Investigating the effect of CB2 receptor of cannabinoid system in CA1 region of hippocampus on D-AP5 induced amnesia in male Wistar rats.

Number of pages: 87 File Format: word File Code: 32050
Year: 2016 University Degree: Master's degree Category: Psychiatry
  • Part of the Content
  • Contents & Resources
  • Summary of Investigating the effect of CB2 receptor of cannabinoid system in CA1 region of hippocampus on D-AP5 induced amnesia in male Wistar rats.

    Dissertation:

    To receive a doctorate degree in pharmacy

    Persian summary

    Learning and memory are among the complex mechanisms of the brain in which different neuronal pathways play a role in their creation and stabilization. According to the researches, the glutamate-dependent system in the hippocampus region of the brain is effective in creating memory, and the cannabinoid system in this region is involved in memory-related pathways. In this research, we investigate the effect of the cannabinoid system through the CB2 receptor on the destroyed memory caused by the NMDA receptor antagonist (D-AP5) in the hippocampal CA1 region of male Wistar rats. In order to check the memory of the rats, the inhibitory avoidance (passive) method with the step-through model was used and the memory of the rats was checked 24 hours after the training. The results of this study show that the intracerebral injection (ICV, Intra-CA1) of D-AP5 (0.5 & 0.75 µg/rat) caused memory destruction, as well as the intracerebral injection of the specific CB2 receptor antagonist (AM630) depending on The dose (100 ng/rat) causes forgetfulness. If the intracerebral injection of GP1a 50, 75, 100 & 125 ng/rat) - specific CB2 agonist - did not cause significant changes in memory consolidation. The injection of AM630 (50ng/rat) and also the ineffective dose of GP1a (50ng/rat five minutes before the effective doses of D-AP5 (0.75 and 0.50µg/rat) were able to block the memory destruction effect of D-AP5. However, the injection of the ineffective dose of AM630 (50ng/µL) and also the ineffective dose of GP1a (50ng/rat five minutes before D-AP5) (µg/rat 0.25) did not cause a significant change in the memory of rats.

    The results of this research showed that both the CB2 receptor agonist and antagonist are able to correct the amnesia caused by D-AP5, and this may indicate the modulatory effect of the CB2 receptor. It can also be said that there is probably an interference between the cannabinoid system and the glutamate system in the CA1 region.

    1-1. Necessity and importance of the topic

    One ??hundred years after Alzheimer's disease was described for the first time, this disease is still recognized as one of the most important and debilitating health problems of societies. Alzheimer's disease is one of the most important causes of forgetfulness, while other diseases such as vascular problems Cerebral, Lewy body amnesia and frontotemporal amnesia, as well as diseases such as Huntington's, Parkinson's and injuries caused by blows to the brain can also be causes of amnesia. Surveys conducted in 2005 show that 24.3 million people in the world suffer from amnesia. 4.6 million cases are added to this figure every year (one new case every 7 seconds). Every twenty years, this number doubles until it reaches 1.81 million in 2040.

    According to the growing statistics of forgetfulness and diseases related to it, the effort to identify the mechanisms and pathways related to memory formation and causing forgetfulness can be a way to find treatment and also prevention of these diseases.

    1-2-Statement Problem

    Glutamate is the most important excitatory neurotransmitter and also the most abundant amino acid in the diet [6]. NMDA receptors are composed of a four-part complex that has many homologous structures. This receptor has an important effect on many forms of memory and learning [7].

  • Contents & References of Investigating the effect of CB2 receptor of cannabinoid system in CA1 region of hippocampus on D-AP5 induced amnesia in male Wistar rats.

    List:

    Persian Summary..1

    Chapter One: Generalities

    1-1. Necessity and importance of the subject..3

    1-2- Statement of the problem..3

    1-3- Objectives of the study.. 4

    1-3-1-Main objective.. 4

    1-3-2-Objectives Sub..4

    Chapter Two: Review of other texts and studies in this field

    2-1-1-Learning and memory..6

    2-1-2 Types of memory from a physiological point of view. 7

    2-1-2-1 Explicit or explicit memory.. 7

    2-1-2-2 Implicit or conceptual memory. 8

    2-1-2-3 stages of explicit memory formation. 8

    2-1-3- Division of memory based on time. 9

    2-1-4- Different brain areas involved in types of memory. 11

    2-1-5- hippocampus formation.. 12

    2-1-6- long-term strengthening (LTP). 13

    2-1-6-1- Molecular mechanisms of synaptic plasticity. 14

    2-1-7- Condition-dependent learning. 17

    2-1-8- Studies of behavioral methods of memory in animals:. 17

    2-1-9-1- passive preventive learning. 18

    2-1-9-2- Use of injection in passive preventive learning. 19

    2-2- Cannabinoid system.. 19

    2-2-1- Cannabinoids and their importance. 19

    2-2-2- Cannabinoid receptors.. 20

    2-2-2-1- CB1 receptor position in the CNS. 20

    2-2-2-3- location of CB2 receptor. 21

    2-2-2-4 location of CB2 in CNS. 21

    2-2-2-5-secondary peaks of cannabinoid receptors. 21

    2-2-2-6-cannabinoid receptor agonists. 22

    2-2-2-7-types of endocannabinoids. 23

    1-2-2-8-endogenous ligands of cannabinoid receptors. 23

    2-2-3- the function of endocannabinoids in a reversible way. 24

    2-3- Glutamatergic system and the special importance of NMDA receptors. 25

    2-3-1- L-Glutamate.. 25

    2-3-2- Physiological roles.. 25

    2-3-3- CNS reserves.. 26

    2-3-4- How to release metabolism and specific transporter. 27

    2-3-5- types of receptors.. 28

    .2-3-6- sites and regulatory agents. 31

    2-3-7- specific agonists and antagonists. 33

    Chapter 3: Materials and methods

    3-1- The type of study and the studied population. 36

    3-2- Place of experiment.. 36

    3-2-1- Animal house. 36

    3-2-2-Surgery room. 36

    3-2-3-Behavioral test room.. 37

    3-3- Time of conducting experiments.. 37

    3-4- Limitations.. 37

    3-4- Ethical considerations.. 37

    3-6- Materials and methods.. 37

    3-6-1- Equipment and devices the need 37

    3-6-2- Materials and medicines used. 38

    3-8- Memory check device (Step-Through). 39

    3-9- Animals.. 40

    3-10- Surgical procedures.. 40

    3-11- Intracerebral injection of drugs.. 45

    3-12- Behavioral tests.. 46

    3-12-1 Training phase.. 46

    3-12-2- Memory test phase. 47

    3-13- Drug treatments and tests performed. 48

    3-13-1- Test No. 2: Investigating the effect of injection after AM630 training on inhibitory avoidance memory (Dose response chart). Number 1: Investigating the effect of D-AP5 injection after training on inhibitory avoidance memory (Dose response graph). done with D-AP5.. 50

    Chapter Four: Results

    4-1- Investigating the effect of injection after D-AP5 training on inhibitory avoidance memory. 54

    4-2- Investigating the effect of AM630 injection after training on inhibitory avoidance memory. 56

    4-3- Investigating the effect of GP1a injection after training on inhibitory avoidance memory. 58

    4-4- Investigating the effect of AM630 injection after training on the memory of rats treated with D-AP5.60

    4-5- Investigating the effect of GP1a injection after training on the memory of rats treated with D-AP5.61

    Chapter Five: Discussion and conclusion

    5-1- The glutamatergic system in the hippocampus and its importance in memory consolidation. 65

    5-2-Cannabinoid system and its importance in memory consolidation.67

    5-3- Investigating the interference of cannabinoid system and glutamate system in memory stabilization. 68

    Conclusion. 70

    Suggestions. 72

     

    English summary. 73

    Resources. 74

    Source:

     

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Investigating the effect of CB2 receptor of cannabinoid system in CA1 region of hippocampus on D-AP5 induced amnesia in male Wistar rats.