Psychology Project Topics

The Behavioral Teratogenic Effect of Cimetidine on the Offspring’s of Albino Rats

The Behavioral Teratogenic Effect of Cimetidine on the Offspring’s of Albino Rats

The Behavioral Teratogenic Effect of Cimetidine on the Offspring’s of Albino Rats

Chapter One


This study aims to examine:

  • If exposure to cimetidine will manifest any significant effect on the behaviour of their offsprings.
  • If the intake of cimetidine during pregnancy have an effect on the birth weight of offspring.
  • If the intake of cimetidine during pregnancy affect learning and memory in offsprings whose mother’s where exposed to cimetidine.




        In most species, sexual behaviour principally serves the purposes of reproduction. In humans and in some other primates, other purposes for sexual behaviour in addition to reproduction have evolved. In the human such purposes have been shaped and influence by cultural factors, so that human sexuality has been expressed in many different ways, varying across cultures and over history. Inspire of these powerful cultural influences, biological factors involved in sexual annual and response remain fundamental to human sexual experience and need to be taken into account in our attempt top understand and explained the complexities and problems as well as the positive aspect of the human sexual condition.


        Sexual response in the adult is characterized by a subjective sense of sexual excitement or arousal and physiological changes in the body, involving the genital but also the cardiovascular system and a tendency, particularly in the male, to pursue sexual stimulation until orgasm occurs. This process is a complex interaction between cognitive (information processing), central brain mechanisms, including sexual arousal and other emotional stated, and peripheral physiological processes such as penis in the male and clitoral, vulvar, and pelvic vaso-congestion in the female. It can usually be regarded as a “psychosomatic circle” in which awareness of changes in the genitalia feeds back to influence the  central processes in either an augmenting, excitatory, or inhibitory fashion. The activation of this psychosomatic system can start at vari9us points in the cycle, such as the occurrence of a sexually exciting thought, a sexually stimulating image or tactile stimulation of those parts of the body which are erotically sensitive. The information processing component identifies what is “sexual” a process which is having influenced by learning and cultural factors. The central brain mechanisms activate the neural signals that descend mainly down the spinal cord, along pathways that include reflex centers at certain level of the cord (Steers, 2000), to evolve the peripheral sexual responses. The sensory input from these peripheral responses and further tactile stimulation, as well as continuing informative processing level of central arousal and excitement to the point when the orgasm is triggered. Conversely, if the ongoing process is interpreted in negative terms suggesting threat, danger, fear of failure, or some other negative consequence, then the process may lead to inhibition of further sexual response.

There is much that we do not understand about this psychosomatic circle. In the case of the cognitive component, a distinction has been made between automatic cognitive processes (of which the subject is more or less unaware) and controlled cognitive processes, involving ongoing awareness of the subject. In addition, the impact of emotional states on these cognitive processes has been recognized as important (Janssen and Everaerd, 1993). As yet, however, we understand little about the nature and origins of these automatic processes. The interface between such information processing (i.e. how we interpret what is happening to us in the sexual context) and the physiological system involved in sexual response is also little understood. Research on brain mechanisms involved in sexual response has largely depended on animal studies, and much has been learned in this area over the past few years, particularly in relation to male sexual response (Steers, 2000). Although such studies are important and helpful, they cannot investigate the role of cognitive processing of the ki9nd that characterizes the human. Also, as we learn more about the physiological processes, so their complexity increases to the extent that our earlier, simple explanatory models become overwhelmed. At an earlier stage, we could envisage most of the key response, both in the brain and in the periphery, as being controlled by a small number of monoamines, like norepihephrine, dopamine, serotonin and acetylcholine. We then learned that neuropathies, a different class of chemical messenger, were involved often working in combination with our more traditional monoamines. Whereas we once knew of a handful of such neuropathies, they now number more than a hundred. Excitatory and inhibitory amino acids such as glutamate and GABA (gamma-aminobutyric acid) then became

Recognized as probably the most ubiquitous neurotransmitters in the central nervous system. Modern techniques of molecular biology are finding more and more different receptors for these chemical messengers, each with potentially different function. According to Heaton (2000) “our current capacity to identify and manipulate these targets of controls in the process of explosive growth from an estimated few hundred identifiable systems to well over 100,000” (P.562). Although, whether this is an exaggeration or not, such growth of inevitable fragmented knowledge may have benefits in our search for treatments for sexual problems, it is arguable that in the face of this overwhelming complexity we should revert to simpler but new conceptual systems to guide our research and shape our explanatory models.





        It involves the use of multi-group experimental design with three independent groups i.e. the control group, the experimental group 1 and the experimental group 2.


        The subject for this study includes three pregnant females albino rats whose pregnancy ranges between one-two days old at the time of purchase, they were purchased from a breeders at the college of medicine, Ambrose Alli University (AAU) Ekpoma. They were all between one-two month old.

19 pups littered by the 3 pregnant albino rats of both the control group and experimental groups were also used as the subject in the study.




Earlier on, three hypotheses were stated and tested scientifically and statistically during the cause of this study.

Hypothesis 1: This state that there will be a significant difference between the offspring’s of albino rats who were injected with cimetidine to those who were not injected with cimetidine on a T-maze test i.e. offspring’s of albino rats who were injected with cimetidine during gestation period will have a significant low memory than those offspring of mothers who were not injected with cimetidine during gestation period. In regard to this, the hypothesis was tested with a one way analysis of variance (ANOVA) presented below:



        In this chapter, short discussions about the hypothesis are made, conclusions reached and recommendation made.


The result of this study extends previous research on the “behavioural teratogenic effects of cimetidine on the offspring’s of albino rats”. The variables in the study include “cimetidine” which is the independent variable and the variable of interest, as well as “the offspring’s born to albino rats” which is the dependent variable.

During the cause of this study, three hypotheses were advanced and tested. The following studies supports the  first hypothesis which stated that there will be a significant difference between the offspring’s of albino rats who were injected with cimetidine to those born of mothers wo were not injected with cimetidine on a T-maze test. This was confirmed (Df (2,9) = 33.96, P< .01) indicating that offspring of albino rats who were injected with cimetidine during gestation will have a significant low memory than those born of mother who were not injected with cimetidine during gestation. This findings is in consonance with the works of singer and others  (2005), who established the fact that prenatal cocaine exposure can impair visual attention, visual memory etc. In infancy and throughout the first year of life. This also corresponds to the work of (Fried, 2002; Fried, Wlatkinson and Gray, 2003; Goldschmidt et al, 2008: Richardson, Goldschmidt, and Larkby, 2007) who observed that prenatal marijuana exposure was related to memory difficulties and that it had persistent negative effects through age 16 on higher-order thinking, including problem solving, memory, planning, impulsive, and attention.

The second hypothesis which stated that offspring’s of albino rats who were injected with cimetidine during gestation will significantly perform low on the performance ability test (classical maze) than those born to mothers who were not injected with cimetidine during gestation was also tested and confirmed (Df (2,9) = 14.15, P> .05). this finding is in consonance with the findings of (Fried, 2002; Herrmann, King, and Weitzman, 2008) who established that prenatal tobacco exposure has been consistently associated with lower IQ throughout childhood. In another study, they concluded that children of women who smoked more than 16 cigarettes a day while pregnant had a mean IQ in the average range, but 6 points lower than those of unexposed children “Fried, Watkinson, and Gray 2003”. This findings corresponds to the work of Goldschmidt (2004) who established the fact that children of women who smoked one or more marijuana joints a day during the first trimesters were more likely than controls to exhibit deficits in school achievement, particularly in reading and spelling.

The third hypothesis which stated that offspring’s born to albino rats who were injected with cimetidine during gestation will have a significant low birth weight than those offspring’s of mother who were not injected with cimetidine during gestation: This finding is in consonance with the findings of Salihu and Wilson (2007) who established that tobacco use had been linked to low birth weight and pregnancy complications etc. This also corresponds to the work of Das, Poole, and Bada, (2004) who established that heroin exposure decreases birth weight, birth weight and head circumference.


It is safe to conclude that cimetidine intake during pregnancy will have effects on the memory and performance ability of child. It was also discovered that cimetidine intake will significantly affects the birth weight of children born of mothers who where exposed to cimetidine during pregnancy. However, substances used during pregnancy can affect the developing fetus both directly, through the passage of the drug through the placenta, and indirectly, through poor maternal health habits and environmental conditions. Numerous well designed studies indicate that specific learning and behavior problems may result from prenatal exposure to cimetidine, tobacco and illicit drugs in combination with negative environmental conditions postpartum. Longitudinal studies indicate that some of the negative effects of cocaine, tobacco, marijuana and other teratogenic agent such as cimetidine exposure persist into late childhood and adolescence. Although, some early CNS symptoms remit over the first year of life, they may be precursors to later developmental outcomes.

Developmental outcomes of prenatal drug-exposed children are determined by factors including the specific drug or drugs, dosage, and timing of prenatal exposure as well as pre- and postnatal environmental conditions, including continued caregiver drug use, psychological symptoms, quality of the home environment, postnatal exposures to lead and other toxins, caregiver stability, and type of caregiver.

Pregnancy is a unique time when a woman may seek treatment out of concern for a health and well-being of her child. To prevent postpartum substance abuse relapse, interventions should focus on cassation rather than temporary abstinence. The ongoing consequences of prenatal substance abuse on child growth and development should be emphasized, and follow up should continue unto the postpartum period (Muhuri and G frorer, 2009). Interventions that reduce substance abuse in the general population are now being investigated in pregnant substance abusers with promising results. Theuse of CM appears to increase treatment retention and prolong abstinence in pregnant women with cocaine, opiate, and nicotine dependence. Some medications used to treat addiction, such as methadone, can be relatively safe for pregnant women and their babies.


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  • Accornero VH, et al. prenatal cocaine exposure: am examination of childhood externalizing and internalizing behavior problems at age 7 years. Epidemiologine, Psichiatria sociale. 2006, 15(1): 20-29. (PMC free article) (PubMed)
  • Accornero VH, et al, impact of prenatal cocaine exposure on attention and response inhibition as assessed by continuous performance tests. Journal of developmental and behavioral pediatrics. 2007, 28(3):195-205. (PMC free article) (PubMed).
  • Addis A, et al. fetal effects of cocaine: an updated metaomalysis. Reproductive toxicology. 2001, 15(4): 341-369. (PubMed)
  • Ajcovson SW, et al. new evidence fro neurobehavioral effects of in utero cocaine exposure journal of pediatrics. 1996; 129(4); 581-590.
  • Anad & Van Thiel (1932)
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