The spinal cord, which is 43cm long, is encased in the vertebrae and is the main communication cable between the CNS and the PNS. ‘The nerve fibres running from various parts of the body to and from the brain are gathered together in the spinal cord, where they are protected by the bony spinal vertebrae.’ (Gregory, 2000) The PNS comprises of the 12 pairs of cranial nerves from the brain and 31 pairs of nerves rooted in the spinal cord. Nerve cells called neurones connect to make pathways. Each cell body comprises of a nucleus, dendrites that carry messages to the cell body, axons that carry messages to other neurones, axon terminals, and a myelin coating which provides insulation and speeds up the rate of conduction of Electro-chemical impulses. There are three types of neurone: sensory/afferent, motor/efferent or interneuron/connector. ‘A nerve is a bundle of elongated axons.’ (Gross, 1999, pg67). The gap between each neurone where information is passed is called a synapse.
The PNS can be further divided into the somatic nervous system (SNS), which receives external sensory information and sends signals to the muscles involved in voluntary movements, and the autonomic nervous system (ANS) which controls the automatic muscle control,
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Arousal and anxiety states both influence significantly our behaviour. Arousal, which is the state of ‘general physiological and psychological activation and alertness’ (Hill, 2001, pg256) is increased with greater activity of the sympathetic ANS, the function of which is to prepare the body for action and causes greater attention and mental processing activity. When this is experienced as a negative emotional state then it becomes anxiety.
‘Many of the bodily reactions which result from the ANS are produced by its effect on the endocrine glands.’ (Gross, 1999, pg64). ‘The ANS exerts its effects by direct neural stimulation of body organs and by stimulating the endocrine glands to secrete hormones.’ (Class handout, Satar, 2002). The major endocrine glands are as follows: pituitary gland situated in the brain, the thyroid gland, the parathyroid gland, the adrenal glands, the pancreas, the gonads (ovaries in women and testes in men). These glands are ductless and secrete hormones directly into the bloodstream and have an effect on behaviour because hormones are chemical messengers that affect our physical state. The endocrine system is regulated by the hypothalamus, which exerts its effect on the pituitary gland. Hormones released by the pituitary gland control the secretion of the other endocrine glands.
Biological systems can effect human behaviour, which can be shown through the effects of the intake of drugs. ‘Drugs influence behaviour through their effect on neurotransmitters. The molecules of many commonly used psychoactive drugs are of a very similar shape to those of neurotransmitters and operate in a similar way.’ (Gross, 1999, pg68). First it is necessary to define the term drugs. ‘Drugs are chemicals which have a biological effect on the body’s tissues.’ (Ridings, 2002, pg13). Drugs can have two effects on the biological system; they are either depressants or stimulants. Here we will look at the effect of depressants, in particular alcohol. Depressants are the drugs that depress the CNS; i.e. they slow down mental processes and behaviour. These include tranquilizers, barbiturates, inhalants and alcohol.
Alcohol causes effects on the brain and behaviour and in low doses it can act as a stimulant. The effects of this are that people become more talkative, more outgoing, and less inhibited. Weiss, Lorang, Bloom and Koob (1993) have found that dopamine levels may be involved in the stimulant effects of low doses of alcohol. However, in higher doses alcohol acts as a depressant, impairing sensory and motor functions. Visual activity, sensitivity to taste and smell are all reduced, reflexes become slower reducing reaction time, speech and movement become ‘sluggish’. Memory processes are also affected. ‘Attention to stimuli, ability to encode new information, and short term memory are all decreased.’ . (Rosenhan & Seligman, 1995, pg526).
Chin and Goldstein (1977) identified one of the main effects of alcohol is a ‘non-specific interaction with neuronal membranes’. The physical state of the membrane lipids is made more fluid through the alcohol dissolving in the membrane. This in turn leads to a reduction in neuronal activity and is what causes the debilitating effects on the sensory and motor functions.
Alcohol also affects the neurotransmitter systems, particularly norepinephrine, dopamine and seratonin. (biogenic amines) and gamma-aminobutyric acid (GABA), which are related to altering mood and anxiety reduction. ‘Alcohol enhances the inhibitory actions of GABA, which is the most important inhibitory transmitter in the brain.’ (Nestoros, 1980; Suzdak, Schwartz, Akolnick, and Paul, 1986; cited by Rosenhan & Seligman, 1995, pg526). ‘Alcohol acts at the same GABA receptor complex as the benzodiazepine anti-anxiety drugs (Librium, Valium, etc.) and it is believed that this action is responsible for the anxiety-relieving properties of alcohol (Lister and Durcan, 1989; Koob, Mendelson, Schafer, Wall, Britton and Bloom, 1989; cited by (Rosenhan & Seligman, 1995, pg526).
Alcohol is a widely used, socially acceptable drug in the majority of western cultures, yet it is rarely seen as a drug that so powerfully impacts our biological systems causing the widely recognised changes in our behaviour. Electrical and neuro-chemical activity in the brain is also related to behaviour. Neurones are the cells that process and transmit information and when one fires it sends its electrical impulse which in turn causes chemical changes to take place in the cell, mainly involving sodium and potassium. One neurone can be connected to thousands of other neurones. ‘Each neurone has a threshold of response-the amount of stimulation it needs to receive from other neurones to ‘fire’ its own electrochemical message.’ (Hill, 2001, pg257).
This electrochemical message is transmitted by neurotransmitters (chemicals). Dendrites receive electrochemical impulses from other neurones and the axon ‘transmits electrochemical impulses away from the cell body towards other neurones.’ (Hill, 2001, pg257). The neurotransmitters pass across the synaptic gap and travel to specialised receptor sites on the post-synaptic membrane. Once here the chemicals trigger off an electric impulse, which has an excitatory effect on the next neurone. However, some synaptic connections have an inhibitory effect whereby ‘the neurotransmitters taken up by the target neurone will prevent it from firing.’ (Gregory, 2000). This makes it possible to control a nerve response.’
Some neurones form synapses with glands and muscles. If a motor neurone forms a synapse with muscle fibres it causes those fibres to contract briefly when an axon transmits a message. ‘The strength of the muscular contraction depends on the number of motor neurones whose action potentials are causing the release of neurotransmitters. Whether muscle contraction, or glandular activity is initiated or inhibited or not depends on which neurotransmitters are released.’ (Ridings, 2002, pg4) An example of how this system affects our actions is when we touch a hot object When we touch a hot object there is an increase in the activity of excitatory neurotransmitters. These neurotransmitters communicate with the motor neurones that control the muscles of the hands causing a reflex reaction.
‘Large numbers of neurotransmitters each have their own excitatory or inhibitory effect on certain neurones and are localized in specific groups of neurones and pathways. Normally a single neuron can be labelled by the transmitter it uses: cholinergic, noradrenergic, dopaminergic and serotenergic neurons use acetlycholine (ACh), noradrenaline, dopamine and serotonin respectively,’ (Gross, 1999, pg67).
Looking at one of these neurotransmitters more closely it is possible to realise the implications of the effects these neurotransmitters. For example ‘ACh is particularly prevalent in an area of the forebrain called the hippocampus, which plays a key role in the formation of new memories (Squire, 1987).’ (Atkinson et al, 1996, pg42). With Alzheimer’s disease it has been shown that the neurones producing ACh tend to degenerate, reducing the production of ACh and therefore causing memory loss. ACh is also released at every synapse where a neurone terminates at a skeletal muscle fibre, affecting muscle contraction. This has meant the certain drugs that affect ACh can produce muscle paralysis.