Older adults with cancer and common comorbidities-challenges and opportunities in improving their cancer treatment outcomes.

The older American population is rapidly increasing, and millions of older adults will be cancer survivors with comorbidities. This population faces specific challenges regarding treatment and has unique clinical needs. Recognizing this need, the National Cancer Institute, in collaboration with the National Institute on Aging, hosted a webinar series, entitled Cancer, Aging, and Comorbidities.

Role of oestrous cycle and orbitofrontal cortex in oxycodone seeking after 15-day abstinence in female rats.

Relapse to oxycodone seeking progressively increases after abstinence in rats, a phenomenon termed incubation of oxycodone craving. We have previously shown that the orbitofrontal cortex (OFC) plays a critical role in incubation of oxycodone craving in male rats. Here, we examined the effect of oestrous cycle on incubated oxycodone seeking in female rats, and whether the critical role of OFC in incubated oxycodone seeking generalizes to female rats.

Incubation of Oxycodone Craving Following Adult-Onset and Adolescent-Onset Oxycodone Self-Administration in Male Rats.

Relapse is a major obstacle to curb the ongoing epidemic of prescription opioid abuse. We and others previously demonstrated that oxycodone seeking in adult rats progressively increases after abstinence from oxycodone self-administration (incubation of oxycodone craving). In humans, the onset of oxycodone use in adolescents may increase individuals' vulnerability to later opioid addiction.

Neural mechanisms underlying incubation of methamphetamine craving: A mini-review.

Cue-induced drug craving and seeking progressively increases during abstinence. This "incubation of drug craving" phenomenon has been observed in both laboratory animals and humans. Preclinical studies identified several neural mechanisms underlying incubation of drug craving after forced abstinence, primarily focusing on cocaine.

Epigenetic Mechanisms in Drug Relapse.

A growing body of evidence from the past 15 years implicates epigenetic mechanisms in the behavioral effects of addictive drugs. The main focus of these studies has been epigenetic mechanisms of psychomotor sensitization and drug reinforcement, as assessed by the conditioned place preference and drug self-administration procedures. Some of these studies have documented long-lasting changes in the expression of epigenetic enzymes and molecules that persist for weeks after the last drug exposure.

PKC inhibition decreases amphetamine-maintained responding under a progressive-ratio schedule of reinforcement.

Protein kinase C (PKC) is important for the mechanism of action of amphetamine (AMPH). Inhibiting PKC blocks AMPH-stimulated increases in extracellular dopamine levels and AMPH-stimulated locomotor activity. This study examined the effects of PKC inhibition on the reinforcing properties of AMPH.

Role of orbitofrontal cortex in incubation of oxycodone craving in male rats.

One of the main challenges in treating opioid-use disorders is relapse during abstinence, triggered by re-exposure to drug-associated cues. Previous studies have demonstrated that drug-seeking in rats progressively increases over time during withdrawal (incubation of drug craving). Here, we used male rats and examined neural mechanisms underlying incubation of craving to oxycodone, a commonly abused prescription opioid, and we focused on orbitofrontal cortex (OFC), a brain region previously implicated in incubation of heroin craving.

Correction to: The protein kinase Cβ-selective inhibitor, enzastaurin, attenuates amphetamine-stimulated locomotor activity and self-administration behaviors in rats.

The middle initial of the author should be "A" instead of "C". The correct presentation of the author name is Colleen A. Carpenter.

The protein kinase Cβ-selective inhibitor, enzastaurin, attenuates amphetamine-stimulated locomotor activity and self-administration behaviors in rats.

Rationale: Pathological amphetamine (AMPH) use is a serious public health concern with no pharmacological treatment options. Protein kinase Cβ (PKCβ) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCβ attenuates AMPH-stimulated dopamine efflux in vivo. With this in mind, inhibition of PKCβ may be a viable therapeutic target for AMPH use disorder.

Direct and Systemic Administration of a CNS-Permeant Tamoxifen Analog Reduces Amphetamine-Induced Dopamine Release and Reinforcing Effects.

Amphetamines (AMPHs) are globally abused. With no effective treatment for AMPH addiction to date, there is urgent need for the identification of druggable targets that mediate the reinforcing action of this stimulant class. AMPH-stimulated dopamine efflux is modulated by protein kinase C (PKC) activation.