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Biomedical subjects

L Kokkinidis

Publications and source records attributed to L Kokkinidis.

At least 55 records · Page 3Linked to original sources
PubMed1983

Region-specific reductions of intracranial self-stimulation after uncontrollable stress: possible effects on reward processes.

Rates of responding for intracranial self-stimulation from the medial forebrain bundle, nucleus accumbens and substantia nigra were evaluated in mice that had been exposed to either escapable shock, yoked inescapable shock or no shock treatment. Whereas performance was unaffected by escapable shock, marked reductions of responding from the medial forebrain bundle and nucleus accumbens were evident following the uncontrollable shock treatment. Responding from the substantia nigra was unaffected by the stress treatment. Uncontrollable shock is thought to reduce the rewarding value of responding for electrical brain stimulation from those brain regions in which stressors are known to influence dopamine activity.

Animals↗
PubMed1982

Preference for fixed vs self-selected durations of brain stimulation in rats administered D-amphetamine sulphate.

Rats implanted with stimulating electrodes in the region of the lateral hypothalamus were allowed the opportunity to respond on (a) a fixed duration lever (b) a variable duration lever or (c) were given a choice between responding on either the lever that delivered the fixed duration of electrical brain stimulation or the lever that allowed the animal to control the duration of electrical brain stimulation. Amphetamine increased rates of responding in both the fixed and variable duration conditions but total duration of brain stimulation was comparable in the two conditions. When given a choice of levers, rats did not prefer either the fixed or variable duration lever. After treatment with d-amphetamine, however, a marked preference for the variable duration lever was observed, although total duration of brain stimulation received in the choice procedure was comparable to that received when either the fixed or variable levers were presented alone. These findings were discussed in terms of brain stimulation preference following amphetamine and its relationship to reward value in the rat.

Animals↗
PubMed1982

Potentiation of d-amphetamine and L-dopa-induced acoustic startle activity after long-term exposure to amphetamine.

The startle response to an auditory stimulus was potentiated by treatment with d-amphetamine sulfate. Administration of L-dopa after pretreatment with the extracerebral decarboxylase inhibitor MK-486 also increased startle activity. After long-term exposure to amphetamine the startle response to L-dopa and d-amphetamine was enhanced. These findings are consistent with the consequences of long-term amphetamine administration on other amphetamine-induced behaviors (e.g. stereotype), and are discussed in terms of the effects of long-term amphetamine treatment on pre- and postsynaptic dopamine receptors and serotonin.

Acoustic Stimulation↗
PubMed1982

Stress-induced facilitation of acoustic startle after d-amphetamine administration.

Administration of d-amphetamine enhanced the startle response to an auditory stimulus. In contrast to saline treated mice, startle activity after amphetamine administration did not wane with repeated exposure to the auditory stimulus. Rather, the effects of amphetamine on startle activity increased as a function of stimulus presentation. Whereas exposure to isolation stress or inescapable shock had no effect on startle activity, both types of stress potentiated the effects of amphetamine on startle arousal. The observation that stress sensitized animals to later amphetamine administration is consistent with the effects of stress on other amphetamine behaviors, e.g., stereotypy. Results were related to the development of dopamine post-synaptic receptor supersensitivity after exposure to stress and were discussed in terms of the role played by stress in the expression of behavioral arousal, in the etiology of schizophrenia.

Acoustic Stimulation↗
PubMed1981

Post-amphetamine depression of self-stimulation behavior in rats: prophylactic effects of lithium.

Rats reliably interrupted a photobeam for electrical brain stimulation when electrodes were situated in the substantia nigra. The reinforcing value of electrical brain stimulation diminished, markedly, when animals were exposed to long-term amphetamine treatment and then tested in the absence of the drug. Chronic lithium treatment administered in conjunction with amphetamine protected against the development of the post-amphetamine depression of self-stimulation responding. These findings were not related to drug-induced changes in locomotor activity.

Animals↗
PubMed1981

Amphetamine psychosis and schizophrenia: a dual model.

Several of the behavioral consequences of acute and chronic amphetamine treatment were evaluated and related to the underlying neurochemical correlates of drug treatment. It was suggested that decreased noradrenergic activity after long-term amphetamine treatment influences stimulus sampling, whereas enhanced dopaminergic activity was responsible for the progressive augmentation of stereotypy and self-stimulation behavior observed after long-term exposure to amphetamine. It was hypothesized that amphetamine-induced psychosis and the symptomatology associated with schizophrenia are related to alterations in both norepinephrine and dopamine activity.

Amphetamine↗
PubMed1980

Response sensitization and depression following long-term amphetamine treatment in a self-stimulation paradigm.

The effects of long-term amphetamine treatment were evaluated on responding supported by self-stimulation of the substantia nigra. Rats repeatedly treated with d-amphetamine, and tested with a low dose of the drug that ordinarily has no behavioral effect, showed higher response rates than animals repeatedly treated with saline and tested with the same dose of amphetamine. In contrast, a depression in responding was observed among animals that received long-term amphetamine administration and were tested with saline. The effects of long-term amphetamine treatment on self-stimulation could not be explained by the intrusion of drug-induced competitive behaviors such as locomotor activity and stereotypy. The results were attributed to changes in dopamine neurotransmission following prolonged exposure to amphetamine and were also discussed in terms of an animal model for 'amphetamine psychosis' and 'postamphetamine depression' in man.

Amphetamine↗
PubMed1980

Intracranial self-stimulation in mice using a modified hole-board task: effects of d-amphetamine.

Mice implanted with stimulating electrodes in the lateral hypothalamus demonstrated reliable self-stimulation rates when given the opportunity to break a photobeam in a modified hole-board task. Self-stimulation rates were enhanced by low dosages of d-amphetamine but were depressed by high dosages. The dose-dependent effects of amphetamine could not be accounted for by changes in exploratory hole-board activity and were discussed in terms of an interaction between the rewarding properties of electrical brain stimulation and the reinforcing properties of amphetamine administration.

Animals↗
PubMed1980

Post-amphetamine depression of self-stimulation responding from the substantia nigra: reversal by tricyclic antidepressants.

The effects of long-term amphetamine treatment were examined on self-stimulation responding from the substantia nigra. Rates of self-stimulation responding were substantially depressed among rats chronically treated with amphetamine and tested in the absence of the drug. When rats were subsequently retested after a two day hiatus in which they received imipramine or amitriptyline, the post-amphetamine depression of rates of self-stimulation responding was mitigated. The efficacy of imipramine and amitriptyline in reversing the post-amphetamine depression of self-stimulation responding was also evident during a continuation of the drug (imipramine or amitriptyline)/test sequence, for seven test sessions. The results of the present investigation were related to changes in dopamine and acetylcholine neurotransmission following long-term amphetamine treatement.

Amitriptyline↗
PubMed1979

Circling behavior following systemic d-amphetamine administration: potential noradrenergic and dopaminergic involvement.

Systemic treatment with d-amphetamine produced a dose-dependent increase in the circling behavior of normal mice. Treatment with both alpha-methyl-p-tyrosine (alpha-MpT) and FLA-63 antagonized the amphetamine-induced circling behavior. Similarly, blockade of B-adrenergic receptors by propranolol and dopamine receptors by haloperidol reversed the circling response elicited by amphetamine. In contrast to alpha-MpT and haloperidol, however, neither FLA-63 nor propranolol attenuated the locomotor excitation engendered by amphetamine. Following repeated d-amphetamine injections the circling ordinarily induced by a single injection was abolished, whereas the locomotor effects of amphetamine remained unaltered. These findings are consistent with earlier work suggesting that tolerance may occur in those behaviors that involve a noradrenergic component.

Animals↗
PubMed1978

Involvement of norepinephrine in startle arousal after acute and chronic d-amphetamine administration.

Treatment with d-amphetamine produced a dose-dependent increase in startle amplitude in response to a buzzer. This increase appeared to be a reflection of a sensitization effect, i.e., enhanced responsivity as a function of repeated stimulus presentations. Treatment with alpha-methyl-p-tyrosine, which reduced whole brain concentrations of dopamine (DA) and norepinephrine (NE), or treatment with FLA-63, which reduced only NE, antagonized the effects of d-amphetamine on the startle reflex, suggesting a role of NE in this behavior. Startle amplitude was also reduced following chronic d-amphetamine treatment. The effect of d-amphetamine on startle was found to be independent of changes in drug-induced locomotor excitation. The data of the present investigation, together with earlier reports, suggests that tolerance occurs to those behaviors that involve a noradrenergic component.

Animals↗