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Biomedical subjects

Gary B Kaplan

Publications and source records attributed to Gary B Kaplan.

9 recordsLinked to original sources
PubMed2005

Cigarette smoking topography in smokers with schizophrenia and matched non-psychiatric controls.

Smoking is highly prevalent among people with schizophrenia, and little is known about factors that affect smoking in these patients. One basic question is whether smoking behavior differs for smokers with schizophrenia compared to equally nicotine-dependent smokers who do not have a major mental illness. In this study, 20 smokers with schizophrenia or schizoaffective disorder (SCZ) and 20 non-psychiatric smokers (CON) underwent smoking topography assessments. The groups were matched on age, gender, daily smoking rate, years of regular smoking and nicotine dependence rating. Results indicate that, compared to the CON participants, the SCZ participants smoked significantly more total puffs (SCZ: 58.5 +/- 48.3; CON: 21.3 +/- 9.4) and puffs per cigarette (SCZ: 12.3 +/- 6.0; CON: 8.9 +/- 2.3) and had shorter inter-puff intervals (SCZ: 21.9 +/- 9.7 s; CON: 42.0 +/- 21.5 s), larger total cigarette puff volumes (SCZ: 583 +/- 169 ml; CON: 429 +/- 159 ml) and higher carbon monoxide boosts (SCZ: 3.8+/-5.4 ppm; CON: 1.0 +/- 2.5 ppm). Test-retest reliabilities were good to excellent for most smoking measures in both groups. These findings suggest that smokers with schizophrenia smoke more intensely than matched non-psychiatric smokers and that their smoking behavior is reliable when assessed under laboratory conditions.

Adolescent↗
PubMed2005

Subjective and physiological responses to smoking cues in smokers with schizophrenia.

The prevalence of smoking is high among people with schizophrenia. Although several research groups are developing smoking treatments for these smokers, abstinence rates to date have been modest. Methodological tools such as cue exposure are useful in clinical research with smokers in general, but the value of these paradigms with smokers with schizophrenia has yet to be established. The aim of the present study was to determine the subjective and physiological effects of exposure to in vivo smoking cues in smokers with schizophrenia. A total of 25 heavy smokers with schizophrenia or schizoaffective disorder were assessed while nonabstinent and after 2-hr smoking abstinence. Urge to smoke, mood, nicotine withdrawal symptoms, heart rate, and blood pressure were measured during a precue relaxation period, after exposure to neutral cues, and after exposure to smoking cues. Results indicate that both exposure to smoking cues and brief abstinence increased urge levels, nicotine withdrawal symptom levels, and negative affect. Abstinence did not amplify the effects of cues on urges or other cue reactivity measures. These results indicate that smoking cue reactivity laboratory models may be useful for investigating potential smoking treatments for, or neurobiological contributions to, smoking behavior in smokers with schizophrenia.

Blood Pressure↗
PubMed2004

Antipsychotics regulate cyclic AMP-dependent protein kinase and phosphorylated cyclic AMP response element-binding protein in striatal and cortical brain regions in mice.

Adenosine 3',5'-monophosphate (cAMP) and cAMP-dependent protein kinase (PKA) signaling have been implicated in antipsychotic drug action. This study examines the effects of acute antipsychotic treatment using typical (haloperidol) and atypical (olanzapine) agents on cAMP signaling in dorsal striatum, nucleus accumbens and medial prefrontal cortex in mice. PKA catalytic subunit (PKA-c) and phosphorylated cAMP response element-binding protein (pCREB) levels were measured to evaluate antipsychotic drug effects. Nuclear PKA-c levels increased in the dorsal striatum after haloperidol and olanzapine treatment. In medial prefrontal cortex, olanzapine produced dose-dependent decreases in PKA-c and pCREB levels. The differential effects of typical versus atypical antipsychotic agents on PKA and pCREB in striatal and cortical regions illustrate the diverging actions of these agents on cAMP pathways.

Animals↗
PubMed2003

GABA(B) receptor activation in the ventral tegmental area inhibits the acquisition and expression of opiate-induced motor sensitization.

Opiate-induced motor sensitization refers to the progressive and enduring motor response that develops after intermittent drug administration, and results from neuroadaptive changes in ventral tegmental area (VTA) and nucleus accumbens (NAc) neurons. Repeated activation of mu-opioid receptors localized on gamma-aminobutyric acid (GABA) neurons in the VTA enhances dopaminergic cell activity and stimulates dopamine release in the nucleus accumbens. We hypothesize that GABA(B) receptor agonist treatment in the VTA blocks morphine-induced motor stimulation, motor sensitization, and accumbal Fos immunoreactivity by inhibiting the activation of dopaminergic neurons. First, C57BL/6 mice were coadministered a single subcutaneous injection of morphine with intra-VTA baclofen, a GABA(B) receptor agonist. Baclofen produced a dose-dependent inhibition of opiate-induced motor stimulation that was attenuated by 2-hydroxysaclofen, a GABA(B) receptor antagonist. Next, morphine was administered on days 1, 3, 5, and 9 and mice demonstrated sensitization to its motor stimulant effects and concomitant induction of Fos immunoreactivity in the NAc shell (NAcS) but not NAc core. Intra-VTA baclofen administered during morphine pretreatment blocked the acquisition of morphine-induced motor sensitization and Fos activation in the NAcS. Intra-VTA baclofen administered only on day 9 blocked the expression of morphine-induced motor sensitization and Fos activation in the NAcS. A linear relationship was found between morphine-induced motor activity and accumbal Fos in single- and repeated-dose treatment groups. In conclusion, GABA(B) receptor stimulation in the VTA blocked opiate-induced motor stimulation and motor sensitization by inhibiting the activation of NAcS neurons. GABA(B) receptor agonists may be useful pharmacological treatments in altering the behavioral effects of opiates.

Animals↗
PubMed2003

Baclofen inhibits opiate-induced conditioned place preference and associated induction of Fos in cortical and limbic regions.

In C57BL/6 mice, pretreatment with GABA(B) receptor agonist baclofen blocked the rewarding effects of morphine as measured by acquisition of conditioned place preference. Fos immunoreactivity, a neuronal activity marker, was induced in opiate conditioned mice in several forebrain regions including the nucleus accumbens core and shell, anterior cingulate cortex, and prelimbic cortex. Baclofen pretreatment blocked the induction of Fos in opiate conditioned subjects. These result suggest that GABA(B) receptor transmission has a role in reversing morphine-induced activation of motivational circuitry and conditioned reward.

Analgesics, Opioid↗
PubMed2002

Opiate-induced motor stimulation is regulated by gamma-aminobutyric acid type B receptors found in the ventral tegmental area in mice.

Recent studies suggest that gamma-aminobutyric acid type B (GABA(B)) receptors located on dopaminergic cells in the ventral tegmental area (VTA) regulate mesolimbic dopaminergic (A10) activity. In the current study, we identified GABA(B) receptor subtypes in the area of the VTA and examined their role in modulating acute opiate actions. We studied the effects of intra-VTA infusions of the selective GABA(B) agonist baclofen on morphine-induced locomotor stimulation and A10 neuronal activation. Drug treatments were followed by ambulatory activity monitoring for 180 min. Intra-VTA baclofen treatment produced a 70% inhibition of morphine-stimulated locomotor activity. Furthermore, functional activation of A10 neurons was assessed by immunohistochemical staining of c-Fos in the nucleus accumbens (NAc), where A10 neurons terminate. We found that morphine treatment increased the levels of Fos-positive nuclei in the NAc, while intra-VTA baclofen treatment reversed morphine's effects. Finally, GABA(B) receptor subtypes and isoforms were identified in the ventromedial mesencephalon using immunoblotting. We demonstrated the presence of GABA(B)R1a (130 kDa), GABA(B)R1b (100 kDa), and GABA(B)R2 (120 kDa) receptor subtypes in this region. These results suggest that GABA(B) receptor isoforms are found in the VTA and their activation results in the blockade of behavioral effects of opiates via inhibition of dopaminergic neurotransmission.

Animals↗