Rats have separate ‘defensive’ and ‘reproductive’ pathways gating innate behavioral response to, respectively, predator or sexual stimuli 
. Given the precipitous evolutionary pressures of both reproduction and predation, these pathways run as direct projections from the olfactory bulb to the limbic system and generate rapid and stereotyped behavioral output (see and ). Although functionally distinct, the limbic ‘defensive’ and ‘reproductive’ pathways run in parallel through the medial amygdala and hypothalamus in close anatomical proximity. Previous findings of increased Toxoplasma
cyst density in these areas compel the possibility that Toxoplasma
is somehow perturbing its surrounding neural environment and thereby manipulating the host response to cat urine. We find, indeed, that Toxoplasma
infection perturbs the ‘defensive’ pathway in the infected rat during exposure to cat urine, shifting neural activity to the nearby ‘reproductive’ pathway, specifically the MEApd (see ).
Schematic Model of Toxoplasma Induced Changes to Host Limbic System.
The MEApd projects robustly to hypothalamic nuclei involved in sexual arousal and the generation of approach behavior. The MEApd is responsive to a variety of social odorants 
, but responds strongest to opposite-sex mating stimuli. Lesioning the MEApd reduces, specifically, attraction to opposite-sex odors 
. Interestingly, Toxoplasma
increased MEApd activity during cat urine exposure to levels mimicking uninfected rats during female exposure (). This suggests that the specifically increased magnitude of MEApd activity in male Toxoplasma
infected rats is biasing the processing of the cat urine toward the sexual, ‘reproductive’ pathway (). Plausibly, this shift is altering the salience of the cat urine stimuli and mitigating the defensive response by creating, in its stead, a competing attraction to the cat urine.
Little is known about how, if at all, Toxoplasma
cysts exert themselves in the host brain. Much work remains to be done, based on striking findings that Toxoplasma
raises whole brain dopamine levels in mice by up to 15% 
and that dopamine receptor antagonists block rodent host attraction to cat urine 
. These data suggest a link between dopamine, a primary neurotransmitter in decision-making and reward, and the altered behavior. Intriguingly, the Toxoplasma
genome contains a homolog of tyrosine hydroxylase 
, the rate-limiting enzyme in the vertebrate synthesis of dopamine, raising the possibility that Toxoplasma
is altering dopamine levels by synthesizing its own tyrosine hydroxylase.
From the ground, Toxoplasma
finds its way into other hosts besides rats, including cows, sheep, pigs and many grazing livestock. Ingestion of undercooked meat from infected livestock and the profligacy of private cat ownership are responsible for a strikingly high number of human chronic Toxoplasma
infections. Approximately one-third of humans are seropositive for Toxoplasma
across the world 
, and several recent studies find infection increases risk for schizophrenia 
and obsessive compulsive disorder 
, diseases noted for elevated dopamine levels and disturbed amygdala function 
. Our results are therefore of wide interest, as the ability of Toxoplasma
to dramatically alter host behavior and proper amygdala functioning may extend beyond the rat into ancillary Toxoplasma
hosts, including humans.