Nutritional depletion of total mixed rations by European starlings: Projected effects on dairy cow performance and potential intervention strategies to mitigate damage.

European starlings are an invasive bird species in North America that are known to cause damage to commercial dairies through the consumption of total mixed rations (TMR) destined for dairy cows. We hypothesized that large foraging flocks of starlings alter the physical composition of TMR, and that this change may be significant enough to affect milk production. To better determine if production losses could potentially occur in commercial dairies as a consequence of feed consumption by foraging flocks of starlings, we conducted controlled feeding experiments using a TMR sourced from a commercial dairy that is chronically plagued with seasonal starling damage. European starlings selected the high-energy fraction of the TMR and reduced starch and crude fat availability. Using the dairy National Research Council production model equations, the nutritional changes measured in the controlled feeding experiments could potentially reduce the productivity of dairies. Model output suggests that for Holsteins producing 32 kg of milk/d, total required net energy intake (NEI) was 31.5 Mcal/d. Within the reference TMR, NEI supplied was 29.3 Mcal/d, whereas within the starling-consumed TMR NEI supplied was 27.7 Mcal/d. Following our nutrition experiments, we assessed the efficacy of pelleted feed as a deterrent strategy for bird damage management in commercial dairies. Six different pelleted feed treatments of differing diameter were offered to starlings. All pellets of 0.95 cm diameter or larger inhibited starling consumption by ≥79%.

Self-organization of foraging behaviour: from simplicity to complexity without goals.

A herbivore faces challenges while foraging-ongoing changes in its physiological condition along with variation in the nutrient and toxin concentrations of foods, spatially and temporally-that make selecting a nutritious diet a vital affair. Foraging behaviours arise from simple rules that operate across levels of resolution from cells and organs to individuals and their interactions with social and physical environments. At all these levels, behaviour is a function of its consequences: a behaviour operating on the environment to induce changes is itself changed by those events. Thus, behaviour emerges from its own functioning-behaviour self-organizes-not from that of its surroundings. This ostensible autonomy notwith-standing, no self-organizing system (cell, organ, or individual) is independent of its environs because existence consists of an ongoing exchange of energy and matter. According to this view, the notion of cause and effect is replaced with functional relationships between behaviours and environmental consequences. Changes in physical environments alter the distribution, abundance, nutritional, and toxicological characteristics of plants, which affect food preference. Social interactions early in life influence behaviour in various ways: animals prefer familiar foods and environments, and they prefer to be with companions. Animals in unfamiliar environments often walk farther, ingest less food, and suffer more from malnutrition and toxicity than animals in familiar environments. An individual's food preferences-and its ability to discriminate familiar from novel foods-arise from the functional integration of sensory (smell, taste, texture) and postingestive (effects of nutrients and toxins on chemo-, osmo-, and mechano-receptors) effects. The ability to discriminate among foods is critical for survival: all problems with poisonous plants are due to an inability to discriminate or a lack of alternatives. Animals eat a variety of foods as a result of nearing or exceeding tolerance limits for sensory and postingestive effects unique to each food. After eating any food too frequently or excessively, the likelihood increases that animals will eat alternative foods owing to exceeding sensory-, nutrient-, and toxin-specific tolerance limits. Cyclic patterns of intake of a variety of foods reflect seemingly chaotic interactions among flavours, nutrients, and toxins interacting along continua.

Long-term effects of excitatory amino acid antagonists NBQX and MK-801 on the developing brain.

Because of the critical role of excitatory amino acids (EAAs) in epileptogenesis and seizure-induced brain damage, EAA antagonists are now being considered as a possible therapy for seizures. However, during development EAAs play a pivotal role in learning, memory, and brain plasticity. To evaluate the long-term effects of a short course of EAA antagonists on the developing brain, a non-NMDA antagonist, NBQX, or a NMDA antagonist, MK-801, were administered over 7 days by osmotic pumps stereotaxically implanted into the lateral ventricles of normal 10 day old rats. Alternatively, 10 and 20 day old rats received a 7 day course of intraperitoneal (i.p.) NBQX. One month later, the NBQX-, MK-801-treated rats, and controls underwent a series of behavioral studies: handling test, open field, and Morris water maze. Flurothyl inhalation was used to test seizure susceptibility in all groups. Although all of the rats treated with NBQX via osmotic pumps has spontaneous seizure, rats surviving infusion of EAAs had no deficits in learning, memory, or behavior and did not differ from controls in seizure susceptibility with flurothyl. In the developing animal, a short-term course of EAA antagonists leads to no long-term adverse effects on behavior or seizure susceptibility.

Effect of kainic acid-induced status epilepticus on inositol-trisphosphate and seizure-induced brain damage in mature and immature animals.

We investigated the role of excitatory amino acids in the activation of the phosphoinositide pathway during kainic acid-induced seizures in mature and immature animals. Kainic acid caused more severe seizures in the immature animals, but no hippocampal damage or induction of phosphoinositide hydrolysis. In mature animals, seizures were mild but severe hippocampal damage was seen and was associated with a marked and sustained release of inositol-trisphosphate, suggesting a role of this pathway and intracellular calcium stores in seizure-induced brain damage.

Long-term behavioral deficits following pilocarpine seizures in immature rats.

The effect of seizures on subsequent long-term behavior was studied in immature rats. A similar severity of seizures were induced in 20-day old rats (P20) and 45-day old rats (P45) by intraperitoneal injections of pilocarpine at doses of 200 mg/kg and 380 mg/kg, respectively. Immediately after injection of pilocarpine, prolonged seizures with electroencephalographic ictal discharges were observed in both groups of rats. These seizures were followed by seemingly complete neurological recovery. In rats that received pilocarpine at P45 spontaneous recurrent seizures appeared after 4-10 days and persisted until completion of the study at P100. Behavioral tests performed when the rats were fully mature demonstrated that they were more aggressive when handled, more active in open field, and had deficits in learning platform position in the water maze as compared to controls. Furthermore, flurothyl seizure latency was significantly lower in pilocarpine-treated P45 rats than controls. Histology examination showed gross cell loss in the CA3 subfield of the hippocampus in four out of six pilocarpine-treated rats while no cell loss was found in control rats. Rats that received pilocarpine at P20, despite having more severe seizures than the P45 rats, had no histological lesions, did not develop spontaneous recurrent seizures, and had no significant difference in the flurothyl seizure latency test when compared to their controls. While there was no difference between the control and pilocarpine-treated rats in the handling and open field test, P20 rats receiving pilocarpine were slower in learning platform position in the water maze than the controls. Rats receiving pilocarpine at P45 performed significantly more poorly than rats treated at P20 in the water maze. These results suggest that prolonged seizures in immature rats can cause long-term behavioral deficits. However, the severity and nature of these deficits are highly age dependent.