pupate in. this manipulated behavior was longer lasting and more prominent the longer the larvae were attached to the spider. strepsiptera strepsiptera of the family myrmecolacidae can cause their ant host to linger on the tips of grass leaves, increasing the chance of being found by the parasite's males (in case of females) and putting them in a good position for male emergence (in case of males). rhizocephala members of the order rhizocephala such as sacculina carcini alter male hosts' hormonal balance, to encourage nurturing behavior similar to that seen in females. the parasite usually spends its entire life within the host; however, if it is removed from the host in a laboratory setting, male hosts will subsequently grow partial or complete female gonads. mechanisms the way in which parasites induce behavioral changes in hosts has been compared to the way a neurobiologist would effect a similar change in a lab. a scientist may stimulate a certain pathway in order to produce a specific behavior, such as increased appetite or lowered anxiety; parasites also produce specific behavioral changes in their hosts, but rather than stimulate specific neurological pathways, they appear to target broader areas of the central nervous system. while the proximate mechanisms underlying this broad targeting have not been fully characterized, two mechanisms used by parasites to alter behavior in vertebrate hosts have been identified: infection of the central nervous system and altered neurochemical communication. central nervous system infection some parasites alter host behavior by infecting neurons in the host's central nervous system. the host's central nervous system responds to the parasite as it would to any other infection. the hallmarks of such response include local inflammation and the release of chemicals such as cytokines. the immune response itself is responsible for induced behavioral changes in many cases of parasitic infection. parasites that are known to induce behavioral changes through central nervous system inflammation in their hosts include toxoplasma gondii in rats, trypanosoma cruzi in mice and plasmodium mexicanum in the mexican lizard. immune response toxoplasma gondii induces behavioural changes in rats by infecting central nervous system neurons. while some parasites exploit their hosts' typical immune responses, others seem to alter the immune response itself. for example, the typical immune response in rodents is characterized by heightened anxiety. infection with toxoplasma gondii inhibits this response, increasing the risk of predation by t. gondii's subsequent hosts. research suggests that the inhibited anxiety-response could be the result of immunological damage to the limbic system. altered neurotransmission parasites that induce behavioral changes in their hosts often exploit the regulation of social behavior in the brain. social behavior is regulated by neurotransmitters, such as dopamine and serotonin, in the emotional centers of the brain – primarily the amygdala and the hypothalamus, and although parasites may be capable of stimulating specific neurochemical pathways to induce behavioral changes, evidence suggests that they alter neurochemical communication through broad rather than specific targeting. for example, toxoplasma gondii attaches to the hypothalamus rather than target a specific cellular pathway; this broad targeting leads to a widespread increase in host dopamine levels, which may in turn account for the loss of aversion to cat odor. in some cases, t. gondii is believed to cause increases in dopamine levels by secreting another compound, l-dopa, which may trigger a rise in dopamine levels, though concrete evidence for this mechanism has not yet been demonstrated. this rise in dopamine levels induces a loss of aversion to cat odor in the rats, increasing the risk of predation by cats, t. gondii's definitive host. the mechanistic details underlying the increase in dopamine levels and the way it affects the rat's behavioral change remain elusive. the emerald cockroach wasp alters behavior through the injection of venom directly into the host's brain, causing hypokinesia. this is achieved by a reduction in dopamine and octopamine activity, which affects the transmission of interneurons involved in the escape response; so while the host's brain circuitry responsible for movement control is still functional – and indeed it will slog along when pulled by the wasp – the nervous system is in a depressed state. put differently: the wasp's toxin affects not the host's ability to move, but its motivation to do so. the original function of such secretions may have been to suppress the immune system of the host, as described above. the trematode schistosoma mansoni secretes opioid peptides into the host's bloodstream, influencing both its immune response and neural function. other sources suggest a possible origin in molecular mimicry. other mechanisms mermithid nematodes infect arthropods, residing in their haemocoel (circulatory cavity) and manipulating their hemolymph osmolality to trigger water-seeking behavior. the means by which they do so are unknown. evolutionary perspective addition of intermediate hosts for complex life cycles to emerge in parasites, the addition of an intermediate host species must be beneficial, i.e. result in a higher fitness. it is probable that most parasites with complex life cycles evolved from simple life cycles; the evolution from simple to complex life cycles has been analyzed theoretically, and it has been shown that trophically transmitted parasites (parasites that transmit from a prey host to a predator host during predation) can be favored by the addition of an intermediate prey host if the population density of the intermediate host is higher than that of the definitive host. additional factors that catalyze this transfer are high predation rates, and a low natural mortality rate of the intermediate host. parasites with a single host species are faced with the problem of not being able to survive in higher trophic levels and therefore dying with their prey host. the development of complex life cycles is most likely an adaptation of the parasite to survive in the predator. the development of parasite increased trophic transmission is a further adaptation in relation to a complex life cycle, where the parasite increases its transmission to a definitive host by manipulating its intermediate host. evolution of induced behaviors the adaptive manipulation hypothesis posits that specific behavioral alterations induced in a host can be used by parasites to increase their fitness. under this hypothesis, induced behaviors are the result of natural selection acting upon the parasite's extended phenotype (in this case its host's behavior). many behaviors induced by obligate parasites to complete their lifecycles are examples of adaptive manipulation because of their clear relationship to parasite fitness. for example, evidence has shown that infection by the parasitic worm pomphorhynchus laevis leads to altered drifting behavior in its intermediate host, the amphipod gammarus pulex; this altered behavior increases its host's predation risk by fish which are p. laevis's definitive hosts. the induced behavioral change in the host thus leads to the parasite's increased success in completing its life cycle. in general, whether a specific behavioral change serves an adaptive purpose for the parasite, the host, or both, depends on the entire "host-parasite system": the life cycle of the pathogen, its virulence and the host's immune response. conversely, evolved behaviors of the host may be a result of adaptations to parasitism.