This paradigm distinguished between two hypotheses not previously directly addressed. Do repeated exposures to cocaine at critical times during pregnancy, when the neural mechanisms that support maternal behavior are being read, alter some fundamental neural underpinning of maternal behavior in rats? Alternatively, does cocaine alter maternal behavior only when circulating? During the 4 hr after cocaine injection (20 or 40 mg/kg), there were significant deficits in maternal behavior. In contrast, 16 hr after cocaine injection, drug-injected females, in which plasma cocaine had fallen to nondetectable levels, showed the normal maternal behavior of saline-injected controls. This pattern of impaired maternal behavior after cocaine injection, followed by normal behavior as blood levels returned to zero, was replicated over 8 days. It was concluded that cocaine impairs maternal behavior only when circulating and does not have a residual effect in the transiently drug-free, chronically drug-treated dam.

The finding that only 8% of a group of regular cola soft drink consumers could detect the effect of the caffeine concentration found in most cola soft drinks is at variance with the claim made by soft drink manufacturers that caffeine is added to soft drinks because it plays an integral role in the flavor profile. It is valuable for the general public, the medical community, and regulatory agencies to recognize that the high rates of consumption of caffeinated soft drinks more likely reflect the mood-altering and physical dependence-producing effects of caffeine as a central nervous system-active drug than its subtle effects as a flavoring agent. Arch Fam Med. 2000;9:727-734

Cocaine was microinfused bilaterally (50 microg/0.5 microl/side) into the medial preoptic area (MPOA) or nucleus accumbens (NA), 2 regions within the rat brain neural circuit known to mediate maternal behavior (MB). Additionally, 2 sites not involved in this neural circuit, the dorsal striatum and dorsal medial hippocampus, were used as control sites. Microinfusion of cocaine into the MPOA or NA impaired MB, whereas infusion into the control sites did not. MB impairment was not temporally coincident with the increased locomotor activity, also documented after cocaine infusion into the MPOA or NA, arguing strongly that impaired MB is a direct, specific effect of cocaine in these areas, not a derivative of increased motor activity. This is the first demonstration that cocaine action on single central nervous system (CNS) sites can impair MB to the same extent as systemic injections. Thus, cocaine's simultaneous effect on multiple CNS sites is not required for MB impairment.

No abstract

Subcutaneous injections of cocaine hydrochloride in sterile physiological saline were administered to rats at a dosage of 20 or 40 mg.kg-1. Resultant skin lesions included focal areas of alopecia (within 1 to 2 days) which progressed to necrosis (within 2 to 7 days). Histologically, the skin lesions were characterized by necrotizing panniculitis and vascular necrosis, with only small numbers of inflammatory cells. The lesions may be ischemic in nature, and associated with cytotoxic properties of cocaine.