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Biomedical subjects

F Bermudez-Rattoni

Publications and source records attributed to F Bermudez-Rattoni.

12 recordsLinked to original sources
PubMed2003

Blockade of noradrenergic receptors in the basolateral amygdala impairs taste memory.

In conditioned taste aversion (CTA), a subject learns to associate a novel taste (conditioned stimulus, CS) with visceral malaise (unconditioned stimulus, US). Considerable evidence indicates that the noradrenergic system in the amygdala plays an important role in memory consolidation for emotionally arousing experiences. The specific aim of the present set of experiments was to determine the involvement of noradrenergic activity in the basolateral amygdala (BLA) during the US presentation and consolidation of CTA as well as during the consolidation of a nonaversive/incidental gustatory memory. Selective bilateral microinfusions of the beta-adrenergic antagonist propranolol administered into the BLA immediately before intraperitoneal (i.p.) lithium chloride (LiCl) injections disrupted CTA memory. Additionally, propranolol infused into the BLA immediately after a pre-exposure to the saccharin (CS) significantly attenuated latent inhibition. The present findings indicating that alterations in noradrenergic function in the BLA affect taste memory formation, provide additional evidence that the BLA plays a critical role in modulating the consolidation of memory and that the influence is mediated by interactions with other brain regions that support memory for different kinds of experiences.

Adrenergic beta-Antagonists↗
PubMed1999

Cholinergic modulation of neostriatal output: a functional antagonism between different types of muscarinic receptors.

It is demonstrated that acetylcholine released from cholinergic interneurons modulates the excitability of neostriatal projection neurons. Physostigmine and neostigmine increase input resistance (RN) and enhance evoked discharge of spiny projection neurons in a manner similar to muscarine. Muscarinic RN increase occurs in the whole subthreshold voltage range (-100 to -45 mV), remains in the presence of TTX and Cd2+, and can be blocked by the relatively selective M1,4 muscarinic receptor antagonist pirenzepine but not by M2 or M3 selective antagonists. Cs+ occludes muscarinic effects at potentials more negative than -80 mV. A Na+ reduction in the bath occludes muscarinic effects at potentials more positive than -70 mV. Thus, muscarinic effects involve different ionic conductances: inward rectifying and cationic. The relatively selective M2 receptor antagonist AF-DX 116 does not block muscarinic effects on the projection neuron but, surprisingly, has the ability to mimic agonistic actions increasing RN and firing. Both effects are blocked by pirenzepine. HPLC measurements of acetylcholine demonstrate that AF-DX 116 but not pirenzepine greatly increases endogenous acetylcholine release in brain slices. Therefore, the effects of the M2 antagonist on the projection neurons were attributable to autoreceptor block on cholinergic interneurons. These experiments show distinct opposite functions of muscarinic M1- and M2-type receptors in neostriatal output, i.e., the firing of projection neurons. The results suggest that the use of more selective antimuscarinics may be more profitable for the treatment of motor deficits.

Acetylcholine↗
PubMed1991

Reversible inactivation of the insular cortex by tetrodotoxin produces retrograde and anterograde amnesia for inhibitory avoidance and spatial learning.

Tetrodotoxin (TTX; a voltage-sensitive sodium channel blocker) was microinjected bilaterally into the insular (IC), frontal (FC), or parietal (PC) cortex or the ventral caudate nucleus of rats either before or after they were trained in an inhibitory avoidance task. When administered either before or after training, injections of TTX into the IC impaired performance on a 48-hr retention test. Injections of TTX into the PC also impaired retention when administered before training. One week later, rats with cannulae in the IC, FC, and PC received microinjections of TTX either before or after training in a water maze (Morris) spatial learning task and retention was tested 24 hr later. TTX impaired retention when administered to the IC either before or after training. These findings indicate that a functionally intact IC during and after training in these tasks appears to be essential for the storage of long-term memory.

Amnesia↗
PubMed1991

Insular cortex and amygdala lesions differentially affect acquisition on inhibitory avoidance and conditioned taste aversion.

These experiments examined the effects of NMDA-induced lesions of the amygdala and insular (gustatory) cortex (IC) on inhibitory avoidance learning and conditioned taste aversion (CTA) in rats. IC lesions, but not amygdala lesions, disrupted CTA. In contrast, lesions of either brain region disrupted inhibitory avoidance learning. These findings support the view that the IC is strongly involved in the acquisition of external as well as visceral aversively motivated behavior. Despite extensive functional interconnections, these 2 brain regions appear to have different roles in mediating different forms of aversively based learning.

Amygdala↗
PubMed1990

The conditioned stimulus-unconditioned stimulus-feedback feeding sequence: reply to Ellins, von Kluge, and Cramer (1990).

Taste-potentiated noise aversions have been demonstrated in rats (Ellins, Cramer, & Whitmore, 1985; Ellins & von Kluge, 1987; Holder, Bermudez-Rattoni, & Garcia, 1988). However, these aversions are apparently less readily established than taste-potentiated odor aversions suggesting that all exteroceptive stimuli are not equally well potentiated by taste (Holder et al., 1988). Despite the claims of Ellins, von Kluge, and Cramer (1990), we replicated their findings and see no inconsistency between our findings and theirs. Both sets of results are explained by a common theory of conditioning (Garcia, 1989; Garcia & Holder, 1985).

Animals↗
PubMed1988

Taste-potentiated noise-illness associations.

In five experiments we attempted to establish aversions to a noise presented each time thirsty rats licked a water source. Using an apparatus and a procedure similar to those of previous studies which reported noise-illness associations, weak taste-potentiated noise-illness associations were found (Experiment 1). However, when the apparatus and procedure were varied, noise-illness associations were not observed (Experiments 3, 4, and 5). The noise used in all of these failures was readily associated with shock (Experiment 2), which indicates that this noise was salient to the rats and could be associated with an aversive event. These failures to find noise-illness associations occurred despite the fact that the conditions were chosen to maximize the likelihood of observing these associations. Taste-illness associations always developed normally. The results are consistent with the idea that conditioned aversions to all exteroceptive stimuli are not equally well potentiated by taste.

Animals↗
PubMed1988

Odor and taste aversions conditioned in anesthetized rats.

Conditioned flavor aversions (CFA) are acquired by anesthetized rats but effects of various anesthetics on acquisition of aversions for separate odor and taste components are unknown. In Experiment 1, rats drank tomato juice and then were tranquilized with "Innovar-Vet" or "Rompun" before receiving injections of lithium chloride. Neither drug interfered with acquisition of aversions. Innovar-Vet alone produced no aversions; Rompun alone produced mild aversions but did not enhance aversions when combined with lithium. In Experiments 2 and 3, rats received a compound odor/taste cue as they drank and then were anesthetized with pentobarbital before lithium injections. Anesthesia alone produced negligible aversions but facilitated taste-lithium aversions. During odor tests, odor aversions were weaker than taste aversions. These data extend previous work and suggest that CFA does not result from ordinary classical conditioning. A tripartite notation that unites CFA and classical conditioning is discussed.

Anesthetics↗
PubMed1983

Addictive agents and intracranial stimulation (ICS): novel antagonists and agonists of morphine and pressing for ICS.

Rats fixed with chronically indwelling bipolar electrodes pressed for intracranial stimulation (ICS) of the lateral hypothalamus during daily sessions. The effects of two antagonists of morphine (Win 44,441 and naloxone) were then assessed. Naloxone (10 mg/kg) produced its characteristic reduction in pressing. Win 44, 441 produced a reliable increase in pressing at doses as small as 1 mg/kg. Large doses of morphine (10 mg/kg) produced its characteristic effects: depression in pressing when given 1 hr before the test session and facilitation when given 3 hr before the test session. Win 44,441 antagonized morphine's depressive effects. Other compounds (Win 44,156, Win 42,156), having similar structure to Win 44,441 but having agonist and mixed agonist-antagonist activity with respect to analgesia, also facilitated pressing for ICS. All three compounds' effects on pressing for ICS were antagonized by naloxone. It is inferred that opioids' facilitatory effects on pressing for ICS are separable from opioids' other capabilities such as production of analgesia.

Animals↗
PubMed1983

Flavor-illness aversions: potentiation of odor by taste is disrupted by application of novocaine into amygdala.

Taste and odor have different properties in toxiphobic conditioning. When each is used alone, taste becomes aversive when followed by immediate or delayed poison, while odor becomes aversive only if followed by immediate poison. However, if odor and taste are presented as a compound and followed by delayed poison, then odor does become aversive when tested alone. It is as if taste has potentiated the odor signal. Several experiments assessed the role of the amygdala in this potentiation effect by anesthetizing the amygdala with 10% novocaine. Novocaine applied 30 min before presentation (Pre-CS) of an odor-taste compound disrupted the potentiated odor aversion but not the taste aversion. In contrast, novocaine applied 1 min after the compound odor-taste or 1 min prior to LiCl poison did not dissociate odor and taste aversions; both odor and taste aversions were facilitated. Novocaine applied 30 min before an odor alone also disrupted an odor aversion induced by immediate LiCl. But identical treatment did not disrupt odor avoidance conditioned by immediate foot-shock, suggesting that amygdala anesthesia does not simply produce anosmia. Pre-CS novocaine treatment also disrupted flavor neophobia prior to conditioning. The results suggest that novocaine applied to the amygdala disrupts the integration of odor with taste and illness during toxiphobic conditioning.

Amygdala↗
PubMed1981

Intracerebral administration of naloxone and drinking in water-deprived rats.

In 24-hr water-deprived rats, naloxone, at various doses (0, 12.5, 25, 50 micrograms/rat), was administered prior to a 15-min drinking period. Infusions were made bilaterally into each lateral ventricle, frontal cortex, lateral preoptic area, lateral hypothalamus, and caudate nucleus. Naloxone reliably reduced water consumption at 50 micrograms/rat when infused into the lateral ventricles and lateral hypothalamic areas. When comparable doses of naloxone were given by peripheral injection, no effect on drinking was observed. There appeared to be a trend developing for greater sensitivity to naloxone when infusions were made into a particular part of the hypothalamus. These data support the idea that naloxone reduces drinking by acting at central opiate receptors.

Animals↗
PubMed1980

Early neuronal alterations caused by experimental thinner inhalation in young rats.

Young rats were treated with thinner inhalations (50 and 100 p.p.m., v/v). The brains of treated and control animals were studied with standard techniques of light and electron microscopy and with ultrastructural cytochemical method for localization of RNA. No alterations were found in the group treated with a single session of inhalation, irrespective of the dose. Animals treated with 10 or 20 sessions showed altered neurons in cerebral cortex, caudate nucleus, hypothalamus and cerebellar cortex. More frequent alterations were: small nucleoli with loss of their reticular structure and a marked decrease of their normal granular component; diminution of perichromatin fibrils and of ribosomes. In the animals treated with high doses of thinner (20 sessions, 100 p.p.m.) a small number of neurons show an increased amount of lysosomes, autophagosomes and neurofibrillar hypertrophy. These results suggest that thinner inhalation causes an initial impairment of gene transcription and of RNA processing followed by neuronal degeneration.

Animals↗