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L A Chiodo

Publications and source records attributed to L A Chiodo.

At least 73 records · Page 4Linked to original sources
PubMed1983

Substantia nigra dopamine neurons: alterations in basal discharge rates and autoreceptor sensitivity induced by estrogen.

Treatment with estrogen was shown to exert differential effects on two subpopulations of putative substantia nigra dopamine-containing neurons as demonstrated by single cell electrophysiological techniques. The acute administration of 17 beta-estradiol to anesthetized, ovariectomized female rats increased the spontaneous activity of Type A, but decreased that of Type B neurons in a dose-dependent manner. Moreover, pretreatment with 17 beta-estradiol benzoate, 48 hr before recording, increased the response of Type A neurons to both small doses of the dopamine receptor agonist, apomorphine, and to microiontophoretically applied dopamine. In contrast, the responsiveness of Type B neurons to these same manipulations was significantly diminished by this pretreatment. Taken together, these data suggest that prior exposure to estrogen enhances the sensitivity of dopamine autoreceptors located on Type A neurons while attenuating the sensitivity of the autoreceptors located on Type B cells. The demonstration that estrogen has complex, bidirectional, rather than simple, unidirectional influences on the activity of dopamine cells of the nigra might aid in the understanding of current controversies in both the experimental animal and human clinical literature bearing on behaviorally relevant interactions between estrogen and brain dopamine systems.

Animals↗
PubMed1983

Typical and atypical neuroleptics: differential effects of chronic administration on the activity of A9 and A10 midbrain dopaminergic neurons.

Extracellular single unit recording techniques were used to study the effects of both acute and repeated oral neuroleptic administration on the in vivo activity of rat A9 and A10 dopaminergic (DA) neurons. All antipsychotic drugs examined acutely (haloperidol, l-sulpiride, chlorpromazine, and clozapine) increased the number of spontaneously firing DA neurons in both A9 and A10 compared to controls. Repeated (21 day) treatment with haloperidol, l-sulpiride, and chlorpromazine (antipsychotic drugs which can cause extrapyramidal side effects) markedly reduced the number of active DA cells below control levels in both regions. The "silent" DA neurons were in an apparent state of tonic depolarization inactivation since they could be induced to discharge by the microiontophoretic application of the inhibitory neurotransmitter gamma-aminobutyric acid, but not the excitatory amino acid glutamate. The depolarization inactivation observed may be specific for antipsychotic drugs since a non-neuroleptic phenothiazine (promethazine), the inactive isomer of sulpiride (d-sulpiride), and a tricyclic antidepressant (desmethylimipramine) neither increased DA activity when given acutely nor induced depolarization inactivation when administered repeatedly. In contrast to the other drugs tested, repeated treatment with clozapine (an effective antipsychotic drug which does not produce extrapyramidal side effects) resulted in the depolarization inactivation of A10 neurons but not A9 cells. These data suggest that neuroleptics which can induce extrapyramidal side effects produce depolarization inactivation of both A9 and A10 neurons whereas antipsychotic drugs which lack this property inactivate only A10 neurons. It is suggested that the time-dependent development of A9 DA neuron inactivation induced by repeated neuroleptic treatment may provide a mechanism for understanding the delayed onset of extrapyramidal side effects often observed with these drugs.

Animals↗
PubMed1980

Glucose suppresses basal firing and haloperidol-induced increases in the firing rate of central dopaminergic neurons.

In the rat, doses of glucose sufficient to raise glucose concentrations in the blood to levels equivalent to those produced by a meal or stress suppress the firing of dopamine-containing neurons located within the substantia nigra. Glucose also prevents or reverses the increase in discharge rates of dopaminergic cells normally elicited by the antipsychotic agent haloperidol.

Action Potentials↗
PubMed1980

Electroconvulsive shock: progressive dopamine autoreceptor subsensitivity independent of repeated treatment.

Repeated electroconvulsive shock, applied to rats, induces a subsensitivity of dopamine autoreceptors located in the substantia nigra as indexed by single-unit electrophysiological techniques. This reduced sensitivity is time-dependent, since effects similar to those seen with repeated treatment were also observed when single electroconvulsive shock was followed by an appropriate treatment-free interval. These data, coupled with identical results after the repeated administration of tricyclic antidepressants, raise the possibility that a reduction of dopamine autoreceptor sensitivity could underlie both electroconvulsive shock and pharmacological treatment of depression.

Animals↗
PubMed1980

Repeated tricyclics induce a progressive dopamine autoreceptor subsensitivity independent of daily drug treatment.

Dopamine (DA) has largely been ignored in considering possible mechanisms underlying the therapeutic effects of tricyclic anti-depressants (TCA). Most previous work done has focused on the ability of some TCAs to block the in vitro re-uptake of DA--an effect which unfortunately requires very high doses. Recently, however, Serra et al. proposed that TCAs may exert their therapeutic effects by inducing a subsensitivity of presynaptic receptors located on the dendrites and soma of DA neurones (DA autoreceptors). This hypothesis was directly tested by examining the influence of TCAs on the demonstrated ability of the DA agonist, apomorphine, to depress selectively the spontaneous activity of single DA cells. We now report that repeated administration of both typical and atypical TCAs induces a progressive subsensitivity of DA autoreceptors, and that this gradual augmentation of DA autoreceptor subsensitivity depends on the passage of time rather than daily TCA administration. The latter finding suggests that daily drug administration may not be therapeutically necessary.

Action Potentials↗
PubMed1977

Impairment in a T-maze task following unilateral lateral hypothalamic lesions.

Rats with unilateral LH lesions showed great difficulty performing a contraversive turn to escape shock in a T-maze. Rats that were required to turn to the side ipsilateral to the side of their lesion did not show this performance deficit. The impairment in contraversive responding was shown to dissipate over time. It is proposed that animals with LH lesions do not suffer learning disabilities in escape-avoidance tasks, but can not activate motor behavior directed toward the side contralateral to their lesion.

Animals↗