with brain stimulation and taste prior to and following LiCl toxicosis displayed a strong conditioned aversion. These data suggest that disruption of conditioned taste aversion with amygdaloid stimulation represents a conditioning effect, not amnesia.

Amygdala↗
PubMed1980

The use of conditioned suppression to evaluate the nature of neuroleptic-induced avoidance deficits.

Three groups (N = 8) of rats received five 10-trial sessions of one-way avoidance training in which each trial was initiated by a 10-sec tone stimulus and terminated either by a shuttle response during the tone (avoidance) or by a response during the electric shock (escape). Rats in groups treated with pimozide (0.5 or 1.0 mg/kg i.p.) failed to acquire to avoidance response although they escaped readily when shock was presented, whereas control rats consistently avoided the shock. The same rats then received several sessions of food-reinforced lever-pressing in a different apparatus; no drugs were given during these sessions. When responding had stabilized, the tone that had signalled shock in the avoidance sessions was presented for a 1-min period. A significant decrease in responding during the tone was observed in all groups when compared to unshocked controls, demonstrating that the pimozide-treated rats, although failing to acquire the avoidance response in the shuttle box, had learned the association between the tone and shock. The results suggested that the neuroleptic-treated animals failed to avoid because of a deficit in the ability to initiate responses rather than a deficit in associative learning.

Animals↗
PubMed1979

Conditioned aversion to brain-stimulation reward: effects of electrode placement and prior experience.

A conditioned aversion to rewarding amygdaloid brain-stimulation was established by injecting rats with toxic doses of 0.15 M LiCl immediately after an initial self-stimulation session. The aversion had extinguished by the third self-stimulation session, 96 h after conditioning. This effect cannot be attributed to general depressant effects of LiCl on self-stimulation as treatment with LiCl 24 h before the second self-stimulation session was ineffective. Furthermore, this conditioned aversion was locus specific as LiCl injections immediately after the first test session had no disruptive effects on self-stimulation in the substantia nigra. The parallels between conditioned aversion to rewarding brain-stimulation in the amygdala and late aversion were strengthened by the fact that the novelty of brain-stimulation reward was an important factor in the conditioning effect. These data have important implications for understanding the sensory properties of brain-stimulation reward.

Amygdala↗
PubMed1979

Intracranial self-stimulation in orbitofrontal cortex and caudate nucleus of rhesus monkey: effects of apomorphine, pimozide, and spiroperidol.

Rhesus monkeys were prepared with stimulating electrodes implanted into the orbitofrontal cortex and head of the caudate nucleus under stereotaxic control. These regions of the brain contain high levels of dopamine, and intracranial self-stimulation was readily elicited from these loci in all animals tested using licking behavior as the operant response. Self-stimulation at both sites was significantly attenuated following peripheral injections of the dopamine receptor blocker spiroperidol (0.02 mg/kg). Similarly, pimozide (0.15 and 0.20 mg/kg) significantly reduced self-stimulation in the orbitofrontal cortex, but the suppression observed at caudate placements did not reach statistical significance. Licking for a reward of blackcurrant juice was unaffected by either drug. Apomorphine (0.2, 0.4 mg/kg) had a differential effect on self-stimulation. This drug significantly attenuated self-stimulation in the orbitofrontal cortex, while the same treatment tended to facilitate self-stimulation in the caudate. Apomorphine did not significantly affect responding for the fruit juice reward. The parallels between the effects of dopamine agonists and antagonists on self-stimulation in the monkey and rat suggest that dopamine influences self-stimulation of some sites in both the primate and the rat.

Animals↗
PubMed1979

Facilitation of self-stimulation behavior following intracerebral microinjections of opioids into the ventral tegmental area.

The intracerebral microinjection technique was used to localize sites in the brain where morphine facilitated the self-stimulation rate at hypothalamic electrode sites. Bilateral injections of morphine (2 x 1 microgram) into the ventral tegmental area and substantia nigra produced the strongest enhancement at the shortest latencies. At these sites, bilateral injections of 200 ng of morphine also produced a significant enhancement whereas a dose of 50 ng was below threshold for the rate increasing effect. The enhancement by morphine was effectively antagonized by naloxone (5 mg/kg). When injected bilaterally into the same area, D-Ala2-Met5-enkephalinamide (2 x 1 microgram) also induced a strong enhancement of self-stimulation lasting for 70 minutes. A possible dopaminergic substrate for the opiate induced behavioral stimulation is discussed.

Animals↗
PubMed1979

Possible involvement of serotonin in extinction.

In Experiment 1, rats were trained to leverpress for continuous reinforcement with food; half were then intubated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA: 400 mg/kg) and half with water. In extinction the PCPA-treated rats responded at a higher rate. In Experiment 2, rats were trained on a random interval schedule and then assigned to two groups, treated as in Experiment 1, and tested in extinction. There was no significant difference in the resistance to extinction of the two groups. In Experiment 3, the responding of rats trained in a punished stepdown response paradigm and then given an intragastric injection of PCPA took longer to recover than the responding of water-injected controls. These observations suggest that serotonergic neurons might play a role in extinction processes.

Animals↗
PubMed1979

Effects of satiety on self-stimulation of the orbitofrontal cortex in the rhesus monkey.

Self-stimulation of the orbitofrontal cortex of the rhesus monkey was found to be attenuated after the monkeys were fed to satiety. Self-stimulation at some other sites (e.g. the nucleus accumbens septi, the region of the substantia nigra, and the caudate nucleus) was relatively unaffected in the same test sessions by the satiety. In recordings from single neurons in the monkey orbitofrontal cortex, neurons of the type found in the lateral hypothalamus with sustained responses associated with the sight of preferred foods were not found. However, some orbitofrontal neurons did respond to the removal of food or other desired objects. These experiments show that self-stimulation of the monkey orbitofrontal cortex in modulated by hunger, and show that some orbitofrontal neurons have complex responses which could be related to the control of feeding.

Animals↗
PubMed1979

Involvement of the trigeminal motor system in brain stem self-stimulation and stimulation-induced behavior.

Anatomical and behavioral correlates of intracranial self-stimulation (ICSS) at sites in the pons suggest the involvement of the trigeminal motor system in brain stimulation reward. 90% of the electrodes terminating in or dorsal to the trigeminal motor nucleus supported ICSS. Stimulation through these ICSS electrodes was usually accompanied by a display of repetitive jaw movement in the period following brain stimulation. There appeared to be a close relation between post-stimulation jaw movement and ICSS. In the motor nucleus there was a positive linear relationship between current intensity and duration of jaw movement. Optimal current intensities for ICSS induced long periods of jaw movement. Extensive lesions of the dorsal pons which included the locus ceruleus had no effect on ICSS in the trigeminal motor system. Therefore it seems unlikely that ICSS in the trigeminal system is mediated by noradrenergic neurons located in the dorsal pontine area. These data suggest that a centripetal analysis of ICSS sites along pathways afferent to the trigeminal motor system may lead to a more complete description of the anatomical correlates of brain stimulation reward. The functional implications of a trigeminal reinforcement mechanism are discussed.

Animals↗
PubMed1978

Electrical stimulation of the amygdala as a conditioned stimulus in a bait-shyness paradigm.

Animals receiving low-intensity electrical stimulation of the basolateral nucleus of the amygdala while drinking plain tap water were injected with toxic doses of lithium chloride to examine whether brain stimulation can serve as a conditioned stimulus in a bait-shyness paradigm. Subjects receiving this pairing greatly reduced their water intake in a retention test, in a similar manner to a group in which saccharin was paired with poisoning. Pairing lithium chloride with stimulation of the amygdala had no effect on subsequent water intake in the absence of brain stimulation. This effect appears to be locus specific, as caudate stimulation could not serve as a conditioned stimulus.

Amygdala↗
PubMed1978

An analysis of dorsal and median raphe self-stimulation: effects of parachlorophenylalanine.

The role of serotonergic systems in intracranial self-stimulation (ICSS) of the dorsal and median raphe nuclei of rats was investigated. Intragastric administration of 400 mg/kg of parachlorophenylalanine (PCPA) depressed ICSS rates in the group with dorsal raphe electrode placements over a similar time course to the depletion of brain serotonin which results from treatment with PCPA. An intrasessional analysis of these behavioral changes on the fourth day after PCPA revealed that dorsal raphe ICSS was depressed over both halves of the 2 hr test session, whereas a significant depression in median raphe ICSS occurred only in the last hr of the session. The data from these studies suggest that brain serotonin systems contribute to the phenomenon of brain-stimulation reward in the dorsal and median raphe nuclei. The involvement of multiple neurochemical substrates of brain stimulation reward is discussed.

Animals↗