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Biomedical subjects

R F Berman

Publications and source records attributed to R F Berman.

At least 55 records · Page 3Linked to original sources
PubMed1984

Anticonvulsant effects of adenosine analogues on amygdaloid-kindled seizures in rats.

Male Long-Evans rats were stereotaxically implanted with a bipolar electrode in the central amygdala and with a stainless-steel cannula in the lateral cerebral ventricle. Rats were then kindled once daily until 3 consecutive Stage 5 kindled seizures were elicited. Adenosine analogues were injected into the lateral cerebral ventricle to examine their effects on behavioral seizures and afterdischarge duration following a kindling stimulus. 5'-N-ethylcarboxamidoadenosine (NECA) and (-)-N-(1-methyl-2-phenylethyl)-adenosine(L-phenylisopropyladenosine) (L-PIA) produced dose-related reductions of amygdaloid-kindled seizures with NECA exhibiting slightly more potent anticonvulsant activity than L-PIA. Parenteral injections of caffeine, at a dose which had no effect on seizure parameters, antagonized the anticonvulsant effects of NECA. These results are consistent with the notion that adenosine is a modulator of synaptic activity in the CNS and methylxanthines exert a specific antagonism of central adenosine receptors.

Adenosine↗
PubMed1984

A procedure to enhance auditory brainstem response reliability in unrestrained rats.

We describe a procedure to record auditory evoked potentials in unrestrained rats. A key feature of this procedure is the attachment of a miniature speaker to the rat's head during recording, so that the distance between the speaker and the rat's ear is held constant. A speaker base is permanently attached to the acrylic supporting the electrode connector. This system enables the recording of reliable auditory evoked potentials over long periods of time with minimal concern for the rat's position or posture.

Acoustic Stimulation↗
PubMed1984

In vivo phosphorylation of postsynaptic density proteins.

In vivo protein phosphorylation was examined in postsynaptic density-enriched fractions isolated from rat brain. In vivo phosphorylation was carried out by injecting rats intraventricularly with [32P]orthophosphate followed by isolation of postsynaptic densities from pooled cerebral cortices. In vivo 32P-labeled postsynaptic densities were then fractionated by sodium dodecylsulfate-polyacrylamide slab gel electrophoresis and stained with Coomassie Blue. The protein banding pattern was typical for postsynaptic densities. The principal polypeptide component occurred in a single band at an apparent molecular weight of 51,000. Autoradiographs of the dried gels showed a major peak of radioactivity associated with the 51,000 molecular weight component for the in vivo labeled postsynaptic density fraction. Additional minor peaks of radioactivity were also observed. These results represent the first demonstration that proteins associated with the postsynaptic density readily incorporate phosphate in vivo and may represent a major and important class of synaptic phosphoproteins.

Animals↗
PubMed1984

Effects of naloxone on ethanol dependence in rats.

Adult male Long-Evans rats were maintained on an ethanol-containing liquid diet. During development of ethanol dependence, the rats were given daily i.p. injections of either naloxone (2 mg/kg) or saline daily. At the beginning of ethanol withdrawal, the rats were injected with either naloxone (10 mg/kg) or saline i.p. Rats injected with naloxone during the development of ethanol dependence consumed significantly more of the ethanol diet and therefore more ethanol than rats injected with saline. Rats treated with naloxone throughout both the development of ethanol dependence and during ethanol-withdrawal showed delayed or reduced withdrawal symptomatology compared to rats injected with only saline, naloxone only during the development of dependence and naloxone only during ethanol withdrawal. These results indicate that naloxone can alter the effects of chronic ethanol exposure and further suggest that ethanol may exert some of its actions via the brain opioid system.

Alcohol Drinking↗
PubMed1983

Amnesia attenuation specificity: propranolol reverses norepinephrine but not cycloheximide-induced amnesia.

Post-trial injections of norepinephrine (NE) or cycloheximide (CHX) into the amygdala produces a long-term retention deficity (amnesia) for a 1-trial footshock experience in rats. concomitant post-trial injections of the adrenergic antagonist, propranolol, prevents NE-, but not CHX-induced amnesia. These results indicate separate mechanisms of action for amnesia produced by intracranial CHX and NE injections.

Amnesia↗
PubMed1982

Opiate modification of amygdaloid-kindled seizures in rats.

Male Long-Evans rats were stereotaxically implanted bilaterally with bipolar electrodes in the central amygdala. Rats were then kindled once daily for 1 sec until 3 consecutive Stage V [25] kindled seizures were elicited. On the following day, animals were injected (IP) with either saline, naloxone (10 mg/kg), naltrexone (10mg/kg) or morphine sulfate (10 mg/kg) and again stimulated at the kindling stimulation parameters. Saline injected animals continued to show long bilateral AD's and behaviors (i.e., forelimb clonus, rearing, falling) typical of Stage V kindled animals. In contrast, rats injected with naloxone or naltrexone showed reduced behavioral seizures. Potentiation of post-ictal spiking by morphine in amygdaloid-kindled rats was also observed supporting previous reports [7,21]. In a second experiment, the reduction of kindled seizure serverity by naloxone was systematically replicated. It is concluded that opiates can significantly modify amygdaloid-kindled seizures, and that brain endorphins may play a role in the development or maintenance of an amygdaloid-kindled seizure focus.

Amygdala↗
PubMed1981

A quantitative regional analysis of protein synthesis inhibition in the rat brain following localized injection of cycloheximide.

Previous work has shown that bilateral injection of as little as 10 microgram of cycloheximide (CHX) into the amygdala, but not into the internal capsule, caused a time-dependent disruption of long-term retention of passive avoidance training. Under these conditions, protein synthesis in the entire brain was inhibited by less than 10%. The present study was undertaken to quantify the resulting inhibition of protein synthesis in various brain regions (amygdala, internal capsule, caudate, cortex, hippocampus, thalamus, hypothalamus and the entire half brain). Rats were subcutaneously injected with L-[14C-methyl]methionine following unilateral administration of CHX via a cannula implanted in either the amygdala or the internal capsule. Regional inhibition of protein synthesis was determined by analysis of autoradiograms from different brain levels using an image analyzing computer to measure the optical densities of microscopic areas corresponding to discrete neuroanatomical structures. Regional patterns of inhibition were assessed: (a) after injection of different doses of CHX (10 or 20 microgram) into the amygdala; (b) after injection of 20 microgram of CHX into the amygdala or internal capsule; and (c) at different times (0.5, 3, 6 and 24 h) after injection of 20 microgram of CHX into the amygdala. Quantitative results are presented for the temporal and spatial patterns of protein synthesis inhibition caused by CHX injection. Since injection of CHX into the amygdala resulted in a profound inhibition of protein synthesis in both the amygdala and internal capsule while injection into the thermal capsule only caused a marked inhibition in the capsule itself, these results provide a possible explanation for our earlier observation that injection of CHX into the amygdala produced a retention deficit while injection into the adjacent internal capsule had no effect on memory function. These observations on protein synthesis inhibition support our earlier hypothesis that CHX injected into the amygdala might impair memory by virtue of its action on amygdaloid function rather than as a result of its effect on the brain as a whole.

Amygdala↗
PubMed1977

Taste aversion disruption by drug pretreatment: dissociative and drug-specific effects.

Disruption of taste aversion learning following the administration of the same drug prior to and during conditioning (intra-agent disruption) was shown to be greater than disruption following the administration of one drug prior to conditioning and another during conditioning (inter-agent disruption). Comparable dosages of ethanol and lithium chloride served as unconditioned stimuli. Inter-agent disruptions are attributed to a dissociation of conditioned and unconditioned stimuli, while intra-agent disruptions are attributed to both a dissociative effect and drug-specific effects. Intra-agent disruption was correlated with an independent measure of tolerance, suggesting tolerance constitutes at least a portion of the drug-specific effects.

Animals↗
PubMed1976

Posttrial hippocampal, amygdaloid, and lateral hypothalamic electrical stimulation: effects on short- and long-term memory of an appetitive experience.

Water-deprived rats were given 150 licks of a 10% sucrose solution, followed 4 sec later by 30 sec of low-intensity electrical brain stimulation applied through bipolar electrodes implanted bilaterally in the dorsal hippocampus, amygdala, or lateral hypothalamus. Retention of the licking experience was then tested either 90 sec or 24 hr after the 150-lick experience by measuring the number of licks taken on an empty drinking tube. Rats that received hippocampal stimulation licked the empty tube less than controls did during the 24-hr, but not during the 90-sec, retention test. These data suggest that the hippocampus may be critically involved in processes (e.g., consolidation) mediating long-term, but not short-term, memory. Compared with controls, rats that received amygdala stimulation did not exhibit any changes in licking at either retention test. Rats that received lateral hypothalamic stimulation showed more licking compared with controls during the 90-sec, but not the 24-hr, retention test. Subsequent tests suggested that facilitation of short-term memory may have been influenced by stimulation-induced motivational changes.

Amygdala↗
PubMed1975

Effect of preconditioning unconditioned stimulus experience on learned taste aversions.

One taste-aversion study using male Long-Evans rats in which ethanol was the unconditioned stimulus (UCS) and six studies in which lithium chloride (LiCl) was the UCS demonstrate that (a) exposure to the UCS prior to conditioning retards subsequent acquisition of learned taste aversions; (b) a single preconditioning UCS exposure is sufficient to attenuate conditioning; (c) the preconditioning UCS exposure must occur within a limited period prior to conditioning to attenuate learning; (d) repeated conditioning trials will override the effect of prior exposure to the UCS; (e) tolerance to the UCS is not a necessary condition for the attenuation effect to occur; (f) pairing the preconditioning UCS with a novel flavor other than the CS does not remove the preexposure effect, although it may reduce its magnitude; and (g) the degree of disruption is a positive function of preconditioning UCS dosage and an inverse function of conditioning UCS dosage.

Animals↗
PubMedDate not supplied

Alcohol and the auditory brain-stem response, brain temperature, and blood alcohol curves: explanation of a paradox.

A previous study found temperature-independent effects of alcohol upon the auditory brain-stem response (ABR): another found only temperature-dependent effects. To understand these paradoxical results, we measured the ABR and brain temperature in unrestrained rats before and after 3 alcohol doses (0.5, 2.5 and 5.0 g/kg). In a separate experiment, blood ethanol concentration (BEC) curves were determined for the same 3 alcohol doses. Integration of dose- and time-related effects of alcohol upon the ABR, brain temperature, and BEC suggested that alcohol has both temperature-dependent and temperature-independent effects, which vary according to dose and BEC curve phase. Temperature-dependent effects are likely during a BEC curve falling phase with a steep slope, following a high alcohol dose. Temperature-independent effects are likely during a BEC curve falling phase with a flatter slope, when BEC is still high following a moderate alcohol dose, or during a BEC curve rising phase soon after alcohol administration. The two previous studies with contradictory results each used procedural combinations likely to produce their respective results. Although both research groups administered similar alcohol doses, their alcohol solutions, administration routes, and time of ABR recording differed; consequently, they probably recorded ABR during different portions of BEC curve falling phases, which differed in slope. In view of the complex interactions among alcohol effects, BEC curve phase, temperature, and the ABR, we recommend temperature measurement during alcohol-ABR studies.

Analysis of Variance↗